Experimental cell research最新文献_第3页

Chronic hypoxia promotes pulmonary venous smooth muscle cell proliferation through the CaSR-TRPC6/ROCE pathway.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-12-03 DOI: 10.1016/j.yexcr.2024.114363

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

{"title":"Chronic hypoxia promotes pulmonary venous smooth muscle cell proliferation through the CaSR-TRPC6/ROCE pathway.","authors":"Shaoxing Li, Zhenli Fu, Wei Hong, Hong Yuan, Weitao Cao, Juan Xu, Rongmin Liu, Zhuandi Lin, Zhiming Xiang, Gongyong Peng","doi":"10.1016/j.yexcr.2024.114363","DOIUrl":"10.1016/j.yexcr.2024.114363","url":null,"abstract":"<p><p>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 Ca<sup>2+</sup> restoration was evaluated, to assess store- and receptor-operated Ca<sup>2+</sup> 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.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114363"},"PeriodicalIF":3.3,"publicationDate":"2024-12-03","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Long non-coding RNAs and their role in breast cancer pathogenesis and drug resistance: Navigating the non-coding landscape review.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-12-01 DOI: 10.1016/j.yexcr.2024.114365

Tohada M Al-Noshokaty, Gharieb S El-Sayyad, Rehab Abdelhamid, Abdallah Mansour, Nourhan Abdellatif, Ayat Alaaeldien, Tasnim Reda, David Gendi, Nourhan M Abdelmaksoud, Shereen Saeid Elshaer, Ahmed S Doghish, Osama A Mohammed, Ahmed I Abulsoud

{"title":"Long non-coding RNAs and their role in breast cancer pathogenesis and drug resistance: Navigating the non-coding landscape review.","authors":"Tohada M Al-Noshokaty, Gharieb S El-Sayyad, Rehab Abdelhamid, Abdallah Mansour, Nourhan Abdellatif, Ayat Alaaeldien, Tasnim Reda, David Gendi, Nourhan M Abdelmaksoud, Shereen Saeid Elshaer, Ahmed S Doghish, Osama A Mohammed, Ahmed I Abulsoud","doi":"10.1016/j.yexcr.2024.114365","DOIUrl":"10.1016/j.yexcr.2024.114365","url":null,"abstract":"<p><p>Despite the progress made in the development of targeted therapies, breast cancer (BC) continues to pose a significant threat to the health of women. Transcriptomics has emerged due to the advancements in high-throughput sequencing technology. This provides crucial information about the role of non-coding RNAs (ncRNAs) in human cells, particularly long ncRNAs (lncRNAs), in disease development and function. When the control of these ncRNAs is disrupted, various illnesses emerge, including cancer. Numerous studies have produced empirical data on the function of lncRNAs in tumorigenesis and disease development. However, the roles and mechanisms of numerous lncRNAs remain unidentified at the molecular level because their regulatory role and the functional implications of abnormalities in cancer biology have yet to be thoroughly defined. The review gives an itemized summary of the most current developments in the role of lncRNA in BC, focusing on three main pathways, PI3K, MAPK, NF-kB, and hypoxia, and their resistance mechanisms.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114365"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767481","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

lncRNA-NEF regulates hepatic stellate cells proliferation, cell cycle, apoptosis and ECM synthesis through the ERK1/2/c-Fos axis.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-11-30 DOI: 10.1016/j.yexcr.2024.114361

Gang-Gang Jia, Li-Xia Lu, Bin- Li, Chu-Yi Li, Ying- Zheng, Jiu-Cong Zhang, Yu-Jing He, Xu-Shi, Xiao-Hui Yu

