Cell Proliferation最新文献

{"title":"MCL restrained ROS/AKT/ASAH1 pathway to therapy tamoxifen resistance breast cancer by stabilizing NRF2","authors":"Xiao Han,&nbsp;Yupeng Zhang,&nbsp;Yin Li,&nbsp;Zhoujun Lin,&nbsp;Zhenkun Fu,&nbsp;Changjun Wang,&nbsp;Shengjie Zhang,&nbsp;Di Shao,&nbsp;Chenggang Li","doi":"10.1111/cpr.13700","DOIUrl":"10.1111/cpr.13700","url":null,"abstract":"<p>Tamoxifen resistance is a common and difficult problem in the clinical treatment of breast cancer (BC). As a novel antitumor agent, Micheliolide (MCL) has shown a better therapeutic effect on tumours; however, little is known about MCL and its role in BC therapy. With tamoxifen stimulation, drug-resistant BC cells MCF7TAMR and T47DTAMR obtained a high oxidative status and Amidohydrolase 1 (ASAH1) was abnormally activated. The inhibition of ASAH1 rescued the sensitivity of resistant cells to tamoxifen. We found that MCL inhibited the expression of ASAH1 and cell proliferation, especially in MCF7TAMR and T47DTAMR cells. The high oxidative stress status of resistant cells stimulated the expression of ASAH1 by positively regulating AKT, which was restrained by MCL. MCL activated NRF2 by directly binding to KEAP1 and promoting the antioxidant level of tamoxifen-resistant (TAMR) cells. In addition, ACT001, the prodrug of MCL, significantly inhibited the tumour growth of TAMR cells in preclinical xenograft tumour models. In conclusion, ASAH1 mediates tamoxifen resistance in ER-positive BC cells. MCL could activate the cellular antioxidant system via NRF2/KEAP1 and inhibit ASAH1 expression through the ROS/AKT signalling pathway, thus suppressing cell proliferation. MCL could be used as a potential treatment for TAMR-BC.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 11","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13700","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141455569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrahedral framework nucleic acids-based delivery of microRNA-155 alleviates intervertebral disc degeneration through targeting Bcl-2/Bax apoptosis pathway","authors":"Zhuhai Li,&nbsp;Yuanlin Tang,&nbsp;Lihang Wang,&nbsp;Kai Wang,&nbsp;Shishu Huang,&nbsp;Yu Chen","doi":"10.1111/cpr.13689","DOIUrl":"10.1111/cpr.13689","url":null,"abstract":"<p>Intervertebral disc degeneration (IDD) is one of the most common causes of chronic low back pain, which does great harm to patients' life quality. At present, the existing treatment options are mostly aimed at relieving symptoms, but the long-term efficacy is not ideal. Tetrahedral framework nucleic acids (tFNAs) are regarded as a type of nanomaterial with excellent biosafety and prominent performance in anti-apoptosis and anti-inflammation. MicroRNA155 is a non-coding RNA involved in various biological processes such as cell proliferation and apoptosis. In this study, a complex named TR155 was designed and synthesised with microRNA155 attached to the vertex of tFNAs, and its effects on the nucleus pulposus cells of intervertebral discs were evaluated both in vitro and in vivo. The experimental results showed that TR155 was able to alleviate the degeneration of intervertebral disc tissue and inhibit nucleus pulposus cell apoptosis via Bcl-2/Bax pathway, indicating its potential to be a promising option for the treatment of IDD.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 11","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13689","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141426406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modelling bone metastasis in spheroids to study cancer progression and screen cisplatin efficacy","authors":"Ceri-Anne E. Suurmond,&nbsp;Sander C. G. Leeuwenburgh,&nbsp;Jeroen J. J. P. van den Beucken","doi":"10.1111/cpr.13693","DOIUrl":"10.1111/cpr.13693","url":null,"abstract":"<p>Most bone metastases are caused by primary breast or prostate cancer cells settling in the bone microenvironment, affecting normal bone physiology and function and reducing 5-year survival rates to 10% and 6%, respectively. To expedite clinical availability of novel and effective bone metastases treatments, reliable and predictive in vitro models are urgently required to screen for novel therapies as current in vitro 2D planar mono-culture models do not accurately predict the clinical efficacy. We herein engineered a novel human in vitro 3D co-culture model based on spheroids to study dynamic cellular quantities of (breast or prostate) cancer cells and human bone marrow stromal cells and screen chemotherapeutic efficacy and specificity of the common anticancer drug cisplatin. Bone metastatic spheroids (BMSs) were formed rapidly within 24 h, while the morphology of breast versus prostate cancer BMS differed in terms of size and circularity upon prolonged culture periods. Prestaining cell types prior to BMS formation enabled confocal imaging and quantitative image analysis of in-spheroid cellular dynamics for up to 7 days of BMS culture. We found that cancer cells in BMS proliferated faster and were less susceptible to cisplatin treatment compared to 2D control cultures. Based on these findings and the versatility of our methodology, BMS represent a feasible 3D in vitro model for screening of new bone cancer metastases therapies.