Experimental cell research最新文献

{"title":"The effect of cancer cell-derived exosomal proteins on macrophage polarization: An in-depth review","authors":"Khandu Wadhonkar ,&nbsp;Soumalya Das ,&nbsp;Ramachandran Subramanian ,&nbsp;Mobbassar Hassan Sk ,&nbsp;Yashi Singh ,&nbsp;Mirza S. Baig","doi":"10.1016/j.yexcr.2024.114393","DOIUrl":"10.1016/j.yexcr.2024.114393","url":null,"abstract":"<div><div>Cancer is characterized by unregulated cell proliferation, enabling it to invade and spread to different organs and tissues in the body. Cancer progression is intricately influenced by the complex dynamics within the tumor microenvironment (TME). The TME is a composite and dynamic network comprising cancer cells and various immune cells, including tumor-associated macrophages. Exosomes facilitate the communication between different cancer cells as well as other types of cells. This review particularly focuses on exosomal proteins derived from different cancer cells in mounting the complex crosstalk between cells of cancer and macrophages within the TME. Most cancer-derived exosomal proteins polarize macrophages towards M2 phenotype, promoting cancer aggressiveness, while a few have role switching towards the M1 phenotype, inhibiting cancer proliferation, respectively. In this review, we summarize, for the first time, the dual impact of cancer cell-derived exosomal proteins on macrophage polarization and the associated signaling pathways, offering valuable insights for developing innovative therapeutic strategies against diverse cancer types.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114393"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876283","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}

{"title":"SEMA3C promotes thyroid cancer via the Wnt/β-catenin pathway","authors":"Shiwei Li ,&nbsp;Yanmei Cheng ,&nbsp;Changhui Gao ,&nbsp;Qingling Yuan ,&nbsp;Xiubo Lu","doi":"10.1016/j.yexcr.2024.114378","DOIUrl":"10.1016/j.yexcr.2024.114378","url":null,"abstract":"<div><div>Semaphorin 3C (SEMA3C) regulates the progression of several tumors. However, the role of SEMA3C in thyroid cancer remains unknow. In the present study, SEMA3C was overexpressed or knocked down in thyroid cancer cell lines BCPAP and IHH-4. It was found that SEMA3C promoted the cell migration, invasion, and mesenchymal–epithelial transition (EMT) process. SEMA3C overexpression enhanced tumor cell stemness, while SEMA3C knockdown showed the opposite effects. In vivo experiments suggested that SEMA3C accelerated the tumor growth and metastasis. Moreover, SEMA3C enhanced β-catenin nuclear translocation. When cells were treated with Dickkopf-1 (DKK1), an inhibitor of Wnt/β-catenin pathway, the promoting effects of SEMA3C on cell migration and stemness were offset. Wnt/β-catenin pathway mediated the roles of SEMA3C in thyroid cancer. Additionally, an upstream regulator of SEMA3C was identified. E1A binding protein P300 (P300) was found to increase the histone three lysine 27 acetylation (H3K27ac) level of SEMA3C, promoting its transcriptional activation. Therefore, we clarify that SEMA3C exerts a tumor-promoting effect on thyroid cancer, and Wnt/β-catenin pathway is the critical downstream pathway.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114378"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817669","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}

