共查询到20条相似文献,搜索用时 15 毫秒
1.
Tao Xu Bang-Shun He Bei Pan Yu-Qin Pan Hui-Ling Sun Xiang-Xiang Liu Xue-Ni Xu Xiao-Xiang Chen Kai-Xuan Zeng Mu Xu Shu-Kui Wang 《Journal of cellular physiology》2020,235(5):4928-4940
MicroRNA-142-3p (miR-142-3p) was previously investigated in various cancers, whereas, it's role in breast cancer (BC) remains far from understood. In this study, we found that miR-142-3p was markedly decreased both in cell lines and BC tumor tissues. Elevated miR-142-3p expression suppressed growth and metastasis of BC cell lines via gain-of-function assay in vitro and in vivo. Mechanistically, miR-142-3p could regulate the ras-related C3 botulinum toxin substrate 1 (RAC1) expression in protein level, which simultaneously suppressed the epithelial-to-mesenchymal transition related protein levels and the activity of PAK1 phosphorylation, respectively. In addition, rescue experiments revealed RAC1 overexpression could reverse tumor-suppressive role of miR-142-3p. Our results showed miR-142-3p could function as a tumor suppressor via targeting RAC1/PAK1 pathway in BC, suggesting a potent therapeutic target for BC treatment. 相似文献
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Zi-Bin Zhang Liu-Lin Xiong Lu-Lu Xue Yan-Ping Deng Ruo-Lan Du Qiao Hu Yang Xu Si-Jin Yang Ting-Hua Wang 《Cell death & disease》2021,12(3)
Neonatal hypoxic–ischemic (HI) injury derived from asphyxia during perinatal period, is a serious complication of neonatal asphyxia and the main cause of neonatal acute death and chronic neurological injury. Aberrant autophagy occurs in many nervous system diseases, but its role and underlying mechanism in HI injury is largely unknown. Here, we successfully constructed a newborn rat model of HI brain injury, and the knockout-miR-127-3p (KO-miR-127-3p) rats were structured by using CRISPR/Cas9. Subsequently, the in vitro functional experiments, in vivo zea-longa scores, as well as bioinformatics analyses and biological experiments were applied. The expression of autophagy-related proteins, including ATG12, P62, Beclin-1, LC3II in HI cortex with miR-127-3p knockout was significantly decreased, and autophagic vacuoles were disappeared. Moreover, miR-127-3p has a specific regulatory effect on CISD1 expression, another crucial molecule in autophagy process. Accordingly, the overexpression of CISD1 effectively inhibited the autophagic cell death and physiological dysfunction in the brain of HI injury, whereas si-CISD1 reversed the neuroprotective effects of KO-miR-127-3p. Our findings explained the underlying mechanism for HI injury, and miR-127-3p targeting CISD1 signal could be supposed as a new treatment strategy to prevent and treat HI injury.Subject terms: Autophagy, Molecular biology 相似文献
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Shaohang Cheng Zhenghong Di Abdul Razaq Hirman Heng Zheng Linna Duo Qianyu Zhai 《Bioscience, biotechnology, and biochemistry》2020,84(10):2005-2013
ABSTRACT Atopic dermatitis (AD) is a relapsing inflammatory skin disease with a complicated pathogenesis. This study aimed to investigate whether miR-375-3p could regulate AD through the Yes-associated protein 1 (YAP1) pathway. In this study, inflammatory response was induced by TNF-α and IFN-γ administration in HaCaT cells. We found that viability and inflammatory factor release, including interleukin-1β (IL-1β) and IL-6, were negatively related to miR-375-3p expression in HaCaT cells. We also found that YAP1 overexpression down-regulated lympho-epithelial Kazal type inhibitor (LEKTI) levels and aggravated viability and inflammation in TNF-α and IFN-γ-treated HaCaT cells. Dual-luciferase reporter assay proved the targeted binding of miR-375-3p and YAP1 3?-UTR. Additionally, the protective effect of miR-375-3p on inflammatory response in TNF-α and IFN-γ-treated HaCaT cells could be impeded by YAP1 overexpression. Collectively, our results suggested that miR-375-3p could modulate HaCaT cell viability and inflammation through the YAP1/LEKTI pathway. 相似文献
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Background
