Human Cell最新文献_第9页

Human amniotic epithelial stem cells, a potential therapeutic approach for diabetes and its related complications. 人羊膜上皮干细胞，糖尿病及其相关并发症的潜在治疗方法。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-01-03 DOI: 10.1007/s13577-024-01171-x

Zhenshuo Chen, Yunfei Luo, Jianping Liu

{"title":"Human amniotic epithelial stem cells, a potential therapeutic approach for diabetes and its related complications.","authors":"Zhenshuo Chen, Yunfei Luo, Jianping Liu","doi":"10.1007/s13577-024-01171-x","DOIUrl":"10.1007/s13577-024-01171-x","url":null,"abstract":"The escalating diabetes prevalence has heightened interest in innovative therapeutic strategies for this disease and its complications. Human amniotic epithelial stem cells (HAESCs), originate from the innermost layer of the placenta closest to the fetus and express stem cell markers in the amniotic membrane's umbilical cord attachment area, which have garnered significant attention. This article critically examines emerging research advancements and potential application values of hAESCs in treating diabetes and its complications. Initially, we will discuss the characteristics, origin, and advantages of hAESCs in differentiating into insulin-secreting cells. Subsequently, we will focus on the potential applications of hAESCs in treating diabetes complications such as diabetic retinopathy, diabetic nephropathy, and diabetic neuropathy, etc. We will scrutinize the progress of relevant clinical studies and trials involving hAESC therapy. In conclusion, as an emerging diabetes treatment method, hAESCs exhibit immense potential and application value. Despite numerous challenges in practical application, we are confident that with scientific advancement and technological progress, hAESCs will play a pivotal role in treating diabetes and its related complications.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"39"},"PeriodicalIF":3.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928446","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

Taxifolin regulates SLC31A1-mediated cuproptosis and tumor progression in hepatocellular carcinoma. Taxifolin调节slc31a1介导的肝细胞癌的铜增生和肿瘤进展。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-01-03 DOI: 10.1007/s13577-024-01168-6

Jike Li, Yuelian Wang, Lei Bao, Guo Chen, Qing Ye, Chengshi He, Lin Liu, Mei Luo

{"title":"Taxifolin regulates SLC31A1-mediated cuproptosis and tumor progression in hepatocellular carcinoma.","authors":"Jike Li, Yuelian Wang, Lei Bao, Guo Chen, Qing Ye, Chengshi He, Lin Liu, Mei Luo","doi":"10.1007/s13577-024-01168-6","DOIUrl":"10.1007/s13577-024-01168-6","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a primary malignant neoplasm exhibiting a high mortality rate. Taxifolin is a naturally occurring flavonoid compound that exhibits a range of pharmacological properties. The effects of taxifolin on HCC remain largely unexplored. Therefore, the aim of this study was to examine the potential roles of taxifolin in the development and progression of HCC. In this study, CCK-8 assay was utilized to examine the impact of taxifolin on the cell viability. The copper ions level and the activity of mitochondrial respiratory chain were determined by the correspondent kits. The biological properties of HCC cells were evaluated using colony formation, transwell, flow cytometry, and TUNEL assays, respectively. Transcriptome sequencing was carried out either with or without taxifolin treatment. The expression of cuproptosis-related proteins was determined by Western blot. We observed significant decrease of cell viability, Glutathione (GSH), and mitochondrial respiratory chain under the treatment of taxifolin, while an increase of copper ions level. Taxifolin was observed to suppress HCC progression both in vitro and in vivo. The intersection analysis was performed between upregulated genes and cuproptosis-related genes to obtain one intersection gene-SLC31A1. The knockdown of SLC31A1 reversed the tumor-suppressive effects induced by taxifolin. Taxifolin inhibited HCC progression through inducing cuproptosis in an SLC31A1-mediated manner.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"37"},"PeriodicalIF":3.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142923762","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

Long non-coding RNA MSC-AS1 confers imatinib resistance of gastrointestinal stromal tumor cells by activating FNDC1 and ANLN-mediated PI3K/AKT pathway. 长链非编码RNA MSC-AS1通过激活FNDC1和anln介导的PI3K/AKT通路，赋予胃肠道间质肿瘤细胞伊马替尼耐药。