{"title":"Exosomes derived from cardiac fibroblasts with Ang-II stimulation provoke myocardial hypertrophy via miR-15b-5p/PTEN-L axis","authors":"Zhiwen Hu ,&nbsp;Dijiu Xiao ,&nbsp;Liang Wang ,&nbsp;Jiaxiang You ,&nbsp;Tao Long ,&nbsp;Jinping Wang ,&nbsp;Yibiao Shang ,&nbsp;Dasong Yi ,&nbsp;Lu Ding ,&nbsp;Xiang Wang ,&nbsp;Xiaoping Peng ,&nbsp;Junyi Zeng","doi":"10.1016/j.yexcr.2024.114380","DOIUrl":"10.1016/j.yexcr.2024.114380","url":null,"abstract":"<div><div>This study aimed to examine the impact of exosomes derived from Ang II-stimulated cardiac fibroblasts (CFs) on myocardial hypertrophy. Neonatal rat CFs were isolated and identified using Vimentin immunofluorescence. Following Ang II stimulation, exosomes were collected, characterized, and subjected to miRNA sequencing. Myocardial hypertrophy models were induced both <em>in vitro</em> and <em>in vivo</em> using Ang II. CFs were transfected with miR-15b-5p mimics or inhibitors, and their exosomes were co-cultured with rat cardiomyocytes (H9C2). Changes in cell viability, myocardial hypertrophy, and the expression levels of PTEN-L, PINK1, and Parkin proteins were assessed using the CCK-8 assay, cell surface area evaluation, and Western blot analysis. Cardiac tissue pathology and myocardial hypertrophy were evaluated through HE and WAG staining, respectively, while PTEN-L expression was detected by immunohistochemistry. The results demonstrated successful isolation of CFs and their exosomes, with miR-15b-5p significantly enriched in the exosomes derived from Ang II-stimulated CFs (Ang II-CFs-Exos). Ang II-CFs-Exos inhibited cell viability, exacerbated myocardial hypertrophy, and activated mitophagy via miR-15b-5p in the <em>in vitro</em> myocardial hypertrophy model. PTEN-L was identified as a downstream target of miR-15b-5p, with its overexpression reversed the effects of miR-15b-5p mimic on myocardial hypertrophy and mitophagy. Additionally, mitochondrial inhibitors also countered the effects of the miR-15b-5p mimic on myocardial hypertrophy. Furthermore, Ang II-CFs-Exos exacerbated myocardial hypertrophy in rats, while knockout of miR-15b-5p in Ang II-CFs-Exos mitigated this effect. To sum up, Ang II-CFs-Exos promote myocardial hypertrophy by modulating PINK1/Parkin signaling -mediated mitophagy through the miR-15b-5p/PTEN-L axis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114380"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824068","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}

{"title":"AZD1390, an Ataxia telangiectasia mutated inhibitor, enhances cisplatin mediated apoptosis in breast cancer cells","authors":"Deniz Özdemir,&nbsp;Can Ali Ağca","doi":"10.1016/j.yexcr.2024.114382","DOIUrl":"10.1016/j.yexcr.2024.114382","url":null,"abstract":"<div><div>Genomic instability is often caused by deficiencies in DNA damage repair pathways, making therapeutic targeting of DDR beneficial for cancer patients with specific DDR functions. ATM kinase plays a critical role in various cellular processes and its deficiency increases sensitivity to DDR-targeted agents in different cancers. Recent studies highlight ATM inhibition as a potential clinical target, with AZD1390 being a notable ATM inhibitor due to its potent and selective inhibition, ability to accumulate at DNA breaks. The study aimed to evaluate the potential anti-cancer effects of AZD1390, a key component of the DNA damage response, in breast cancer cells. The impact of the combination of AZD1390 and cisplatin on various parameters such as cell viability, proliferation, colony formation capacity, DNA damage, reactive oxygen species (ROS) levels, mitochondrial membrane potential, cell cycle progression, and cell death in breast cancer cells was evaluated using several methodologies, including WST-1 assays, real-time cell analysis, colony formation assays, comet assays, DCF-DA, MMP/JC-1 staining assays, flow cytometry along with Western blot analysis. We found that AZD1390 and cisplatin displayed synergistic antitumor effects in breast cancer cells at low doses. Addinationaly exhibited significant anti-proliferative effects in colony formation and real-time cell proliferation experiments, increasing intracellular ROS levels and mitochondrial membrane potential.The combined treatment also arrested the cell cycle at the G2-M point. Furthermore, combination of AZD1390 with cisplatin enhances its apoptotic effects in MCF-7 and MDA-MB-231 cells. These findings could aid in developing new treatments for breast cancer that exploit the genomic instability of cancer cells.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114382"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142834858","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}