MiR-155 has emerged as an “oncomiR”, which is the most significantly up-regulated miRNA in breast cancer. However, the mechanisms of miR-155 functions as an oncomiR are mainly unknown. In this study, the aims were to investigate the effects of miR-155 on cell proliferation, cell cycle, and cell apoptosis of ERalpha (+) breast cancer cells and to verify whether TP53INP1 (tumor protein 53-induced nuclear protein 1) is a target of miR-155, and tried to explore the mechanisms of miR-155 in this process.Results
The expression of miR-155 is significantly higher in MCF-7 cells compared with MDA-MB-231 cells. Ectopic expression of TP53INP1 inhibits growth of MCF-7 cells by inducing cell apoptosis and inhibiting cell cycle progression. Overexpression of miR-155 increases cell proliferation and suppress cell apoptosis, whereas abrogating expression of miR-155 suppress cell proliferation and promotes cell apoptosis of MCF-7 cells. In addition, miR-155 negatively regulates TP53INP1 mRNA expression and the protein expression of TP53INP1, cleaved-caspase-3, -8, -9, and p21, and luciferase reporter reveals that TP53INP1 is targeted by miR-155.Conclusions
TP53INP1 is the direct target of miR-155. MiR-155, which is overexpressed in MCF-7 cells, contributes to proliferation of MCF-7 cells possibly through down-regulating target TP53INP1. 相似文献7.
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Zhou Rongjun Luo Zhen Yin Guanqun Yu Lanting Zhong Hao 《Journal of molecular histology》2022,53(2):297-308
Journal of Molecular Histology - Breast cancer bone metastases may block normal bone remodeling and promote bone degradation, during which several signaling pathways and small non-coding miRNAs... 相似文献
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Ovarian cancer is one of the leading malignancies in women and the 5-year survival rate of ovarian cancer still remains poor. In the present study, we aimed to investigate the interaction between the miR-126-3p and PLXNB2 in the progression of ovarian cancer. The qRT-PCR data revealed a reduction of miR-126-3p level in ovarian cancer tissues comparing to the adjacent normal tissues. Over-expression of miR-126-3p in ovarian cancer cells suppressed cell proliferation and invasion and the phosphorylation of AKT and ERK1/2. The cell cycle assay results showed that the over-expression of miR-126-3p induced cells in G1-phase and reduced cells in S-phase. We further performed bioinformatics analysis and luciferase assay to investigate the relationship between miR-126-3p and PLXNB2 in ovarian cancer cells. The results of TargetScan suggested that PLXNB2 is a direct target of miR-126-3p in ovarian cancer cells, and luciferase assay confirmed bioinformatics prediction. Knocking down of PLXNB2 with PLXNB2 siRNA results in repressed ovarian cancer cell proliferation and invasion, and decreased phosphorylation of AKT and ERK1/2, which is similar to the effect of over-expression of miR-126-3p in OC cells. The synergistic effect of combination of miR-126-3p over-expression and PLXNB2 down-regulation on the cell growth viability, cell colony, and cell invasion was also identified. All these findings indicated that miR-126-3p is involved in the progression of ovarian cancer via direct regulating PLXNB2. 相似文献
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Xiaolin Wang Jialun Shi Zhigao Niu Jianwu Wang 《Bioscience, biotechnology, and biochemistry》2020,84(10):2014-2027
ABSTRACT Effect of miR-216a-3p on lung cancer hasn’t been investigated. Here, we explored its effects on lung cancer. MiR-216a-3p expression in lung cancer tissues and cells was detected by RT-qPCR. The target gene of miR-216a-3p was predicted by bioinformatics and confirmed by luciferase-reporter assay. After transfection, cell viability, migration, invasion, proliferation, and apoptosis were detected by MTT, scratch, transwell, colony formation, and flow cytometry. The expressions of COPB2 and apoptosis-related factors were detected by RT-qPCR or western blot. MiR-216a-3p was low-expressed and COPB2 was high-expressed in lung cancer tissues and cells. MiR-216a-3p targeted COPB2 and regulated its expression. MiR-216a-3p inhibited lung cancer cell viability, migration, invasion, and proliferation, while promoted apoptosis. Effect of miR-216a-3p on lung cancer was reversed by COPB2. MiR-216a-3p regulated proliferation, apoptosis, migration, and invasion of lung cancer cells via targeting COPB2. 相似文献
