Cell Proliferation[JOURNAL]
Sun
200 papers
Endocrine Resistance Score Based on Three Key Genes Predicts Prognosis and Reveals Potential Therapeutic Targets for ER+HER2- Breast Cancer.
Ping L, Zhu L, Chen N … +5 more , Liu X, Zhong J, Sun X, Tang H, Zhang K
Cell Prolif · 2026 Mar · PMID 40664624 · Full text
Endocrine resistance is a leading cause of mortality in oestrogen receptor-positive and human epidermal growth factor receptor 2-negative (ER+HER2-) breast cancer (BC), highlighting the urgent need to understand its unde...
Endocrine resistance is a leading cause of mortality in oestrogen receptor-positive and human epidermal growth factor receptor 2-negative (ER+HER2-) breast cancer (BC), highlighting the urgent need to understand its underlying molecular mechanisms and identify potentially resistant patients for effective management. In this study, we constructed endocrine-resistant cell lines through long-term oestrogen deprivation and identified differentially expressed genes (DEGs) via transcriptome analysis. Key endocrine-resistant genes were defined through Cox regression analysis. Our findings revealed that the genes CLEC3A, PCDH10, and ST3GAL1 were significantly upregulated in endocrine-resistant cells and serve as independent prognostic factors for ER+HER2- BC patients. We developed an endocrine resistance score (ERS), and a nomogram model incorporating ERS demonstrated robust predictive capabilities for patient prognosis. Single-cell RNA sequencing analysis demonstrated that the ERS and the three core genes constituting the ERS were significantly upregulated in tissue specimens from patients with resistance to endocrine neoadjuvant therapy. Additionally, knocking down CLEC3A, PCDH10, and ST3GAL1 led to reduced malignancy progression in endocrine-resistant BC cells. Mechanistic studies revealed that CLEC3A promotes endocrine resistance by upregulating the PI3K-AKT pathway. This study suggests that CLEC3A, PCDH10, and ST3GAL1 are associated with endocrine resistance and can reflect the prognosis of ER+HER2- BC patients receiving endocrine therapy, providing potential therapeutic targets and a valuable prognostic indicator for clinicians.
Establishment and Validation of a C57BL/6J Mouse Model for Melasma.
Wang W, Sun X, Liu Y … +7 more , Yang Y, Yang H, Zhang X, Li X, Xu H, Chen X, Lin T
Cell Prolif · 2026 Jan · PMID 40640993 · Full text
Melasma is a recurrent and treatment-resistant hyperpigmentation disorder characterized by a complex and multifactorial pathogenesis. However, the lack of a stable and reliable animal model has hindered systematic invest...
Melasma is a recurrent and treatment-resistant hyperpigmentation disorder characterized by a complex and multifactorial pathogenesis. However, the lack of a stable and reliable animal model has hindered systematic investigations into its onset and progression. In this study, we established a melasma-like model in C57BL/6J mice by combining broadband UVB irradiation, intramuscular progesterone administration, and induced emotional stress. The affected skin areas exhibited irregular, brown hyperpigmented patches. Histopathological analysis revealed an accumulation of melanin granules in the epidermis and superficial dermis, elevated levels of tyrosinase (TYR) in both skin and plasma, systemic oxidative stress imbalance, and reduced autophagic activity in the lesional skin. Furthermore, this model displayed distinct differences from a UV-induced post-inflammatory hyperpigmentation (PIH) model. Notably, the melasma-like mice responded to tranexamic acid treatment in a manner that closely resembled clinical outcomes observed in human patients. Collectively, these findings establish a stable, reproducible, and clinically relevant mouse model of melasma, providing a valuable platform for future research into its pathogenesis and treatment.
High-Resolution Single-Neuron Reconstruction Analysis in Golgi-Stained Brain Tissues.
Tang Q, Fan B, Cai X … +5 more , Shen Z, Zhang J, Hu J, Li J, Zhu Y
Cell Prolif · 2026 Feb · PMID 40619275 · Full text
Understanding the structural and functional organisation of brain networks is a fundamental objective in neuroscience, with three-dimensional (3D) reconstruction of single-neuron morphology serving as a critical foundati...