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 9","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13693","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141426405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes on the development and progression of renal fibrosis","authors":"Peihan Wang,&nbsp;Wu Chen,&nbsp;Bojun li,&nbsp;Songyuan Yang,&nbsp;Wei Li,&nbsp;Sheng Zhao,&nbsp;Jinzhuo Ning,&nbsp;Xiangjun Zhou,&nbsp;Fan Cheng","doi":"10.1111/cpr.13677","DOIUrl":"10.1111/cpr.13677","url":null,"abstract":"<p>Renal fibrosis is a prevalent pathological alteration that occurs throughout the progression of primary and secondary renal disorders towards end-stage renal disease. As a complex and irreversible pathophysiological phenomenon, it includes a sequence of intricate regulatory processes at the molecular and cellular levels. Exosomes are a distinct category of extracellular vesicles that play a crucial role in facilitating intercellular communication. Multiple pathways are regulated by exosomes produced by various cell types, including tubular epithelial cells and mesenchymal stem cells, in the context of renal fibrosis. Furthermore, research has shown that exosomes present in bodily fluids, including urine and blood, may be indicators of renal fibrosis. However, the regulatory mechanism of exosomes in renal fibrosis has not been fully elucidated. This article reviewed and analysed the various mechanisms by which exosomes regulate renal fibrosis, which may provide new ideas for further study of the pathophysiological process of renal fibrosis and targeted treatment of renal fibrosis with exosomes.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 11","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13677","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141426404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MRE11 is essential for the long-term viability of undifferentiated spermatogonia","authors":"Zhenghui Tang,&nbsp;Zhongyang Liang,&nbsp;Bin Zhang,&nbsp;Xiaohui Xu,&nbsp;Peng Li,&nbsp;Lejun Li,&nbsp;Lin-Yu Lu,&nbsp;Yidan Liu","doi":"10.1111/cpr.13685","DOIUrl":"10.1111/cpr.13685","url":null,"abstract":"<p>In the meiotic prophase, programmed SPO11-linked DNA double-strand breaks (DSBs) are repaired by homologous recombination (HR). The MRE11-RAD50-NBS1 (MRN) complex is essential for initiating DNA end resection, the first step of HR. However, residual DNA end resection still occurs in <i>Nbs1</i> knockout (KO) spermatocytes for unknown reasons. Here, we show that DNA end resection is completely abolished in <i>Mre11</i> KO spermatocytes. In addition, <i>Mre11</i> KO, but not <i>Nbs1</i> KO, undifferentiated spermatogonia are rapidly exhausted due to DSB accumulation, proliferation defects, and elevated apoptosis. Cellular studies reveal that a small amount of MRE11 retained in the nucleus of <i>Nbs1</i> KO cells likely underlies the differences between <i>Mre11</i> and <i>Nbs1</i> KO cells. Taken together, our study not only demonstrates an irreplaceable role of the MRE11 in DNA end resection at SPO11-linked DSBs but also unveils a unique function of MRE11 in maintaining the long-term viability of undifferentiated spermatogonia.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 9","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13685","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141418022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein phosphatase SCP4 regulates cartilage development and endochondral osteogenesis via FoxO3a dephosphorylation","authors":"Pinger Wang,&nbsp;Kaiao Zou,&nbsp;Jin Cao,&nbsp;Zhengmao Zhang,&nbsp;Wenhua Yuan,&nbsp;Jiali Chen,&nbsp;Jianbo Xu,&nbsp;Zhen Zou,&nbsp;Di Chen,&nbsp;Hongfeng Ruan,&nbsp;Jianying Feng,&nbsp;Xia Lin,&nbsp;Hongting Jin","doi":"10.1111/cpr.13691","DOIUrl":"10.1111/cpr.13691","url":null,"abstract":"<p>The regulatory mechanisms involved in embryonic development are