{"title":"Chronic hypoxia promotes pulmonary venous smooth muscle cell proliferation through the CaSR-TRPC6/ROCE pathway","authors":"Shaoxing Li ,&nbsp;Zhenli Fu ,&nbsp;Wei Hong ,&nbsp;Hong Yuan ,&nbsp;Weitao Cao ,&nbsp;Juan Xu ,&nbsp;Rongmin Liu ,&nbsp;Zhuandi Lin ,&nbsp;Zhiming Xiang ,&nbsp;Gongyong Peng","doi":"10.1016/j.yexcr.2024.114363","DOIUrl":"10.1016/j.yexcr.2024.114363","url":null,"abstract":"<div><div>The mechanism underlying chronic hypoxia (CH)-induced pulmonary venous remodeling remains unclear. Cell proliferation is key in vascular remodeling, and the calcium-sensing receptor (CaSR) protein contributes to CH-induced pulmonary venous smooth muscle cell (PVSMC) proliferation. In pulmonary arterial smooth muscle cells, CaSR and transient receptor potential canonical (TRPC) proteins interact, contributing to CH-induced cell proliferation via CaSR-TRPC1/6 signaling. We investigated whether a similar pathway exists in PVSMCs. Rat PVSMCs were isolated and subjected to CH. Cell proliferation was assessed by cell counting, CCK-8, and BrdU incorporation assays. Expression of CaSR and TRPC was analyzed by qPCR and western blotting, while interactions between CaSR and TRPC were detected by co-immunoprecipitation assay. Extracellular Ca²⁺ restoration was evaluated, to assess store- and receptor-operated Ca²⁺ entry (SOCE and ROCE, respectively). CH enhanced PVSMC numbers, viability, and DNA synthesis, and upregulated CaSR and TRPC6 expression. Further, CaSR and TRPC6 interacted with one another. CaSR inhibitors (NPS2143, NPS2390) reduced, whereas activators (spermine, R568) enhanced, CH-induced increases in PVSMC numbers, viability, DNA synthesis, and TRPC6 expression. CaSR knockdown using siRNA inhibited CH-induced TRPC6 upregulation and attenuated CH-induced increases in PVSMC numbers, viability, and DNA synthesis. TRPC6 knockdown had no significant effect on CH-induced CaSR upregulation, but significantly attenuated CH-induced increases in PVSMC number, viability, and DNA synthesis. CaSR knockdown reduced ROCE, but not SOCE, enhancement. Overall, CH promotes PVSMC proliferation through the CaSR-TRPC6/ROCE pathway.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114363"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785075","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}

{"title":"Quercetin promotes osteogenic differentiation of bone marrow mesenchymal stem cells by modulating the miR-214-3p/Wnt3a/β-catenin signaling pathway","authors":"Xueling Hu ,&nbsp;Xiaotong Lei ,&nbsp;Weiwen Lin ,&nbsp;Xiaoyun Li ,&nbsp;Wenqiang Zhong ,&nbsp;Bingjie Luo ,&nbsp;Ji Xie ,&nbsp;Ziwen Liang ,&nbsp;Yunchuan Li ,&nbsp;Jingli Qiu ,&nbsp;Panpan Wang ,&nbsp;Xiaofeng Zhu ,&nbsp;Ronghua Zhang ,&nbsp;Li Yang","doi":"10.1016/j.yexcr.2024.114386","DOIUrl":"10.1016/j.yexcr.2024.114386","url":null,"abstract":"<div><div>Postmenopausal osteoporosis, primarily driven by estrogen deficiency, is predominantly mediated through estrogen receptors such as ERα. However, the underlying mechanisms necessitate further investigation. In this study, we established an ERα-deficient model in rBMSCs to elucidate the role of ERα in osteogenic differentiation and miRNA expression profiles. Our findings demonstrate that knockdown of ERα inhibits osteogenic differentiation in rBMSCs, resulting in upregulation of 25 miRNAs and downregulation of 184 miRNAs, including a significant increase in the expression of miR-214-3p. Validation using qPCR, Western blotting, and bioinformatics analysis revealed that miR-214-3p negatively regulates osteogenic differentiation via the Wnt/β-catenin signaling pathway. Furthermore, we explored the potential therapeutic effects of quercetin (QUE) on rBMSCs. CCK8, alkaline phosphatase activity assays, and Alizarin Red staining demonstrated that QUE dose-dependently enhances rBMSCs proliferation, alkaline phosphatase activity, and mineralization within the concentration range of 0.1–1 μM. Importantly, QUE was found to downregulate miR-214-3p expression and activate the Wnt3a/β-catenin signaling pathway. Rescue experiments confirmed that QUE could counteract the inhibitory effects of miR-214-3p on the Wnt3a/β-catenin signaling pathway. Collectively, our study provides compelling evidence that knockdown of ERα inhibits the osteogenic differentiation of rBMSCs by affecting the miRNA expression profile, while QUE can reverse the inhibitory effect exerted by miR-214-3p on the Wnt3a/β-catenin signaling pathway, thereby offering novel insights into diagnosis, prevention, and treatment strategies for postmenopausal osteoporosis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114386"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853600","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}