Understanding the structural and functional organisation of brain networks is a fundamental objective in neuroscience, with three-dimensional (3D) reconstruction of single-neuron morphology serving as a critical foundation. The Golgi staining method, which enables random neuronal labeling and provides high-contrast signals in both optical and X-ray microscopy, remains a valuable tool for morphological analysis. However, its widespread application in large-scale neuronal reconstructions is hindered by signal discontinuities in neuronal branches, high-density labeling, and complex background interference. While automated reconstruction methods perform well in sparsely labelled and morphologically simple neuronal populations, their effectiveness is limited in Golgi-stained samples. Here we develop a semi-automated single-neuron reconstruction method for Golgi-stained mouse brain neurons (SNR-Golgi). By integrating three key technical modules-background denoising, single-neuron extraction, and branch repair-SNR-Golgi significantly enhances the accuracy and completeness of neuronal reconstruction. In fluorescence micro-optical sectioning tomography (fMOST) datasets, SNR-Golgi demonstrated superior performance in neuronal reconstruction within the mouse somatosensory cortex, achieving a 30% increase in reconstructed branch count, a 76% improvement in total branch length, and a 3.7-fold increase in axonal length. Additionally, in synchrotron-based X-ray imaging datasets, SNR-Golgi enabled submicron-resolution 3D reconstruction of single neurons. These results demonstrate that SNR-Golgi effectively addresses the complexity of Golgi-stained samples and provides robust technical support for the structural analysis of brain neurons across various imaging modalities.
Targeting ROCK1/YAP1 Axis Ameliorates Inflammation-Induced Prostatic Hyperplasia via Stabilising SIRT1-Dependent Mitochondrial Dynamics.
Lin D, Wei P, Zhang M … +7 more , Li K, Li L, Li Z, Luo C, Kuang W, Cui K, Chen Z
Cell Prolif · 2026 Feb · PMID 40616266 · Full text
Benign prostatic hyperplasia (BPH) is a common condition in older men, with its prevalence increasing as age advances. Chronic inflammation orchestrates oxidative stress to exacerbate BPH. YAP1, which regulates organ siz...
Benign prostatic hyperplasia (BPH) is a common condition in older men, with its prevalence increasing as age advances. Chronic inflammation orchestrates oxidative stress to exacerbate BPH. YAP1, which regulates organ size, cellular homeostasis, and tissue fibrosis, can be activated by ROCK1. Given the urgent clinical need for more effective therapies, this study explored whether targeting the ROCK1/YAP1 axis could mitigate BPH progression. Here, rats received in situ adeno-associated virus (AAV) injection to induce prostate-specific YAP1 overexpression. An inflammation-associated experimental autoimmune prostatitis (EAP) model was established by prostate antigen immunisation, followed by treatment with ROCK1 inhibitor fasudil and YAP1 inhibitor verteporfin. Cell models were treated with specific inhibitors to confirm the critical role of YAP1 in modulating mitochondrial function. As a result, YAP1 overexpression was sufficient to induce a pathological BPH phenotype. Specifically, YAP1 activated the inflammatory cascade to provoke an immune response, disrupted proliferation/apoptosis balance to induce tissue hyperplasia, triggered epithelial-mesenchymal transition (EMT) and reactive stroma to drive fibrosis, and promoted NOX4/ROS generation and antioxidant depletion to cause oxidative stress. The inflammation-induced experimental autoimmune prostatitis (EAP) model also presented analogous BPH lesions, which were significantly alleviated when treated with ROCK1 inhibitor fasudil and YAP1 inhibitor verteporfin. Mechanistically, YAP1 activation under inflammatory conditions suppressed SIRT1 expression, thereby exacerbating oxidative stress through the disruption of DRP1/MFN2-mediated mitochondrial dynamics. Overall, inflammation-driven activation of the ROCK1/YAP1 axis aggravates oxidative stress, promoting BPH hyperplasia and fibrosis by impairing SIRT1-regulated mitochondrial dynamics. These findings provide a preclinical rationale for developing ROCK1 or YAP1 inhibitors as targeted therapies for BPH patients with chronic inflammation.