{"title":"lncRNA-NEF regulates hepatic stellate cells proliferation, cell cycle, apoptosis and ECM synthesis through the ERK1/2/c-Fos axis.","authors":"Gang-Gang Jia, Li-Xia Lu, Bin- Li, Chu-Yi Li, Ying- Zheng, Jiu-Cong Zhang, Yu-Jing He, Xu-Shi, Xiao-Hui Yu","doi":"10.1016/j.yexcr.2024.114361","DOIUrl":"https://doi.org/10.1016/j.yexcr.2024.114361","url":null,"abstract":"<p><p>In this study, we investigated the role of lncRNA-NEF in modulating hepatic stellate cell (HSC) activation, a key process in liver fibrosis. Using the GSE78160 dataset, we identified lncRNA-NEF as downregulated in liver cirrhosis patients. Gene Ontology and KEGG analyses implicated it in transcriptional regulation and cell cycle control. We established an activated HSC model with TGF-β1-treated LX-2 cells and employed RT-qPCR and Western blot to assess lncRNA-NEF and ERK1/2 expression. Lentiviral transfection was used to overexpress lncRNA-NEF in activated LX-2 cells, and its effects on proliferation, apoptosis, and cell cycle were evaluated using EdU staining, CCK-8, Annexin-V PE/7-AAD, TUNEL, and PI-FACS analysis. Overexpression of lncRNA-NEF led to reduced cell proliferation, increased apoptosis, and cell cycle arrest at the S and G2/M phases. We also observed a decrease in ERK1/2, c-Fos, Collagen I, α-SMA, and Bcl-2 expression, and an increase in Caspase-3 expression, as confirmed by Western blot. These results suggest that lncRNA-NEF regulates HSC activation via the ERK1/2/c-Fos axis, potentially offering a therapeutic target for antifibrotic drug development. Our findings provide a molecular basis for understanding the role of lncRNAs in liver fibrosis and highlight the potential of lncRNA-NEF as a novel antifibrotic target.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"114361"},"PeriodicalIF":3.3,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767586","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

The anillin knockdown in the Drosophila nervous system shows locomotor and learning defects.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-11-30 DOI: 10.1016/j.yexcr.2024.114364

Man Anh Huynh, Dang Thi Phuong Thao, Hideki Yoshida

引用次数: 0

Knockdown of PELI1 promotes Th2 and Treg cell differentiation in juvenile idiopathic arthritis.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-11-29 DOI: 10.1016/j.yexcr.2024.114360

Dan Li, Xiaoqing Li, Mingyue Duan, Xiuhong Xue, Xianyan Tang, Nan Nan, Rui Zhao, Wenhua Zhang, Wanggang Zhang

{"title":"Knockdown of PELI1 promotes Th2 and Treg cell differentiation in juvenile idiopathic arthritis.","authors":"Dan Li, Xiaoqing Li, Mingyue Duan, Xiuhong Xue, Xianyan Tang, Nan Nan, Rui Zhao, Wenhua Zhang, Wanggang Zhang","doi":"10.1016/j.yexcr.2024.114360","DOIUrl":"10.1016/j.yexcr.2024.114360","url":null,"abstract":"<p><p>Pellino1 (PELI1) is a key regulator of inflammatory and autoimmune diseases. The role of PELI1 in juvenile idiopathic arthritis (JIA) is unclear. The correlation between serum PELI1 mRNA levels and clinical indicators of JIA patients was evaluated by Pearson correlation analysis. The percentage of Th1, Th2, Th17 and Treg cells was analyzed by flow cytometry. ELISA kits were used to detect cytokine levels in serum and cell supernatants. Co-immunoprecipitation experiments were performed to validate PELI1 and TCF-1 interactions. The protein and ubiquitination levels of TCF-1 were detected by western blot. The results showed that JIA patients have high serum PELI1 levels. PELI1 levels were positively correlated with erythrocyte sedimentation rate, C-reactive protein levels and JADAS27 scores in JIA patients. Interfering with PELI1 promoted naïve CD4<sup>+</sup> T cell differentiation to Th2 and Treg cells and increased IL-4 and IL-10 levels, while inhibiting their differentiation to Th1 and Th17 cells and decreasing IFN-γ and IL-17 levels. PELI1 increased TCF-1 ubiquitination levels and accelerated its degradation. Inhibition of TCF-1 reduced the effects of interfering with PELI1 on cell differentiation and cytokine levels. In conclusion, Silencing of PELI1 facilitated the naïve CD4<sup>+</sup> T cell differentiation into Th2 and Treg cells by TCF-1.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114360"},"PeriodicalIF":3.3,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767477","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