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Li Jingyan Zhang Zhanlei Hu Jieting Wan Xiaoting Huang Wei Zhang Hong Jiang Ningyi 《Molecular and cellular biochemistry》2022,477(3):649-661
Molecular and Cellular Biochemistry - One of the most prevalent forms of endocrine malignancies is thyroid cancer. Herein, we explored the mechanisms whereby miR-1246 is involved in thyroid cancer.... 相似文献
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《Genomics》2021,113(4):1689-1704
Maternally expressed 3 (MEG3) and RNA binding motif single stranded interacting protein 3 (RBMS3) are abnormally expressed in breast cancer susceptibility genes (BRCA), but the mechanism of the two in breast cancer (BC) is unclear. By performing in vivo and in vitro experiments, we found that MEG3 and RBMS3 were low-expressed, negatively correlated with high-expressed miR-141-3p, were positively correlated with each other in BC. MEG3 targeted miR-141-3p, and miR-141-3p targeted RBMS3. MEG3, which was mainly distributed in BC cytoplasm, could down-regulate miR-141-3p and up-regulate RBMS3, and reverse effect of miR-141-3p on related gene expressions and on promoting cancer development. Overexpressed MEG3 inhibited growth of xenografts, promoted cell apoptosis via regulating apoptosis related factors, and up-regulated RBMS3 expression but down-regulated miR-141-3p. The findings of this study showed that MEG3 inhibited proliferation and promoted apoptosis of BC cells through the miR-141-3p/RBMS3 axis, and MEG3 inhibited growth of xenografts through miR-141-3p. 相似文献
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Lina Bu Yingxuan Tian Hongqing Wen Weihong Jia Shuanying Yang 《Acta biochimica et biophysica Sinica》2021,(2):189-200
miR-195-5p has been widely explored in various cancers and is considered as a tumor-suppressive microRNA.However,its roles in human lung cancer pathogenesis are not fully elucidated.In this study,we aimed to explore how miR-195-5p is involved in malignant behaviors of lung adenocarcinoma(LUAD)cells.miR-195-5p expression was examined in the tumor tissues of patients with LUAD and human LUAD cell lines including A549 and PC-9.Thioredoxin reductase 2(TrxR2)was predicted to be an mRNA target of miR-195-5p using online tools and validated by the Dual-Luciferase Reporter Assay.Lentivirus infection was used for gene overexpression,while gene knockdown was achieved by RNA interference.Cell proliferation was determined by Cell Counting Kit-8 and 5-ethynyl-2′-deoxyuridine methods,and cell migration and invasion were assayed with transwell experiments.Cell apoptosis was determined by annexin V staining-based flow cytometry.The antitumor effects of miR-195-5p were also evaluated in nude mice xenografted with A549 cells.We found that miR-195-5p was lowly expressed in human LUAD cells,and its overexpression markedly suppressed cell proliferation,migration,and invasion and increased the apoptosis of LUAD cells in vitro.TrxR2 knockdown phenocopied the tumor-suppressive effects of miR-195-5p overexpression,while simultaneous TrxR2 overexpression remarkably reversed the effects of miR-195-5p overexpression on malignant behaviors of A549 and PC-9 cells.Additionally,miR-195-5p overexpression inhibited the growth of xenografted A549 tumor in nude mice.Our work verified that miR-195-5p exerts tumor-suppressive functions in LUAD cells through targeting TrxR2 and suggested that the miR-195-5p/TrxR2 axis is a potential biomarker for LUAD therapy. 相似文献
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《FEBS letters》2014,588(9):1644-1651