CDK12 Inactivation Attenuates Prostate Cancer Progression by Inhibiting BNIP3-Mediated Mitophagy.
Huang M, Lei H, Tong T … +11 more , Zou H, Yan B, Cao F, Wang Y, Teng Q, Xu B, Luo J, Guan Y, Lai S, Li P, Pang J
Cell Prolif · 2026 Feb · PMID 40605142 · Full text
Mitochondrial stress-induced mitophagy plays a critical role to maintain cellular homeostasis; however, in cancer cells, this process may also contribute to drug resistance. Our previous work identified CDK12 as a critic...
Mitochondrial stress-induced mitophagy plays a critical role to maintain cellular homeostasis; however, in cancer cells, this process may also contribute to drug resistance. Our previous work identified CDK12 as a critical regulator of prostate cancer (PCa) cell survival under sustained enzalutamide exposure, though the precise mechanism remains to be elucidated. In this study, we hypothesize that CDK12 plays a key role in mitophagy regulation under mitochondrial stress, potentially modulating PCa cell resistance to enzalutamide, the first-line clinical medication in PCa therapy. Utilising multiple in vitro PCa cell models, we demonstrate that both CDK12 knockdown and pharmacological inhibition with THZ531 impaired mitophagy following treatment with enzalutamide and mitophagy inducer CCCP. Mechanistically, our finding reveal that CDK12 inhibition disrupts FOXO3-induced BNIP3 transcription, thereby preventing receptor-mediated mitophagy and sensitising PCa cells to enzalutamide. This study identifies the CDK12-FOXO3-BNIP3 pathway as a novel regulatory mechanism governing mitophagy under mitochondrial stress. Importantly, these results underscore CDK12's role in preserving mitochondrial function and promoting PCa cell survival during enzalutamide treatment. These findings highlight the therapeutic potential of targeting the CDK12-BNIP3-mitophagy axis in combination with antiandrogen therapies, offering a promising strategy to overcome drug resistance in PCa and improve clinical outcomes.
Single-Nucleus Transcriptomics Uncovers Xaf1-Driven PANoptosis as a Therapeutic Target in Aminoglycoside-Induced Hearing Loss.
Wang X, Xiao H, Wu J … +8 more , Lin Y, Ao Y, Ye Z, Tan X, Kong F, Chen X, Chai R, Zhang S
Cell Prolif · 2026 Jan · PMID 40600354 · Full text
Aminoglycoside antibiotics are essential in managing many life-threatening diseases. However, their derivatives, such as neomycin, are associated with severe side effects such as persistent sensorineural hearing loss. Th...
Aminoglycoside antibiotics are essential in managing many life-threatening diseases. However, their derivatives, such as neomycin, are associated with severe side effects such as persistent sensorineural hearing loss. Therefore, it is essential to elucidate the molecular and biochemical mechanisms of aminoglycoside-induced ototoxicity and identify targets for alleviating ototoxic injury. Here, we provide a detailed cochlear cell atlas of neomycin-induced acute and chronic ototoxicity-related changes through single-nucleus RNA sequencing profiling. Utilising this cochlear cell atlas, we used the Augur and scDist algorithms to evaluate cell-type-specific susceptibility to neomycin injury. We observed aberrant expression of X-linked inhibitor of apoptosis (Xiap)-associated factor 1 (Xaf1) in neomycin-exposed cochleae using the cochlear cell atlas, and we identified a novel role for Xaf1 in facilitating PANoptosis through overexpression and knockdown assays in vitro. Finally, we assessed the protective role of Xaf1 against neomycin-induced ototoxicity by Xaf1 knockdown in cochlear hair cells using adeno-associated virus-based gene delivery. Mechanistically, Xaf1 orchestrates PANoptosis activation through direct interaction with and transcriptional regulation of ZBP1, establishing its hierarchical position upstream in the signalling cascade. This study presents detailed cochlear cellular maps of neomycin-induced ototoxicity and serves as a valuable resource for identifying transcriptome-wide disease-driving perturbations at the single-cell level. More importantly, we identified Xaf1 as a critical target for modulating the PANoptosis pathway, offering a promising treatment strategy for aminoglycoside-induced ototoxicity.