complex and yet remain unclear. SCP4 represents a novel nucleus-resident phosphatase identified in our previous study. The primary aim of this study was to elucidate the function of SCP4 in the progress of cartilage development and endochondral osteogenesis. <i>SCP4</i>^{<i>−/−</i>} and <i>SCP4</i>^{<i>Col2ER</i>} mice were constructed to assess differences in bone formation using whole skeleton staining. ABH/OG staining was used to compare chondrocyte differentiation and cartilage development. Relevant biological functions were analysed using RNA-sequencing and GO enrichment, further validated by immunohistochemical staining, Co-IP and Western Blot. Global <i>SCP4</i> knockout led to abnormal embryonic development in <i>SCP4</i>^{<i>−</i>/<i>−</i>} mice, along with delayed endochondral osteogenesis. In parallel, chondrocyte-specific removal of <i>SCP4</i> yielded more severe embryonic deformities in <i>SCP4</i>^{<i>Col2ER</i>} mice, including limb shortening, reduced chondrocyte number in the growth plate, disorganisation and cell enlargement. Moreover, RNA-sequencing analysis showed an association between SCP4 and chondrocyte apoptosis. Notably, Tunnel-positive cells were indeed increased in the growth plates of <i>SCP4</i>^{<i>Col2ER</i>} mice. The deficiency of SCP4 up-regulated the expression levels of pro-apoptotic proteins both in vivo and in vitro. Additionally, phosphorylation of FoxO3a (pFoxO3a), a substrate of SCP4, was heightened in chondrocytes of <i>SCP4</i>^{<i>Col2ER</i>} mice growth plate, and the direct interaction between SCP4 and pFoxO3a was further validated in chondrocytes. Our findings underscore the critical role of SCP4 in regulating cartilage development and endochondral osteogenesis during embryonic development partially via inhibition of chondrocytes apoptosis regulated by FoxO3a dephosphorylation.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 9","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13691","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141418023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulated vascular smooth muscle cell death in vascular diseases","authors":"Zheng Yin,&nbsp;Jishou Zhang,&nbsp;Zican Shen,&nbsp;Juan-Juan Qin,&nbsp;Jun Wan,&nbsp;Menglong Wang","doi":"10.1111/cpr.13688","DOIUrl":"10.1111/cpr.13688","url":null,"abstract":"<p>Regulated cell death (RCD) is a complex process that involves several cell types and plays a crucial role in vascular diseases. Vascular smooth muscle cells (VSMCs) are the predominant elements of the medial layer of blood vessels, and their regulated death contributes to the pathogenesis of vascular diseases. The types of regulated VSMC death include apoptosis, necroptosis, pyroptosis, ferroptosis, parthanatos, and autophagy-dependent cell death (ADCD). In this review, we summarize the current evidence of regulated VSMC death pathways in major vascular diseases, such as atherosclerosis, vascular calcification, aortic aneurysm and dissection, hypertension, pulmonary arterial hypertension, neointimal hyperplasia, and inherited vascular diseases. All forms of RCD constitute a single, coordinated cell death system in which one pathway can compensate for another during disease progression. Pharmacologically targeting RCD pathways has potential for slowing and reversing disease progression, but challenges remain. A better understanding of the role of regulated VSMC death in vascular diseases and the underlying mechanisms may lead to novel pharmacological developments and help clinicians address the residual cardiovascular risk in patients with cardiovascular diseases.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 11","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13688","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141316807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal cell landscape of human embryonic tooth development","authors":"Yueqi Shi,&nbsp;Yejia Yu,&nbsp;Jutang Li,&nbsp;Shoufu Sun,&nbsp;Li Han,&nbsp;Shaoyi Wang,&nbsp;Ke Guo,&nbsp;Jingang Yang,&nbsp;Jin Qiu,&nbsp;Wenjia Wei","doi":"10.1111/cpr.13653","DOIUrl":"10.1111/cpr.13653","url":null,"abstract":"<p>Understanding the cellular composition and trajectory of human tooth development is valuable for dentistry and stem cell engineering research. Previous single-cell studies have focused on mature human teeth and developing mouse teeth, but the cell landscape of human embryonic dental development is still unknown. In this study, tooth germ tissues were collected from aborted foetus (17–24 weeks) for single-cell RNA sequence and spatial transcriptome