IF 3.4 3区生物学

Human Cell Pub Date : 2025-01-03 DOI: 10.1007/s13577-024-01167-7

Lin Chen, Yongjian Gao, Huaixi Yang, Yanzhuo Su, Yunxin Zhang, Lin Lou, Xuefeng Wang, Dayong Ding

{"title":"Long non-coding RNA MSC-AS1 confers imatinib resistance of gastrointestinal stromal tumor cells by activating FNDC1 and ANLN-mediated PI3K/AKT pathway.","authors":"Lin Chen, Yongjian Gao, Huaixi Yang, Yanzhuo Su, Yunxin Zhang, Lin Lou, Xuefeng Wang, Dayong Ding","doi":"10.1007/s13577-024-01167-7","DOIUrl":"10.1007/s13577-024-01167-7","url":null,"abstract":"Imatinib resistance is a major obstacle to the successful treatment of gastrointestinal stromal tumors (GIST). Long non-coding RNAs (LncRNAs) have been identified as important regulatory factors in chemotherapy resistance. This study aimed to identify key lncRNAs involved in imatinib resistance of GISTs. First, MSC-AS1 was found to be upregulated in imatinib-resistant GIST tissues and imatinib-resistant GIST cells. Cellular experiments demonstrated that MSC-AS1 overexpression decreased imatinib sensitivity of GIST cells, evidenced by increased cell survival, colony formation, migration, and invasion. Moreover, suppression of MSC-AS1 improved the imatinib resistance of imatinib-resistant GIST cells. Furthermore, MSC-AS1 upregulated the expression of FNDC1 and Anillin via sponging miR-200b-3p, activated the phosphatidylinositol-3-kinase-AKT signaling pathway, and thereby driving imatinib resistance in vitro and in vivo. Overall, this study elucidates the crucial role and mechanism of MSC-AS1 in the imatinib resistance of GIST, providing the potential therapeutic strategy for overcoming the imatinib resistance of GIST.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 2","pages":"38"},"PeriodicalIF":3.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142923761","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

Loss of hepatocyte growth factor activator inhibitor type 1 (HAI-1) upregulates MMP-9 expression and induces degradation of the epidermal basement membrane. 肝细胞生长因子激活因子抑制剂1型（HAI-1）的缺失可上调MMP-9的表达并诱导表皮基底膜的降解。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-12-28 DOI: 10.1007/s13577-024-01159-7

Liang Weiting, Makiko Kawaguchi, Tsuyoshi Fukushima, Yuichiro Sato

{"title":"Loss of hepatocyte growth factor activator inhibitor type 1 (HAI-1) upregulates MMP-9 expression and induces degradation of the epidermal basement membrane.","authors":"Liang Weiting, Makiko Kawaguchi, Tsuyoshi Fukushima, Yuichiro Sato","doi":"10.1007/s13577-024-01159-7","DOIUrl":"10.1007/s13577-024-01159-7","url":null,"abstract":"Hepatocyte growth factor activator inhibitor type 1 (HAI-1), which is encoded by the SPINT1 gene, is a membrane-associated serine proteinase inhibitor abundantly expressed in epithelial tissues. We had previously demonstrated that HAI-1 is critical for placental development, epidermal keratinization, and maintenance of keratinocyte morphology by regulating cognate proteases, matriptase and prostasin. After performing ultrastructural analysis of Spint1-deleted skin tissues, our results showed that Spint1-deleted epidermis exhibited partially disrupted epidermal basement-membrane structures. Matrix metalloproteinases-9 (MMP-9) expression levels were upregulated in Spint1-deleted primary cultured keratinocytes and SPINT1 knockout (KO) HaCaT cells. Furthermore, gelatin zymography of the conditioned medium showed increased MMP activities in keratinocytes with reduced HAI-1 expression. Treating SPINT1 KO HaCaT cells with dehydroxymethylepoxyquinomicin (DHMEQ), a small molecule inhibitor of NF-κB, abrogated the upregulation of MMP9 and the gelatinolytic activity associated with MMP-9. These results suggest that HAI-1 may play a critical role in epidermal basement membrane integrity by regulating NF-κB activation-induced upregulation of MMP-9.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 1","pages":"36"},"PeriodicalIF":3.4,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142899652","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