Homoharringtonine Promotes FTO Degradation to Suppress LILRB4-Mediated Immune Evasion in Acute Monocytic Leukaemia.
Huang F, Luo X, Zhang M … +16 more , Jin L, Sun W, Chen P, Hong X, Xu C, Jiang M, Hu D, Zhang B, Hu S, Yang C, Gao R, Zeng J, Lu Q, Luo Q, Wu J, Chen S
Cell Prolif · 2026 Feb · PMID 40590394 · Full text
Acute monocytic leukaemia, a subtype of acute myeloid leukaemia (AML), is a highly aggressive malignancy characterised by a poor prognosis, primarily due to the ability of leukaemic cells to evade immune surveillance. In...
Acute monocytic leukaemia, a subtype of acute myeloid leukaemia (AML), is a highly aggressive malignancy characterised by a poor prognosis, primarily due to the ability of leukaemic cells to evade immune surveillance. In this study, we demonstrate that homoharringtonine (HHT), an FDA-approved therapeutic agent for chronic myeloid leukaemia (CML), inhibits this immune evasion by targeting the FTO/m6A/LILRB4 signalling pathway in monocytic AML. Utilising RNA sequencing (RNA-seq) and various functional assays, we reveal that HHT treatment significantly reduces LILRB4 expression at both the RNA and protein levels, suggesting that the effects of HHT on LILRB4 are distinct from its well-established role as a protein synthesis inhibitor. Mechanistically, HHT treatment markedly increases global levels of RNA m6A in THP-1 cells by promoting the degradation of FTO, which subsequently diminishes the expression of its downstream targets, MLL1 and LILRB4. Furthermore, in vitro and in vivo analyses employing monocytic AML cell lines, mouse-derived AML xenograft models, and patient samples collectively support the conclusion that HHT suppresses immune evasion in monocytic AML by reducing LILRB4 expression. Importantly, the downregulation of LILRB4 resulting from HHT treatment enhances the susceptibility of THP-1 cells to CD8 T cell cytotoxicity, accompanied by increased markers of immune activation. Overall, our findings position HHT as a promising clinical agent for enhancing CD8 T cell-based cancer immunotherapy by mitigating immune evasion in monocytic AML.
Myeloid PD-1 Regulates Astrocyte Development and Leads to Active Behaviours.
Qin J, Wang C, Li S … +4 more , Wang Y, He T, Jiao J, Ji F
Cell Prolif · 2026 Feb · PMID 40582992 · Full text
During early brain development, the nervous system evolves as cells connect to form a unique neural network, with communication between cell populations vital for neurological balance. This study investigates how the los...
During early brain development, the nervous system evolves as cells connect to form a unique neural network, with communication between cell populations vital for neurological balance. This study investigates how the loss of PD-1 in myeloid cells disrupts nervous system development. Specific ablation of PD-1 affects myeloid cell proliferation and classification. As astrogenesis begins, astrocyte proliferation ceases, continuous astrocyte proliferation is observed. Immunofluorescence staining revealed high expression of astrocyte-related genes in PD-1 mice, which also exhibited more extroverted behaviour. Additionally, the absence of PD-1 enhances CXCL1 expression through the NF-κB pathway, promoting astrocyte proliferation by interacting with CXCR2. These findings underscore PD-1's regulatory role in myeloid cells and its implications for the myeloid-brain axis.
LncRNA H19-Encoded Micropeptide altH19 Promotes DNA Replication and Mitosis in Myeloma Cells by Enhancing the Phosphorylation of CDK2 at Threonine 160.
Zhang Y, Li W, Cao X … +4 more , Mao J, Zhou X, Liu L, Yao R
Cell Prolif · 2026 Feb · PMID 40579124 · Full text
Micropeptides are endogenous peptides translated from alternative open reading frames (alt-ORFs) within coding or non-coding genes. Emerging evidence suggests that some micropeptides play critical roles in both physiolog...