{"title":"Combined injection of pristane and Bacillus Calmette-Guerin Vaccine successfully establishes a lupus model with atherosclerosis","authors":"Chunru Jiang ,&nbsp;Zhenduo Zhu ,&nbsp;Yu Tai ,&nbsp;Meiyue Lu ,&nbsp;Huijuan Cheng ,&nbsp;Tiantian Su ,&nbsp;Paipai Guo ,&nbsp;Ruhong Fang ,&nbsp;Feng He ,&nbsp;Mingli Ge ,&nbsp;Qiuyun Guan ,&nbsp;Yongsheng Han ,&nbsp;Shangxue Yan ,&nbsp;Wei Wei ,&nbsp;Qingtong Wang","doi":"10.1016/j.yexcr.2024.114381","DOIUrl":"10.1016/j.yexcr.2024.114381","url":null,"abstract":"<div><div>Cardiovascular disease (CVD) induced by atherosclerosis (AS) is the main fatal complication of systemic lupus erythematosus (SLE). Establishing an appropriate animal model of SLE with AS is of great value for investigating the pathogenesis and therapeutic targets of SLE-CVD. In the present work, pristane was injected intraperitoneally into C57BL/6J mice to establish the SLE model and Bacillus Calmette-Guerin Vaccine (BCG) was injected intradermally one month later to enhance immunity and induce AS. Both pristane or pristane and BCG treated C57BL/6J mice exhibit a classical lupus-like phenotype which manifested as proteinuria and high levels of serum anti-ANA and anti-dsDNA autoantibodies, in conjunction with pathological changes in spleen and kidney, complement C3 deposition in the kidney, overactivation of T and B cells, a decreased proportion of splenic CD19⁺ B cells, and an increased frequency of CD19⁻CD138⁺ plasma cells, CD19⁺CD27⁺ memory B cells, CD3⁺CD4⁺ helper T (Th) cells, and CD3⁺CD4⁺CXCR5⁺PD-1⁺ T follicular helper cells. The combined pristane and BCG challenge aggravated AS in SLE mice, which had an enlarged thymus gland, an increased T cell proliferative vitality, an expanded Th cell pool, severe perivascular lymphocytes, and CD68⁺ macrophage infiltration, in addition to an intimal lipid deposition, and further elevation of Toll-like receptor 2 (TLR2), TLR4, and the transcription factor nuclear factor-κB (NF-κB) expression in kidney tissue and blood vessels when comparing with pristane or BCG injection alone. Pristane combined BCG challenge is able to establish a validated SLE-AS mouse model in C57BL/6J mice.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114381"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827974","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}

{"title":"Targeting METTL8 with Rabdosiin overcomes lenvatinib resistance in hepatocellular carcinoma","authors":"Yunpeng Liu ,&nbsp;Muhua Chen ,&nbsp;Xiang-Xu Wang ,&nbsp;Yuan Gao ,&nbsp;Xiao Han ,&nbsp;Shuning Wang ,&nbsp;Wangqian Zhang ,&nbsp;Xiaoying Lei ,&nbsp;Pengfei Yu ,&nbsp;Lei Liu ,&nbsp;Hong-Mei Zhang ,&nbsp;Kuo Zhang","doi":"10.1016/j.yexcr.2024.114389","DOIUrl":"10.1016/j.yexcr.2024.114389","url":null,"abstract":"<div><div>In hepatocellular carcinoma (HCC), lenvatinib is a key first-line treatment that significantly improves survival in some patients with advanced stage. However, lenvatinib resistance presents a major clinical challenge. This study aims to identify key molecular factors driving lenvatinib resistance in HCC and propose intervention strategies to overcome this resistance, thereby enhancing therapeutic efficacy. A genome-wide CRISPR-Cas9 activation screen identified METTL8 as a crucial gene associated with lenvatinib resistance. Validation through <em>in vitro</em> and <em>in vivo</em> assays confirmed METTL8's role in mediating lenvatinib resistance. Higher METTL8 expression was observed in lenvatinib-resistant HCC cells compared to parental cells. Immunohistochemical staining of tissue sections from HCC patients revealed a negative correlation between high METTL8 expression and lenvatinib sensitivity. To inhibit the function of METTL8 that mediate lenvatinib resistance, we conducted a screening using a natural compound library, virtual drug screening identified Rabdosiin as a potential METTL8 inhibitor, subsequent experiments demonstrated that Rabdosiin could effectively overcome METTL8-mediated lenvatinib resistance. In conclusion, this research highlights METTL8 as a novel target for mitigating lenvatinib resistance, proposing that targeting METTL8 could restore lenvatinib sensitivity in HCC, and underscores its value as a biomarker for lenvatinib application in clinical settings.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114389"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863897","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}

