Experimental cell research最新文献_第3页

Deciphering significances of autophagy in the development and metabolism of adipose tissue

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-18 DOI: 10.1016/j.yexcr.2025.114478

Zitao Liu , Haoyuan Peng , Pengfei Liu , Feiyi Duan , Yutian Yang , Pengkun Li , Zhihao Li , Jiaoyan Wu , Jiayi Chang , Dandan Shang , Qiwen Tian , Jiawei Zhang , Yucheng Xie , Zhenzhen Liu , Yang An

{"title":"Deciphering significances of autophagy in the development and metabolism of adipose tissue","authors":"Zitao Liu , Haoyuan Peng , Pengfei Liu , Feiyi Duan , Yutian Yang , Pengkun Li , Zhihao Li , Jiaoyan Wu , Jiayi Chang , Dandan Shang , Qiwen Tian , Jiawei Zhang , Yucheng Xie , Zhenzhen Liu , Yang An","doi":"10.1016/j.yexcr.2025.114478","DOIUrl":"10.1016/j.yexcr.2025.114478","url":null,"abstract":"<div><div>The mechanisms of adipose tissue activation and inactivation have been a hot topic of research in the last decade, from which countermeasures have been attempted to be found against obesity as well as other lipid metabolism-related diseases, such as type 2 diabetes mellitus and non-alcoholic fatty liver disease. Autophagy has been shown to be closely related to the regulation of adipocyte activity, which is involved in the whole process including white adipocyte differentiation/maturation and brown or beige adipocyte generation/activation. Dysregulation of autophagy in adipose tissue has been demonstrated to be associated with obesity. On this basis, we summarize the pathways and mechanisms of autophagy involved in the regulation of lipid metabolism and present a review of its pathophysiological roles in lipid metabolism-related diseases, in the hope of providing ideas for the treatment of these diseases.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114478"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

EBP50 regulates senescence and focal adhesion in endometrial carcinoma

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-17 DOI: 10.1016/j.yexcr.2025.114465

Ako Yokoi , Ryoya Ogomori , Yasuko Oguri, Miki Hashimura, Makoto Saegusa

{"title":"EBP50 regulates senescence and focal adhesion in endometrial carcinoma","authors":"Ako Yokoi , Ryoya Ogomori , Yasuko Oguri, Miki Hashimura, Makoto Saegusa","doi":"10.1016/j.yexcr.2025.114465","DOIUrl":"10.1016/j.yexcr.2025.114465","url":null,"abstract":"<div><div>Ezrin-radixin-moesin (ERM)-binding phosphoprotein 50 (EBP50) is a multifunctional scaffold protein that is highly expressed in polarized epithelial cells. Here, we focused on the functional roles of EBP50 in endometrial carcinoma (Em Ca). We analyzed immunohistochemical sections from 121 Em Ca and 30 normal samples. We also characterized EBP50 overexpression or knockout (KO) Em Ca cell lines. High levels of membranous (Me) EBP50 expression were observed in endometrial tissues from normal menstrual cycles, in contrast to the transient upregulation of cytoplasmic (Cyt) EBP50 in tissues in the proliferative phase; this was probably in response to estrogenic effects. There was a significant stepwise reduction of Me-EBP50 expression from grade (G) 1 to G3 Em Cas, which was consistent with the loss of glandular structures. Conversely, Cyt-EBP50 levels increased with in the higher tumor grades. Low Me-EBP50 expression was significantly associated with tumor lymphovascular invasion and short overall survival. Whereas EBP50 KO led to senescence and reduced proliferation and motility, overexpression elicited the opposite phenotypes. Moreover, the number of focal adhesions (FAs), which mediate cell migration, was significantly increased in EBP50 overexpressing cells but decreased in the KO cells. In conclusion, Me- and/or Cyt-EBP50 expression contributes to acceleration of cell motility through enhancement of FA formation, and inhibits senescence to promote cytokinesis. Together, these effects contribute to Em Ca aggressiveness.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114465"},"PeriodicalIF":3.3,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143437187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endoplasmic reticulum stress and unfolded protein response in renal lipid metabolism

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-17 DOI: 10.1016/j.yexcr.2025.114463

Xinyi Zhou , Ziyi Li , Fajian Ren , Hua Deng , Jiayu Wen , Qiwen Xiang , Zhihui Zhou , Xiyun Yang , Chaolong Rao