Micropeptides are endogenous peptides translated from alternative open reading frames (alt-ORFs) within coding or non-coding genes. Emerging evidence suggests that some micropeptides play critical roles in both physiological and pathological processes. Multiple myeloma (MM), a haematological malignancy, remains incurable due to frequent relapses and a limited understanding of its underlying mechanisms. In this study, we sought to investigate the function and molecular mechanism of a novel micropeptide in MM pathogenesis. We identified a novel micropeptide, altH19, encoded by the lncRNA H19, which is highly expressed in patients of MM. Functional assays revealed that altH19 promotes myeloma cell proliferation and colony formation significantly. Furthermore, altH19 induces multipolar mitosis by upregulating the expression of Aurora B, Centrin 2 and phosphorylated histone H3. Flow cytometry analyses confirmed that overexpression of altH19 enhances DNA replication and accelerates the transition from early to mid-late stages of the DNA replication process. Conversely, knockout of altH19 reverses these effects. Mechanistically, altH19 directly interacts with phosphorylated CDK2 at threonine 160, thereby enhancing CDK2 T160 phosphorylation and activating the downstream E2F1 target RB phosphorylation. Notably, altH19 was able to restore phosphorylation levels of CDK2 and RB that were otherwise suppressed by the CDK2-selective inhibitor Seliciclib. In summary, we identify altH19 as a novel lncRNA-derived micropeptide with a pivotal role in myeloma progression, highlighting the therapeutic potential of targeting the altH19-CDK2-RB axis in MM treatment.
Lactate Promotes the Second Cell Fate Decision in Blastocysts by Prompting Primitive Endoderm Formation Through an Intercellular Positive Feedback Loop That Couples Paracrine FGF Signalling.
Hu X, Tang Y, Zhao W … +7 more , Liu J, Liu Z, Yang Q, Chu M, Tian J, An L, Wang S
Cell Prolif · 2025 Oct · PMID 40579118 · Full text
Lactate has been widely recognised as an energy source and metabolic by-product, but increasing evidence supports its critical role as a signalling molecule or epigenetic substrate. During early embryogenesis, lactate pr...
Lactate has been widely recognised as an energy source and metabolic by-product, but increasing evidence supports its critical role as a signalling molecule or epigenetic substrate. During early embryogenesis, lactate production increases during the transition from early to late blastocyst, coinciding with the differentiation of inner mass cell (ICM) into epiblast (EPI) and primitive endoderm (PrE), termed the second cell fate decision. However, the role of this hallmark metabolic change in the second cell fate segregation remains unknown. Herein, using in vitro and in vivo models, we found lactate production is preferentially increased in PrE cells and is essential for ICM differentiation into PrE. Mechanically, increased lactate in PrE precursor cells and FGF signalling in EPI precursor cells reciprocally activate each other and synergise to prompt PrE specification, forming an intercellular positive feedback loop essential for this lineage commitment. Additionally, lactate enhanced histone lactylation levels during differentiation into PrE fate. Thus, our findings construct a complex multilayer model in which intracellular metabolite in PrE cooperates with intercellular growth factor signalling from EPI to regulate early embryonic lineage commitment. Highlighting the multifaceted lactate's function, our findings also advance the current knowledge that bridges epigenetic reprogramming and metabolic remodelling during early embryonic development.
Maternal Nutritional Status Governs Fetal Development by Modulating Imprinting Gene GAB1-Mediated Trophoblast Differentiation in the Placenta.
Fan M, Wu H, Xie Y … +7 more , Liu M, Yu X, Wang F, Xiao Z, Wang H, Shao X, Wang YL
Cell Prolif · 2025 Dec · PMID 40550626 · Full text
The appropriate allocation of nutrients between the mother and the fetus during mammalian pregnancy primarily depends on a healthy placenta. Fetal growth restriction (FGR) is frequently associated with inadequate materna...