Ganoderma lucidum extract reverses multidrug resistance in breast cancer cells through inhibiting ATPase activity of the P-glycoprotein via MAPK/ERK signaling pathway.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-11-28 DOI: 10.1016/j.yexcr.2024.114355

Chunwei Jiao, Jinshou Qiu, Congcong Gong, Xiaoyi Li, Huijia Liang, Chunyan He, Sien Cen, Yizhen Xie

{"title":"Ganoderma lucidum extract reverses multidrug resistance in breast cancer cells through inhibiting ATPase activity of the P-glycoprotein via MAPK/ERK signaling pathway.","authors":"Chunwei Jiao, Jinshou Qiu, Congcong Gong, Xiaoyi Li, Huijia Liang, Chunyan He, Sien Cen, Yizhen Xie","doi":"10.1016/j.yexcr.2024.114355","DOIUrl":"10.1016/j.yexcr.2024.114355","url":null,"abstract":"<p><p>Breast cancer represents a persistent global health challenge, with multidrug resistance (MDR) posing a significant obstacle to effective treatment. In this study, we investigate the potential of Ganoderma lucidum extract (GLE) in reversing MDR in breast cancer and delve into the underlying mechanisms. We establish a robust in vitro 3D model of breast cancer with acquired MDR induced by paclitaxel. Utilizing the CCK-8 method, we assess the impact of GLE on cytotoxic drug sensitivity to determine its in vitro MDR reversal activity. Our results reveal that GLE enhances the toxicity of paclitaxel in breast cancer cells by inhibiting the ATPase activity of P-glycoprotein (P-gp) and increasing the intracellular and extracellular excretion of P-gp substrates, all without significantly altering P-gp protein expression. Additionally, GLE inhibits the phosphorylation of ERK1/2, suggesting that the enhanced sensitivity of breast cancer cells to paclitaxel by GLE is associated with the MAPK pathway. These findings indicate that GLE may inhibit P-gp-mediated drug efflux via the MAPK pathway, thus effectively overcoming paclitaxel resistance in breast cancer. This study provides valuable insights into the potential clinical applications of GLE in reversing multidrug resistance, offering hope for improved breast cancer treatment strategies.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114355"},"PeriodicalIF":3.3,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754920","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

Mechanism of METTL3 in the proliferation, invasion, and migration of intrahepatic cholangiocarcinoma cells via m6A modification.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-11-26 DOI: 10.1016/j.yexcr.2024.114353

Xinmiao Jiang, Hui Tan

{"title":"Mechanism of METTL3 in the proliferation, invasion, and migration of intrahepatic cholangiocarcinoma cells via m6A modification.","authors":"Xinmiao Jiang, Hui Tan","doi":"10.1016/j.yexcr.2024.114353","DOIUrl":"10.1016/j.yexcr.2024.114353","url":null,"abstract":"<p><p>Intrahepatic cholangiocarcinoma (ICC) is a primary invasive malignant tumor. This study was conducted to explore the role of methyltransferase-like 3 (METTL3)-mediated m6A modification in ICC cells and provide novel targets for ICC treatment. Levels of METTL3/YTH N6-methyladenosine RNA binding protein 2 (YTHDF2)/Nedd4 family interacting protein 1 (NDFIP1) in cells were determined. Cell viability, proliferation, invasion, and migration were evaluated. The enrichments of METTL3, YTHDF2, and m6A on NDFIP1 mRNA were analyzed. The mRNA stability was determined. Inhibition of YTHDF2 or NDFIP1 was combined with si-METTL3 to confirm the mechanism. The role of METTL3 in vivo was verified. METTL3 was overexpressed in ICC cells. METTL3 silencing suppressed ICC cell malignant behaviors, which were reversed by METTL3 overexpression. METTL3 increased m6A modification on NDFIP1 mRNA, facilitated YTHDF2 recognition of m6A, and promoted NDFIP1 mRNA degradation, thereby suppressing NDFIP1 expression. YTHDF2 inhibition increased NDFIP1 mRNA levels. NDFIP1 downregulation partially reversed the inhibitory effects of si-METTL3 on ICC cell behaviors, while NDFIP1 overexpression partially reversed the promotive effects of METTL3 on ICC cell behaviors. METTL3 downregulation suppressed ICC growth by increasing NDFIP1 expression. In conclusion, METTL3 aggravates ICC cell proliferation, invasion, and migration by promoting the degradation of NDFIP1 mRNA in a YTHDF2-dependent manner.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114353"},"PeriodicalIF":3.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750419","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