{"title":"Endoplasmic reticulum stress and unfolded protein response in renal lipid metabolism","authors":"Xinyi Zhou , Ziyi Li , Fajian Ren , Hua Deng , Jiayu Wen , Qiwen Xiang , Zhihui Zhou , Xiyun Yang , Chaolong Rao","doi":"10.1016/j.yexcr.2025.114463","DOIUrl":"10.1016/j.yexcr.2025.114463","url":null,"abstract":"<div><div>The endoplasmic reticulum (ER) is a crucial cellular organelle involved in protein synthesis, folding, modification, and transport. Exposure to internal and external stressors can induce endoplasmic reticulum stress (ERS), leading to abnormal protein folding and ER malfunction. This stress can disrupt lipid synthesis, metabolism, and transport processes. Fatty acid oxidation is the primary energy source for the renal system. When energy intake exceeds the storage capacity of adipose tissue, lipids accumulate abnormally in non-adipose tissues, including kidneys, liver, and pancreas. Lipids accumulate in the kidneys of nearly all cell types, including thylakoid membranous, pedunculated, and proximal renal tubular epithelial cells. Intracellular free fatty acids can significantly disrupt renal lipid metabolism, contributing to ischemia-reperfusion acute kidney injury, diabetic nephropathy, renal fibrosis, and lupus nephritis. Consequently, this study delineated the primary signaling pathways and mechanisms of the ERS-induced unfolded protein response, explored the mechanistic link between ERS and lipid metabolism, and elucidated its role in renal lipid metabolism. This study aimed to offer new perspectives on managing and treating renal disorders.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114463"},"PeriodicalIF":3.3,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143454329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HSPD1-facilitated formation of CTPS cytoophidia promotes proliferation in C2C12 cells

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-17 DOI: 10.1016/j.yexcr.2025.114462

Lili Liu , Wen Chen , Haijing Luo , Weiwei Zhang , Zhenzhu Zhang , Xin Huang , Xuepeng Fu

{"title":"HSPD1-facilitated formation of CTPS cytoophidia promotes proliferation in C2C12 cells","authors":"Lili Liu , Wen Chen , Haijing Luo , Weiwei Zhang , Zhenzhu Zhang , Xin Huang , Xuepeng Fu","doi":"10.1016/j.yexcr.2025.114462","DOIUrl":"10.1016/j.yexcr.2025.114462","url":null,"abstract":"<div><div>CTP synthase (CTPS) is a rate-limiting enzyme that controls CTP synthesis and can polymerize to form a filamentous structure called cytoophidia. The presence of cytoophidia affects the enzymatic activity of CTPS. However, whether CTPS can form cytoophidia in C2C12 cells and whether it affects the proliferation of skeletal muscle satellite cells needs to be further studied. In this study, we found that CTPS could form cytoophidia during C2C12 cell proliferation, and that overexpression of <em>CTPS</em> significantly promoted the formation of CTPS cytoophidia and increased the viability and proliferation rate of C2C12 cells. However, the CTPS H355A mutation hindered the formation of CTPS cytoophidia and inhibited the viability and proliferation of C2C12 cells. In addition, we found that the HSPD1 protein could interact with the CTPS protein and interference with <em>Hspd1</em> gene expression inhibited the formation of CTPS cytoophidia, even with the overexpression of the <em>CTPS</em> gene. Subsequently, it inhibited C2C12 cells proliferation. Thus, these findings reveal the role of CTPS cytoophidia formation in C2C12 cells proliferation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114462"},"PeriodicalIF":3.3,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A phenotypic journey into NT5DC proteins in cancer and other diseases

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-17 DOI: 10.1016/j.yexcr.2025.114468

Emeline Cros-Perrial, Lars Petter Jordheim

引用次数: 0

Phthalocyanine and photodynamic therapy relieve albumin paclitaxel and gemcitabine chemoresistance in pancreatic cancer

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-17 DOI: 10.1016/j.yexcr.2025.114455

Zeru Li , Cheng Qin , Xiaoying Yang , Bangbo Zhao, Tianyu Li, Yutong Zhao, Xiangyu Zhang, Weibin Wang