The appropriate allocation of nutrients between the mother and the fetus during mammalian pregnancy primarily depends on a healthy placenta. Fetal growth restriction (FGR) is frequently associated with inadequate maternal nutrition supply and impaired placental function. The precise mechanisms linking maternal nutrient deficiency to compromised fetal and placental development remain largely elusive. In this study, we conducted an in-depth analysis by integrating single-cell/single-nucleus RNA sequencing data from human and mouse placentas along with transcriptomic data from FGR placenta, identifying the GAB1 (GRB2-associated binding protein 1) gene as a potential mediator of dysregulated maternal-fetal exchange, thereby affecting fetal growth. Using a mouse model, we demonstrated that food restriction significantly impeded fetal growth and disrupted placental labyrinth development. Through an in vitro trophoblast differentiation model, we revealed that nutritional restriction impaired GAB1 stability via LC3-interacting region (LIR) motif-mediated selective autophagic degradation, thereby hindering GAB1-MAPK signalling-enhanced trophoblast syncytialisation. These findings elucidate the mechanisms by which placental GAB1 links maternal nutrition status with fetal growth and suggest potential therapeutic strategies for managing pregnancy complications such as FGR.
Correction to "Targeting RORα in Macrophages to Boost Diabetic Bone Regeneration".
Cell Prolif · 2025 Aug · PMID 40539449 · Full text
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TRAPPC2l Participates in Male Germ Cell Development by Regulating Cell Division.
Wang M, Li J, Liu B … +6 more , Shen Z, Chen M, Cui X, Liu H, Gao F, Zhao H
Cell Prolif · 2025 Jun · PMID 40539230 · Full text
TRAPPC2L is a core subunit of the Transport Protein Particle (TRAPP) complex, which is involved in vesicle transport and autophagy. Mutations in Trappc2l gene are associated with neurodevelopmental disorders, characteris...
TRAPPC2L is a core subunit of the Transport Protein Particle (TRAPP) complex, which is involved in vesicle transport and autophagy. Mutations in Trappc2l gene are associated with neurodevelopmental disorders, characterised by severe neurodevelopmental delays and varying degrees of muscle abnormalities. In this study, we found that the knockout of Trappc2l did not cause developmental abnormalities in both male and female mice. However, the male mice were completely infertile. Histological examination revealed that germ cell syncytial structures with multiple nuclear were formed in Trappc2l knockout mice from embryonic day 17.5 (E17.5) and the number and size of these structures gradually were increased at later developmental stages. The germ cells were completely lost at 2 weeks after birth. Further study found that germ cell syncytial structures were most likely formed by abnormal cell division but not cell fusion. We also found that meiosis-associated genes Stra8 and Sycp3 were expressed in Trappc2l-deficient germ cells during the embryonic stage. Our study demonstrated that Trappc2l is essential for germ cell development in male mice which is probably involved in keeping the mitotic quiescent state of male germ cells during the embryonic stage.
Organoids in Haematologic Research: Advances and Future Directions.
Chang L, Li L, Han Y … +2 more , Cheng H, Yang L
Cell Prolif · 2025 Jun · PMID 40538372 · Full text
Organoid technology, as a revolutionary biomedical tool, has shown immense potential in haematological research in recent years. By using three-dimensional (3D) cell culture systems constructed from pluripotent stem cell...
Organoid technology, as a revolutionary biomedical tool, has shown immense potential in haematological research in recent years. By using three-dimensional (3D) cell culture systems constructed from pluripotent stem cells (PSCs) or adult stem cells (ASCs), organoids can highly mimic the characteristics of in vivo organs, thereby offering significant potential for investigating human organ development, disease processes and treatment strategies. This review introduces the development of organoids and focuses on their progress in haematological research, including haematopoietic-related organoids, immune-related organoids and organoids used for studying blood system diseases. It discusses the prospects, challenges and future outlook of organoids in the field of haematology. This review aims to provide the latest advancements and future directions of organoid technology in haematological research, offering references and insights into further exploration in this field.
RETRACTION: CBX8 Interacts with Chromatin PTEN and Is Involved in Regulating Mitotic Progression.