Curzerenone inactivates the nuclear factor-kappa B signaling to suppress malignancy and immune evasion in cervical cancer by targeting CSNK2B. Curzerenone通过靶向CSNK2B使核因子κ B信号失活以抑制宫颈癌的恶性和免疫逃避。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-12-24 DOI: 10.1007/s13577-024-01164-w

Yangyan Sun, Min Wang, Jing Ling, Qunying Wu, Guorong Han, Junxu Zhou

{"title":"Curzerenone inactivates the nuclear factor-kappa B signaling to suppress malignancy and immune evasion in cervical cancer by targeting CSNK2B.","authors":"Yangyan Sun, Min Wang, Jing Ling, Qunying Wu, Guorong Han, Junxu Zhou","doi":"10.1007/s13577-024-01164-w","DOIUrl":"10.1007/s13577-024-01164-w","url":null,"abstract":"Curzerenone is a major component of the traditional herbal medicine Curcumae Rhizoma with potential cancer-suppressing effects. This study aims to investigate the treatment effect of Curzerenone on cervical cancer cells and the underpinning mechanism. HeLa and SiHa cells were treated with Curzerenone. The 100 μM Curzerenone treatment repressed proliferation, migration, and invasion of the cells. The Curzerenone treatment also reduced cellular expression of programmed death ligand 1, which increased the proliferation and activity of CD8+ T cells in a co-culture system with cancer cells. Casein kinase 2 beta (CSNK2B), a predicted physiological target of Curzerenone, was found to be suppressed by Curzerenone. Further overexpression of CSNK2B blocked the treatment effects of Curzerenone. Curzerenone inhibited while CSNK2B triggered activation of the nuclear factor-kappa B (NF-κB) pathway. The oncogenic and immunosuppressive effects of CSNK2B were blocked by an NF-κB-specific inhibitor. In vivo, Curzerenone treatment inhibited the tumorigenic activity of cancer cells, and it increased the proportion of CD8+ T cells in the xenograft tumor tissues. However, these anti-tumor effects were diminished by the CSNK2B overexpression as well. In conclusion, this research suggests that Curzerenone targets CSNK2B and inactivates the NF-κB signaling to suppress malignancy and immune evasion in cervical cancer.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 1","pages":"35"},"PeriodicalIF":3.4,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883417","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

Bone marrow stromal cell antigen 2 is broadly expressed in the different pluripotent states of human pluripotent stem cells and regulates the expression of pluripotency genes and three germ layer markers. 骨髓基质细胞抗原2在人多能干细胞的不同多能状态下广泛表达，调控多能基因和三种胚层标记物的表达。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-12-24 DOI: 10.1007/s13577-024-01160-0

Hong Seo Choi, Ji Yoon Lee, Mun Ju Choi, Min Seong Kim, Chun Jeih Ryu

{"title":"Bone marrow stromal cell antigen 2 is broadly expressed in the different pluripotent states of human pluripotent stem cells and regulates the expression of pluripotency genes and three germ layer markers.","authors":"Hong Seo Choi, Ji Yoon Lee, Mun Ju Choi, Min Seong Kim, Chun Jeih Ryu","doi":"10.1007/s13577-024-01160-0","DOIUrl":"10.1007/s13577-024-01160-0","url":null,"abstract":"Human pluripotent stem cells (hPSCs) have at least three distinct states: naïve pluripotency that represents the cellular states of the pre-implantation epiblast cells, primed pluripotency that represents the cellular states of the post-implantation epiblast cells, and formative pluripotency that represents a developmental continuum between naïve and primed pluripotency. Various cell surface markers have been used to define and analyze primed and naïve hPSCs within heterogeneous populations. However, not much is known about common cell surface markers for the different pluripotent states of hPSCs. To study surface molecules important for maintaining naive pluripotency, in this study, we generated murine monoclonal antibodies (MAbs) specific to naïve hPSCs. Subsequent studies showed that N15-F8, one of the MAbs, bound to both naïve and primed hPSCs. Cell surface biotin labeling and subsequent immunoprecipitation proved that N15-F8 recognized bone marrow stromal antigen 2 (BST2) in a conformation-dependent manner. Quantitative polymerase chain reaction (qPCR) revealed that BST2 expression was decreased during the early stages of differentiation via embryoid body (EB) formation in primed hPSCs. BST2 knockdown in primed hPSCs resulted in reduced expression of pluripotency genes. BST2 knockdown in naïve hPSCs also resulted in reduced expression of pluripotency genes and several naïve and primed pluripotent state-specific genes. BST2 knockdown induced the expression of ectoderm and endoderm markers in primed hPSCs, whereas it suppressed the expression of mesoderm markers. The results suggest that BST2 is broadly expressed in the different pluripotent states of hPSCs and regulates the expression of pluripotency genes and three germ layer markers.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 1","pages":"34"},"PeriodicalIF":3.4,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883413","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