{"title":"Phthalocyanine and photodynamic therapy relieve albumin paclitaxel and gemcitabine chemoresistance in pancreatic cancer","authors":"Zeru Li , Cheng Qin , Xiaoying Yang , Bangbo Zhao, Tianyu Li, Yutong Zhao, Xiangyu Zhang, Weibin Wang","doi":"10.1016/j.yexcr.2025.114455","DOIUrl":"10.1016/j.yexcr.2025.114455","url":null,"abstract":"<div><div>Pancreatic cancer (PCa) is a solid tumor with extremely high malignancy and poor prognosis. Chemotherapy is an important treatment option. Compared with gemcitabine alone, albumin paclitaxel plus gemcitabine (AG) is more effective in the treatment of advanced PCa. The NCCN guidelines also list AG regimen as one of the first-line recommended schemes for PCa. As for the mechanism of drug resistance of AG regimen, there is no relevant literature report at present. MIA PaCa-2 and BxPC-3, two PCa cell lines, were utilized to construct stable cell lines (AG-resistant cell lines) resistant to paclitaxel plus gemcitabine via gradually increased drug concentration of gemcitabine and albumin paclitaxel. AG-resistant cell lines are more malignant than parental cell lines in proliferation, invasion and chemoresistance. 5 genes, including ALDH3A1, ALDH3B1, CDA, MUC1, C15orf48 were found significantly high expression in AG-resistant cell lines. By utilizing PDB database and drugbank, a large-scale virtual screening of target drugs is carried out to screen for possible small molecule targeted drugs, and phthalocyanine was selected and proved to sensitize AG-resistant cell lines. We also validated the mechanism of phthalocyanine sensitizing chemoresistance, demonstrating that it leads to cell death by stimulating intracellular ROS level.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114455"},"PeriodicalIF":3.3,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

USP48 inhibits colorectal cancer progression and promotes M1-like macrophage polarization by stabilizing TAK1

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-17 DOI: 10.1016/j.yexcr.2025.114469

Xinwen Zhang , Jiawei Zhao , Guangying Qi , Yujing Chen , Xiaotong Guo , Juzheng Zhang , Siqi Chen , Xiaochen Xu , Jiayuan Feng , Qinyu Zhang , Bin Gao , Zhenran Wang , Jiamin Jin

{"title":"USP48 inhibits colorectal cancer progression and promotes M1-like macrophage polarization by stabilizing TAK1","authors":"Xinwen Zhang , Jiawei Zhao , Guangying Qi , Yujing Chen , Xiaotong Guo , Juzheng Zhang , Siqi Chen , Xiaochen Xu , Jiayuan Feng , Qinyu Zhang , Bin Gao , Zhenran Wang , Jiamin Jin","doi":"10.1016/j.yexcr.2025.114469","DOIUrl":"10.1016/j.yexcr.2025.114469","url":null,"abstract":"<div><div>Ubiquitination and deubiquitination have emerged as pivotal regulators of the development of colorectal cancer (CRC). However, the precise role of USP48 in CRC tumorigenesis is poorly understood. In this study, immunohistochemistry, protein blotting, MTT assays, plate cloning, scratch assays, transwell assays, and Hoechst 33258 staining were utilized to assess the expression level of USP48 and its involvement in CRC. The interaction between USP48 and Transforming growth factor-β activated kinase-1(TAK1) was confirmed using co-IP. Additionally, the impact of deubiquitination on downstream signaling was determined through qRT-PCR. Furthermore, the associations between USP48 and tumor-associated macrophages within the tumor microenvironment were investigated using flow cytometry. The findings of our study demonstrated that USP48 expression is downregulated in CRC patients. Through deubiquitination, USP48 interacts with and stabilizes TAK1, leading to the inhibition of TAK1-triggered NF-κB activation and effectively suppresses CRC tumorigenesis. Moreover, this study showed a positive correlation between USP48 expression and M1-type TAM polarization, revealed the potential of USP48 as a molecular target for the effective treatment of CRC in the future.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114469"},"PeriodicalIF":3.3,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143437792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to “Chronic hypoxia promotes pulmonary venous smooth muscle cell proliferation through the CaSR-TRPC6/ROCE pathway” [Exp. Cell Res. 2024 Dec 3;444(2):114363. doi: 10.1016/j.yexcr] “慢性缺氧通过CaSR-TRPC6/ROCE通路促进肺静脉平滑肌细胞增殖”的修正[j] .细胞科学，2024,12月3日；444(2):114363。doi: 10.1016 / j.yexcr]。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-15 DOI: 10.1016/j.yexcr.2024.114403

Shaoxing Li, Zhenli Fu, Wei Hong, Hong Yuan, Weitao Cao, Juan Xu, Rongmin Liu, Zhuandi Lin, Zhiming Xiang, Gongyong Peng

引用次数: 0

Threonine and tyrosine kinase promotes multiple myeloma progression by regulating regucalcin expression