Cell Prolif · 2025 Aug · PMID 40538052 · Full text
B. H. Choi, T. M. Colon, E. Lee, Z. Kou, W. Dai, "CBX8 Interacts with Chromatin PTEN and Is Involved in Regulating Mitotic Progression," Cell Proliferation 54, no. 11 (2021): e13110. https://doi.org/10.1111/cpr.13110. Th...
B. H. Choi, T. M. Colon, E. Lee, Z. Kou, W. Dai, "CBX8 Interacts with Chromatin PTEN and Is Involved in Regulating Mitotic Progression," Cell Proliferation 54, no. 11 (2021): e13110. https://doi.org/10.1111/cpr.13110. The above article, published online on 15 December 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Deputy Editor, Yunfeng Lin; and John Wiley & Sons Ltd. A third party reported that the PTEN control bands in Figure 1A had previously been published in another article by some of the same authors (Choi et al. 2017 [https://doi.org/10.1186/s40164-017-0079-0]). Author W. Dai responded to an inquiry by the publisher, but the authors were not able to locate the original data for further analysis. The publisher has confirmed that both articles report on different experimental conditions and time points for both sets of PTEN controls. The retraction has been agreed to because the duplication of the PTEN control data from an earlier publication fundamentally compromises the reliability of the reported results. The authors did not respond to our notice regarding the retraction.
Correction to "YTHDF1 Mediates N-Methyl-N-Nitrosourea-Induced Gastric Carcinogenesis by Controlling HSPH1 Translation".
Cell Prolif · 2025 Jul · PMID 40537914 · Full text
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Deciphering Age-Dependent ECM Remodelling in Liver: Proteomic Profiling and Its Implications for Aging and Therapeutic Targets.
Liu J, Song Q, Li C … +6 more , Yan J, An N, Yin W, Diao J, Su Y, Wang Y
Cell Prolif · 2025 Sep · PMID 40537154 · Full text
Aging is characterised by progressive structural and functional changes in the liver, with the extracellular matrix (ECM) playing a key role in modulating these changes. Our study presents a comprehensive proteomic analy...
Aging is characterised by progressive structural and functional changes in the liver, with the extracellular matrix (ECM) playing a key role in modulating these changes. Our study presents a comprehensive proteomic analysis of the liver ECM across different age stages, uncovering significant age-related changes. Through the identification of 158 ECM proteins in decellularised rat liver scaffolds, we reveal the intricate relationship between ECM composition and liver maturation, as well as the decrease in regenerative capacity. Lumican was identified as a critical regulator with heightened expression in neonatal livers, which is associated with enhanced hepatocyte proliferation and maintenance of stem cell characteristics. Temporal expression analysis distinguished four distinct clusters of ECM proteins, each reflecting the liver's functional evolution from early development to old age. Early developmental stages were marked by proteins essential for liver growth, while adulthood was characterised by a robust ECM supporting metabolic functions. Middle age showed a regulatory shift towards protease balance, and later life was associated with haemostasis-related processes. Our findings underscore the multifaceted role of the ECM in liver health and aging, offering potential opportunities for therapeutic intervention to counteract age-induced liver dysfunction. This study provides a foundational understanding of ECM dynamics in liver aging and sets the stage for the development of innovative strategies to mitigate the effects of age-related liver decline.
YKT6 Is Essential for Male Fertility by Promoting Meiosis Progression During Spermatogenesis of Mice.
Cen J, Yu X, Wang Z … +6 more , Liu W, Xu J, Fang Q, Gao F, Cao Y, Liu H
Cell Prolif · 2026 Jan · PMID 40528727 · Full text
SNARE proteins are required for membrane fusion events throughout the endomembrane system, and are therefore associated with vesicular transport. Here, we found that the SNARE family member, YKT6, is indispensable for ma...