{"title":"Mechanism of RBM15 in the malignant proliferation of colorectal cancer cells through regulating the stability of LncRNA FGD5-AS1 via m6A modification","authors":"Lin Ma ,&nbsp;Weihua Liu ,&nbsp;Xin Wang ,&nbsp;Dezheng Li ,&nbsp;Chuankui Wei","doi":"10.1016/j.yexcr.2024.114384","DOIUrl":"10.1016/j.yexcr.2024.114384","url":null,"abstract":"<div><div>Colorectal cancer (CRC) is the third most prevalent cancer all around the world. This study explored the mechanism of RBM15-mediated m6A modification in CRC cell malignant proliferation. The expression of RBM15, LncRNA FGD5-AS1, and HOXC10 was detected in CRC cells. m6A levels in cells and m6A enrichment on FGD5-AS1 RNA were analyzed. FGD5-AS1 RNA stability and localization in CRC cells were analyzed. The binding of LncRNA FGD5-AS1 to YBX1 and YBX1 to the HOXC10 promoter was analyzed. Combined experiments were conducted to validate the mechanism. Tumor xenografts in nude mice were used to verify the mechanism of RBM15 <em>in vivo</em>. RBM15 was highly expressed in CRC cells. RBM15 inhibition suppressed CRC cell proliferation and reduced PCNA expression. RBM15 increased m6A modification on FGD5-AS1 RNA, enhancing FGD5-AS1 stability and expression. FGD5-AS1 promoted HOXC10 expression by recruiting YBX1 to the HOXC10 promoter. YBX1 inhibition suppressed HOXC10 expression. Overexpression of FGD5-AS1 or HOXC10 partially reversed the alleviative effect of RBM15 inhibition on CRC cell proliferation. RBM15 downregulation attenuated <em>in vivo</em> CRC cell proliferation by inhibiting the FGD5-AS1/HOXC10 axis. In conclusion, RBM15 promotes the FGD5-AS1/HOXC10 axis via m6A modification to promote CRC cell proliferation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114384"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863898","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}

{"title":"Paradigm shift: microRNAs interact with target gene promoters to cause transcriptional gene activation or silencing","authors":"Neelanjana Sarkar,&nbsp;Arun Kumar","doi":"10.1016/j.yexcr.2024.114372","DOIUrl":"10.1016/j.yexcr.2024.114372","url":null,"abstract":"<div><div>MicroRNAs (miRNAs/miRs) are small (18–25 nucleotides in length), endogenous, non-coding RNAs that typically repress gene expression by interacting with the 3′untranslated regions (3′UTRs) of target mRNAs in the cytoplasm. While most of the scientific community still views miRNAs as repressors of gene expression, this review highlights their non-canonical novel role in the nucleus as activators or silencers of target gene transcription through miRNA-promoter interaction. The mechanistic details of the transcriptional role of miRNAs are yet to be elucidated, however, they can be explained by prospective models. In this review, we aim to discuss the different examples of transcriptional regulation by miRNAs and their possible mechanism of action, thereby offering a comprehensive perspective on the role of miRNAs in gene regulation and their importance in health and diseases.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114372"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812409","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}