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-15 DOI: 10.1016/j.yexcr.2025.114454

Xiaofeng Zhu , Zuxi Feng , Xiaohuan Peng , Tianning Di , YanHong Li , Jun Bai , Tao Ma , Lijuan Li , Liansheng Zhang

{"title":"Threonine and tyrosine kinase promotes multiple myeloma progression by regulating regucalcin expression","authors":"Xiaofeng Zhu , Zuxi Feng , Xiaohuan Peng , Tianning Di , YanHong Li , Jun Bai , Tao Ma , Lijuan Li , Liansheng Zhang","doi":"10.1016/j.yexcr.2025.114454","DOIUrl":"10.1016/j.yexcr.2025.114454","url":null,"abstract":"<div><div>Multiple myeloma (MM) is a malignant proliferative disorder of plasma cells and remains an incurable disease. Threonine and tyrosine kinase (TTK) is a dual-specific protein kinase that targets serine/threonine and tyrosine residues for phosphorylation. Its elevated expression has been linked to unfavorable outcomes in several types of cancer. Although the role of TTK in MM are still incompletely understood. In this research, we assessed TTK mRNA and protein expression levels in 51 MM patients and 30 healthy donors using qRT-PCR and western blotting. The impact of TTK expression on MM cell apoptosis, proliferation, and the cell cycle were assessed through CCK-8 assay, flow cytometry, and western blotting. Our findings revealed a significant overexpression of TTK in multiple myeloma patients and cell lines. TTK knockdown promoted apoptosis and G0/G1 phase arrest while inhibiting proliferation in MM cells, whereas TTK overexpression reduced apoptosis and G0/G1 phase arrest, enhancing proliferation in MM cells. Next, we identified regucalcin (RGN) as a downstream target of TTK through proteomic analysis. In NDMM, the expression of RGN was decreased. Cell function experiments showed that RGN knockdown significantly promoted MM cell proliferation, inhibited apoptosis and reduced cell cycle arrest, and reversed the increased apoptosis, weakened proliferation, and enhanced cell cycle arrest caused by TTK knockdown. Finally, a xenograft mouse model showed that TTK significantly promotes MM development. In summary, we demonstrated that the TTK-RGN axis regulates cell apoptosis, G0/G1 phase arrest, and proliferation in MM, highlighting TTK as a potential target for therapeutic intervention in this cancer.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114454"},"PeriodicalIF":3.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ACSS3 promotes the tumorigenesis of non-small cell lung cancer via suppressing p53-mediated ferroptosis

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-15 DOI: 10.1016/j.yexcr.2025.114438

Jing Zhang , Xiuhong Wang , Jingyi Wang , Xiao Wen , Siyuan Chen , Tao Wang , Bei Wang , Wenquan Hu

{"title":"ACSS3 promotes the tumorigenesis of non-small cell lung cancer via suppressing p53-mediated ferroptosis","authors":"Jing Zhang , Xiuhong Wang , Jingyi Wang , Xiao Wen , Siyuan Chen , Tao Wang , Bei Wang , Wenquan Hu","doi":"10.1016/j.yexcr.2025.114438","DOIUrl":"10.1016/j.yexcr.2025.114438","url":null,"abstract":"<div><div>Non-small cell lung cancer (NSCLC) is a subtype of the most frequently diagnosed cancer, causing a considerable number of deaths globally. Mitochondrial dysfunction was found to promote malignant progression. However, the underlying mechanism remains unclear. Acyl-CoA synthetase short chain family member 3 (ACSS3) is mainly located in mitochondria, which abnormal regulation is usually accompanied by the occurrence and development of tumors. In this study, we found that the expression level of ACSS3 was correlated with poor prognosis in patients with NSCLC. Moreover, we demonstrated that ACSS3 knockdown led to mitochondrial contraction, increased reactive oxygen species levels, decreased mitochondrial membrane potential, and subsequently inhibited tumor growth of NSCLC cells <em>in vitro</em> and <em>in vivo</em>, whereas its overexpression promoted these processes. Mechanistically, ACSS3 knockdown promoted ferroptosis through transcriptional control of SLC7A11 and GPX4. Further investigations indicated that ACSS3 loss inhibited the SLC7A11/GPX4 axis by enhancing p53 stability. Taken together, our data confirmed that ACSS3 promotes NSCLC tumorigenesis through inhibiting the p53-mediated ferroptosis. Hence, ACSS3 emerges as a promising therapeutic target for NSCLC treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114438"},"PeriodicalIF":3.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0