β-Asarone regulates microglia polarization to alleviate TBI-induced nerve damage via Fas/FasL signaling axis. β-细丁酮通过Fas/FasL信号轴调控小胶质细胞极化，减轻脑外伤引起的神经损伤。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-12-24 DOI: 10.1007/s13577-024-01161-z

Mingyue Xia, Min Yi, Chunyuan Guo, Yeli Xie, Wenting Yu, Dongsheng Wang, Xingping Dai

{"title":"β-Asarone regulates microglia polarization to alleviate TBI-induced nerve damage via Fas/FasL signaling axis.","authors":"Mingyue Xia, Min Yi, Chunyuan Guo, Yeli Xie, Wenting Yu, Dongsheng Wang, Xingping Dai","doi":"10.1007/s13577-024-01161-z","DOIUrl":"10.1007/s13577-024-01161-z","url":null,"abstract":"Acute injury and secondary injury caused by traumatic brain injury (TBI) seriously threaten the health of patients. The purpose of this study was to investigate the role of β-Asarone in TBI-induced neuroinflammation and injury. In this work, the effects of β-Asarone on nerve injury and neuronal apoptosis were investigated in mice with TBI by controlled cortical impingement. The results of this research implied that β-Asarone dose-dependently decreased the mNSS score, brain water content and neuronal apoptosis, but increased the levels of the axonal markers Nrp-1 and Tau in TBI mice. In addition, β-Asarone caused a decrease in the levels of Fas, FasL, and inflammatory factors in cerebrospinal fluid and serum of TBI mice. Therefore, β-Asarone inhibited neuroinflammation and promoted axon regeneration in TBI mice. Besides, β-Asarone treatment inhibited M1 phenotype polarization but promoted M2 phenotype polarization in microglia of TBI mice. Overexpression of Fas and FasL reversed the above effects of β-Asarone. Thus, β-Asarone regulated microglial M1/M2 polarization balance in TBI mice by suppressing Fas/FasL signaling axis. In conclusion, β-Asarone inhibited Fas/FasL signaling pathway to promote the M1/M2 polarization balance of microglia toward M2 polarization, thus alleviating TBI-induced nerve injury.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 1","pages":"33"},"PeriodicalIF":3.4,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883506","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

MiR-34a regulates renal circadian rhythms during cisplatin-induced nephrotoxicity. MiR-34a在顺铂引起的肾毒性过程中调节肾脏昼夜节律。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-12-22 DOI: 10.1007/s13577-024-01163-x

Mohnad Abdalla, Amr Ahmed El-Arabey, Zhongtao Gai

引用次数: 0

Exosomal miR-146a-5p derived from bone marrow mesenchymal stromal cells regulate Th1/Th2 balance and alleviates immune thrombocytopenia in pregnancy. 来自骨髓间充质基质细胞的外泌体miR-146a-5p调节Th1/Th2平衡，缓解妊娠期免疫性血小板减少症。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-12-19 DOI: 10.1007/s13577-024-01162-y

Yanyan Rong, Wei Lu, Xianbao Huang, Dexiang Ji, Dehong Tang, Ruibin Huang, Wenhua Zhou, Guoan Chen, Yue He