Protective effects of tissue factor pathway inhibitor on mice with lipopolysaccharide-induced acute lung injury 组织因子通路抑制剂对脂多糖诱发急性肺损伤小鼠的保护作用

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-11-26 DOI: 10.1016/j.yexcr.2024.114357

Posum Wan , Kaiheng Gao , Feng Miao, Meng Shi, Xiaofeng Chen

{"title":"Protective effects of tissue factor pathway inhibitor on mice with lipopolysaccharide-induced acute lung injury","authors":"Posum Wan , Kaiheng Gao , Feng Miao, Meng Shi, Xiaofeng Chen","doi":"10.1016/j.yexcr.2024.114357","DOIUrl":"10.1016/j.yexcr.2024.114357","url":null,"abstract":"<div><div>Acute lung injury (ALI) resulting from bacterial infection poses a significant risk, and its etiology involves the complex interplay of harmful immune responses and blood coagulation. Despite this understanding, the roles and mechanisms of tissue factor pathway inhibitor (TFPI) in LPS-induced ALI remain insufficiently elucidated. In this study, we aimed to explore the effects of TFPI in LPS-induced ALI. Our investigations revealed that TFPI exerts multiple beneficial effects in LPS-induced ALI. Specifically, TFPI reduces microvascular permeability, Myeloperoxidase (MPO) activity, and cytokine production while inhibiting blood coagulation. Moreover, TFPI demonstrates the capacity to promote proliferation and suppress apoptosis in Human microvascular endothelial cells (HMEC-1) and Human umbilical vein endothelial cells (HUVEC) through the inhibition of the caspase pathway and mitochondrial apoptosis pathway. Furthermore, our findings indicate a correlation between tissue factor (TF) and TFPI expression, with TFPI regulation observed in HMEC-1 cells following LPS treatment. This novel insight suggests that TFPI plays a regulatory role in TF expression. Overall, the protective effect of TFPI on LPS-induced ALI is unveiled by its ability to enhance endothelial cell proliferation and inhibit apoptosis through the modulation of caspase and Bcl-2/Bax pathways. These results underscore the potential of TFPI as a promising therapeutic target for ALI treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114357"},"PeriodicalIF":3.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738909","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

COPS5 regulates osteosarcoma progression by upregulating KHSRP to promote Per2 mRNA decay

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-11-26 DOI: 10.1016/j.yexcr.2024.114358