SNARE proteins are required for membrane fusion events throughout the endomembrane system, and are therefore associated with vesicular transport. Here, we found that the SNARE family member, YKT6, is indispensable for male fertility in mice. Conditional Ykt6 knockout in pre-meiotic and meiotic germ cells leads to complete sterility and meiotic arrest in male mice, which exhibit loss of spermatocytes in seminiferous tubules, but without obvious disruption of chromosomal behaviours during meiosis. We observed that the abundance of syncytia increases along with abnormal morphology of the Golgi apparatus, while lysosomes decrease in Ykt6-cKO testes. Quantitative proteomics and immunofluorescent staining both showed dysregulation of vesicular transport in YKT6-deficient spermatocytes. Additionally, the recombinant mouse proteins, HA::YKT6 and MYC::STX1A, could interact in vitro, further supporting a likely role in mediating transport vesicle fusion with the plasma membrane. Finally, the absence of TEX14 signal within syncytia and enlarged TEX14 rings between spermatocytes together suggest a failure to stabilise intercellular bridges in Ykt6-cKO testes. These results demonstrate that YKT6 is required for male fertility by promoting meiosis progression through vesicular transport regulation during spermatogenesis in mice, expanding our understanding of YKT6 functions, and suggesting a possible strategy for future interventions for male infertility in humans.
Tumour Cell Size Control and Its Impact on Tumour Cell Function.
Zhou M, Zhou M, Jin Y
Cell Prolif · 2025 Dec · PMID 40525649 · Full text
Cell size is an important component of cell morphological characteristics. It reflects the characteristics of the cell type, nutritional status, growth stage and physiological function. The cell size of cells of the same...
Cell size is an important component of cell morphological characteristics. It reflects the characteristics of the cell type, nutritional status, growth stage and physiological function. The cell size of cells of the same type tends to be homogeneous and stable. However, in tumour cells, mutations in cell cycle genes and cytoskeletal genes and overexpression of the corresponding signalling pathways often lead to large variations in tumour cell size. Tumour cells regulate cell size and growth and proliferation through multiple signalling pathways, such as PI3K/Akt/mTOR, Myc and Hippo pathways, which work together to regulate cell size and proliferation. This allows tumour cells to adapt to different survival environments. Alterations in cell size also cause tumours to perform different functions, leading to alterations in tumour stemness, invasive migration and anti-tumour immunity by affecting immune cells in the tumour immune microenvironment. In this review, we describe the endogenous and exogenous factors affecting tumour cell size, analyse the mechanisms by which tumour cells regulate cell size and the effects of cell size on tumour malignancy and tumour immunity, summarise the potential therapeutic targets for cell size, and look forward to possible future research directions and clinical applications.
FKBP5 Mediates Alveolar Fibroblast Necroptosis During Acute Respiratory Distress Syndrome.
Zhang D, Liu W, Sun T … +7 more , Xiao Y, Chen Q, Huang X, Wang X, Qi Q, Wang H, Wang T
Cell Prolif · 2026 Jan · PMID 40525648 · Full text
The inflammatory storm is a hallmark of acute respiratory distress syndrome (ARDS), yet effective therapies remain unavailable. FK506-binding protein 51 (FKBP5) has emerged as a regulator of inflammatory responses. In th...
The inflammatory storm is a hallmark of acute respiratory distress syndrome (ARDS), yet effective therapies remain unavailable. FK506-binding protein 51 (FKBP5) has emerged as a regulator of inflammatory responses. In this study, FKBP5 expression was markedly increased in patients with sepsis and correlated with both cytokine levels and disease severity. Using sepsis-induced ARDS models in Fkbp5 and bone marrow chimeric mice, this study demonstrated that non-haematopoietic FKBP5 mitigates inflammatory injury. Single-cell transcriptomic analysis identified fibroblasts and epithelial cells as the primary sources of non-haematopoietic FKBP5 in the lung injury. Conditional deletion of FKBP5 in fibroblasts (Col1a2-iCre Fkbp5) confirmed the essential role of fibroblast FKBP5 in the inflammatory response during ARDS. Mechanistically, FKBP5-mediated necroptosis of alveolar fibroblasts triggered NF-κB activation, proinflammatory cytokine release, neutrophil recruitment, and the establishment of an inflammatory microenvironment in alveolar epithelial tissue. These findings suggest a potential therapeutic strategy targeting fibroblast FKBP5 and provide a foundation for future clinical investigation in ARDS management.
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