{"title":"Exosomal miR-146a-5p derived from bone marrow mesenchymal stromal cells regulate Th1/Th2 balance and alleviates immune thrombocytopenia in pregnancy.","authors":"Yanyan Rong, Wei Lu, Xianbao Huang, Dexiang Ji, Dehong Tang, Ruibin Huang, Wenhua Zhou, Guoan Chen, Yue He","doi":"10.1007/s13577-024-01162-y","DOIUrl":"10.1007/s13577-024-01162-y","url":null,"abstract":"Immune thrombocytopenia (ITP) is a common hematological disorder. Our previous study has found that exosomal miR-146a-5p derived from bone marrow mesenchymal stromal cells (BMSCs) regulate Th17/Treg balance to alleviate ITP. This work further investigated the role of miR-146a-5p in ITP with pregnancy. Compared with healthy pregnant volunteers, the levels of Th1 cells and IFN-γ were increased, the levels of Th2 cells and IL-4 were decreased in peripheral blood of ITP patients with pregnancy. Then, human BMSCs-exosomes repressed the ratio of Th1/Th2 cells in CD4+ T cells, while BMSCs-exosomes with miR-146a-5p inhibitor increased Th1/Th2 cell ratio. Moreover, an ITP mouse model with pregnancy was constructed by administering anti-CD41 antibody in pregnant mice to verify the role of BMSCs-Exo in vivo. BMSCs-Exo elevated the number of platelet and megakaryocyte, improved the function of gastric, spleen and thymus tissues in ITP mice with pregnancy, which attributed to delivery miR-146a-5p. Furthermore, miR-146a-5p interacted with CARD10, and then repressed CARD10/NF-κB signaling pathway. BMSCs-exosomes promoted proliferation and inhibited apoptosis of Dami cells. In conclusion, BMSCs-exosomal miR-146a-5p reduced Th1/Th2 cell ratio to elevate proliferation and inhibit apoptosis of Dami cells, thereby alleviating ITP with pregnancy development. Therefore, miR-146a-5p may be a target for ITP with pregnancy treatment.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 1","pages":"31"},"PeriodicalIF":3.4,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856035","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

N6-methyladenosine-modified SRD5A3, identified by IGF2BP3, sustains cisplatin resistance in bladder cancer. 经 IGF2BP3 鉴定的 N6-甲基腺苷修饰 SRD5A3 可维持膀胱癌的顺铂耐药性。

IF 3.4 3区生物学

Human Cell Pub Date : 2024-12-16 DOI: 10.1007/s13577-024-01136-0

Kai Liao, Jing Li, Caixian He, Jiyong Peng

{"title":"N6-methyladenosine-modified SRD5A3, identified by IGF2BP3, sustains cisplatin resistance in bladder cancer.","authors":"Kai Liao, Jing Li, Caixian He, Jiyong Peng","doi":"10.1007/s13577-024-01136-0","DOIUrl":"10.1007/s13577-024-01136-0","url":null,"abstract":"Resistance to cisplatin-based chemotherapy limits the clinical benefit to some bladder cancer patients, and understanding the epigenetic regulation mechanism of cisplatin (CDDP) resistance in bladder cancer from the perspective of N6-methyladenosine (m6A) modification may optimize CDDP-based treatments. The study identified SRD5A3 as an oncogene for bladder cancer and stabilized by a m6A reader, IGF2BP3, to sustain CDDP resistance. Our results revealed that the expression of SRD5A3 was elevated in human bladder cancer tissues and cell lines, and this elevation was more evident in CDDP-resistant T24 and 5637 cells. Results of CCK-8 assay, colony formation assay, EdU staining, and flow cytometric analysis revealed that SRD5A3 knockdown and IGF2BP3 knockdown reduced cell proliferation and prevented chemoresistance in CDDP-resistant T24 and 5637 cells. Results of methylated RNA immunoprecipitation-PCR, RNA immunoprecipitation assay, and luciferase reporter assay showed IGF2BP3 recognized the SRD5A3 m6A modification and stabilized its mRNA. Nude mice implanted subcutaneously with CDDP-resistant T24 cells were injected intraperitoneally with CDDP (2 mg/kg) every 3 days for 35 days and the results demonstrated that SRD5A3 knockdown and IGF2BP3 knockdown effectively inhibited the tumor growth in subcutaneous implantation model. Collectively, the study unveils that IGF2BP3-mediated SRD5A3 m6A modification facilitates bladder cancer progression and induces CDDP resistance, providing rational therapeutic targets for bladder cancer patients.","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 1","pages":"30"},"PeriodicalIF":3.4,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11649775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830445","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