analysis. The cells were classified into seven subclusters of epithelium, and seven clusters of mesenchyme, as well as other cell types such as Schwann cell precursor and pericyte. For epithelium, the stratum intermedium branch and the ameloblast branch diverged from the same set of outer enamel-inner enamel-<i>ALCAM</i>+ epithelial cell lineage, but their spatial distribution of two branches was not clearly distinct. This trajectory received spatially adjacent regulation signals from mesenchyme and pericyte, including JAG1 and APP. The differentiation of pulp cell and pre-odontoblast showed four waves of temporally distinct gene expression, which involved regulation networks of LHX9, DLX5 and SP7, and these genes were regulated by upstream ligands such as the BMP family. This provides a reference landscape for the research on early human tooth development, covering different spatial structures and developmental periods.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 9","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13653","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141310090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Procyanidin B2 improves developmental capacity of bovine oocytes via promoting PPARγ/UCP1-mediated uncoupling lipid catabolism during in vitro maturation","authors":"Yuwen Luo,&nbsp;Jun Li,&nbsp;Lv Zheng,&nbsp;Yizaitiguli Reyimjan,&nbsp;Yan Ma,&nbsp;Shuaixiang Huang,&nbsp;Hongyu Liu,&nbsp;Guizhen Zhou,&nbsp;Jiachen Bai,&nbsp;Yixiao Zhu,&nbsp;Yidan Sun,&nbsp;Xinhua Zou,&nbsp;Yunpeng Hou,&nbsp;Xiangwei Fu","doi":"10.1111/cpr.13687","DOIUrl":"10.1111/cpr.13687","url":null,"abstract":"<p>Metabolic balance is essential for oocyte maturation and acquisition of developmental capacity. Suboptimal conditions of in vitro cultures would lead to lipid accumulation and finally result in disrupted oocyte metabolism. However, the effect and mechanism underlying lipid catabolism in oocyte development remain elusive currently. In the present study, we observed enhanced developmental capacity in Procyanidin B2 (PCB2) treated oocytes during in vitro maturation. Meanwhile, reduced oxidative stress and declined apoptosis were found in oocytes after PCB2 treatment. Further studies confirmed that oocytes treated with PCB2 preferred to lipids catabolism, leading to a notable decrease in lipid accumulation. Subsequent analyses revealed that mitochondrial uncoupling was involved in lipid catabolism, and suppression of uncoupling protein 1 (UCP1) would abrogate the elevated lipid consumption mediated by PCB2. Notably, we identified peroxisome proliferator-activated receptor gamma (PPARγ) as a potential target of PCB2 by docking analysis. Subsequent mechanistic studies revealed that PCB2 improved oocyte development capacity and attenuated oxidative stress by activating PPARγ mediated mitochondrial uncoupling. Our findings identify that PCB2 intricately improves oocyte development capacity through targeted activation of the PPARγ/UCP1 pathway, fostering uncoupling lipid catabolism while concurrently mitigating oxidative stress.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 11","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.13687","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141305532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Long Non-Coding RNA CRNDE Sponges miR-384 to Promote Proliferation and Metastasis of Pancreatic Cancer Cells through Upregulating IRS1","authors":"","doi":"10.1111/cpr.13690","DOIUrl":"10.1111/cpr.13690","url":null,"abstract":"<p>G. Wang, J. Pan, L. Zhang, Y. Wei, C. Wang, “Long Non-Coding RNA CRNDE Sponges miR-384 to Promote Proliferation and Metastasis of Pancreatic Cancer Cells through Upregulating IRS1,” <i>Cell Proliferation</i> 50, no. 6 (2017): e12389, https://doi.org/10.1111/cpr.12389</p><p>The above article, published online on 21 September 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the Deputy Editor-in-Chief, Yunfeng Lin, and John Wiley and Sons Ltd. The retraction has been agreed following a request by the authors to retract the article due to unreliable results and a lack of original data. Further investigation revealed multiple images previously published elsewhere in a different scientific context. Thus, the editors consider the conclusions of this manuscript substantially compromised. The corresponding author Cheng Wang agrees with this decision on behalf of all authors.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"57 8","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141295618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}