Jie Bu, Xuezheng Xu, Yi Luo, Jianfan Liu, Xinyu Yao

{"title":"COPS5 regulates osteosarcoma progression by upregulating KHSRP to promote Per2 mRNA decay","authors":"Jie Bu, Xuezheng Xu, Yi Luo, Jianfan Liu, Xinyu Yao","doi":"10.1016/j.yexcr.2024.114358","DOIUrl":"10.1016/j.yexcr.2024.114358","url":null,"abstract":"<div><div>Osteosarcoma (OS) is a common bone sarcoma that is often seen in children and adolescents. This study delves into the intricate regulatory network involving COP9 signalosome subunit 5 (COPS5), KH-type splicing regulatory protein (KHSRP), and Period circadian clock 2 (Per2) in the context of osteosarcoma cell malignant phenotype. CCK-8 assay was applied to assess cell proliferation. Wound healing or transwell assay was selected to evaluate cell migration or invasion. Apoptosis was determined employing flow cytometry assay. Co-IP and GST-pull down determined the interaction between COPS5 and KHSRP. The interaction relationship between KHSRP and Per2 mRNA was detected by RNA-pull down and RIP assays. We found that COPS5 knockdown repressed proliferation, migration, and invasion and facilitated apoptosis of OS cells. Knockdown of COPS5 also restrained the tumor growth in the nude mice tumor xenograft model. COPS5 interacted with KHSRP to maintain the protein stability of KHSRP. Furthermore, there was a binding relationship between KHSRP and Per2 mRNA. Besides, COPS5 promoted OS cell tumorigenesis by mediating the decay effect of KHSRP on Per2 mRNA. Collectively, COPS5 promoted the decay of Per2 mRNA via contacting and mediating KHSRP, thereby facilitating OS progression. Our study unveils COPS5 as a key modulator in OS.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114358"},"PeriodicalIF":3.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142744083","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

Exosomal noncoding RNA (ncRNA) in breast cancer pathogenesis and therapy; two sides of the same coin

IF 3.3 3区生物学

Experimental cell research Pub Date : 2024-11-26 DOI: 10.1016/j.yexcr.2024.114359

Fatma Magdi Ibrahim , Raed Obaid Saleh , Herlina Uinarni , Dmitry Olegovich Bokov , Soumya V. Menon , Khamdamov Baxtiyor Zarifovich , Neeti Misra , Mais Mazin Al-Hamdani , Beneen Husseen , Mohammed Abed Jawad

{"title":"Exosomal noncoding RNA (ncRNA) in breast cancer pathogenesis and therapy; two sides of the same coin","authors":"Fatma Magdi Ibrahim , Raed Obaid Saleh , Herlina Uinarni , Dmitry Olegovich Bokov , Soumya V. Menon , Khamdamov Baxtiyor Zarifovich , Neeti Misra , Mais Mazin Al-Hamdani , Beneen Husseen , Mohammed Abed Jawad","doi":"10.1016/j.yexcr.2024.114359","DOIUrl":"10.1016/j.yexcr.2024.114359","url":null,"abstract":"<div><div>Over the past few years, breast cancer has become the most prevalent type of cancer globally, with the primary cause of death from the disease being metastatic cancer. This has led to the development of early detection techniques, mainly using non-invasive biomarkers in a range of body fluids. Exosomes are unique extracellular vesicles (EVs) transmitting cellular signals over great distances via various cargo. They are readily apparent in physiological fluids due to release by breast cancer cells or breast cancer-tumor microenvironment (TME) cells. In light of this, numerous biological and functional facets of human tumours, such as breast cancer, are intimately associated with exosomal noncoding RNAs (ncRNAs), containing miRNAs (microRNAs), lncRNAs (long noncoding RNAs), and circRNAs (circular RNAs). Exosomal ncRNAs serve a critical role in various steps of breast cancer development, enabling the exchange of genetic information between cancer cells and other cells (e.g., immune cells), thus regulating tumour angiogenesis, growth, metastasis, immune responses and drug resistance. They interact with multiple regulatory complexes with dissimilar enzymatic actions, which, in turn, modify the chromatin sceneries, including nucleosome modifications, DNA methylation, and histone modifications. Herein, we look into the exosomes' underlying regulatory mechanisms in breast cancer. Furthermore, we inspect the existing understanding of the functions of exosomal miRNAs, lncRNAs, and circRNAs in breast cancer to authenticate their possible significance in identifying biomarkers, deciphering their role in immune escape and drug resistance, and finally, analyzing treatment practices.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114359"},"PeriodicalIF":3.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142744082","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