Dysregulation of the REarranged during Transfection proto-oncogene (RET) pathway and microRNA (miRNAs) are crucial for the development of medullary thyroid carcinomas (MTC). Here we demonstrate that miR-129-5p is down-regulated in MTC tissues and cell lines and inhibits RET expression by directly binding its 3′ untranslated regions. Ectopic expression of miR-129-5p significantly decreases cell growth, induces apoptosis and suppresses migration ability in MTC cells through decreasing the phosphorylated AKT, thus functioning as a tumor suppressor. These findings give new clues for understanding MTC carcinogenesis and may help in developing a therapeutic approach for the treatment of RET-activated MTC. 相似文献
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Yanmei Zou Shuo Yao Xiuqiong Chen Dian Liu Jianhua Wang Xun Yuan Jie Rao Huihua Xiong Shiying Yu Xianglin Yuan Feng Zhu Guohong Hu Yihua Wang Hua Xiong 《European journal of cell biology》2018,97(5):369-378
Object
This study aimed to investigate the role of lncRNA OIP5-AS1 in regulating radioresistance of colorectal cancer (CRC) cells.Methods
Microarray analysis was used to screen out lncRNAs differentially expressed in radio-resistant CRC cell lines. Expression levels of OIP5-AS1, miR-369-3p and DYRK1A in CRC cell lines were measured by qRT-PCR. Protein expression of DYRK1A was determined by western blot. The target relationships among OIP5-AS1, miR-369-3p and DYRK1A were validated by dual luciferase reporter assay. Impacts of OIP5-AS1 or DYRK1A on CRC cellular activity and apoptosis were investigated by MTT assay, clonogenic survival assay and flow cytometry to analyze OIP5-AS1 or DYRK1A’s effect on radioresistance of CRC cells.Results
LncRNA OIP5-AS1 and DYRK1A were down-regulated in radio-resistant CRC cell lines. OIP5-AS1 suppressed the expression of miR-369-3p, thus up-regulating DYRK1A, the downstream gene of miR-369-3p. OIP5-AS1 and DYRK1A impaired cell clonogenic survival and promoted cell apoptosis after irradiation, improving radiosensitivity of CRC cells.Conclusion
LncRNA OIP5-AS1 suppressed cell viability, promoted radio-induced apoptosis, and enhanced the radiosensitivity of CRC cells by regulating DYRK1A expression through miR-369-3p. 相似文献18.
Ming Li Zhimin Qian Xiaoling Ma Xiaolong Lin Yanan You Yiying Li Tong Chen Hua Jiang 《Biochemical and biophysical research communications》2018,495(2):2085-2091
Micro RNAs (miRNAs) are small non-coding RNAs which are 19–24 nucleotides in length. MiRNAs play a vital role in the whole process of tumour development, but how they influence the tumourigenecity of epithelial ovarian cancer (EOC)cells is rarely researched. In our study, it was verified that miR-628-5p decreased the stem like cell percentage of EOC cells by inducing their apoptosis. The animal experiments showed that miR-628-5p decreased the tumourigenecity of EOC cells. Besides, we found miR-628-5p targeted at and down-regulated the expression of fibroblast growth factor receptor 2 (FGFR2). FGFR2 expressed higher in ovarian cancer tissues and was correlated with worse prognosis. Our findings indicated that miR-628-5pplays an important role in ovarian cancer stem cell driven tumorigenesis. 相似文献
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Shi ZM Wang J Yan Z You YP Li CY Qian X Yin Y Zhao P Wang YY Wang XF Li MN Liu LZ Liu N Jiang BH 《PloS one》2012,7(3):e32709
MicroRNAs are a class of small noncoding RNAs that function as critical gene regulators through targeting mRNAs for translational repression or degradation. In this study, we showed that miR-128 expression levels were decreased in glioma, and identified p70S6K1 as a novel direct target of miR-128. Overexpression of miR-128 suppressed p70S6K1 and its downstream signaling molecules such as HIF-1 and VEGF expression, and attenuated cell proliferation, tumor growth and angiogenesis. Forced expression of p70S6K1 can partly rescue the inhibitory effect of miR-128 in the cells. Taken together, these findings will shed light to the role and mechanism of miR-128 in regulating glioma tumor angiogenesis via miR-128/p70S6K1 axis, and miR-128 may serve as a potential therapeutic target in glioma in the future. 相似文献