The Long Non-coding RNA ILF3-AS1 Inhibited Proliferation of Cervical Cancer Cells Through the MiR-130a-3p/PTEN Axis / 中国生物化学与分子生物学报

ILF3 antisense RNA 1 (ILF3-AS1), the antisense RNA of interleukin enhancer binding factor 3 (ILF3), is a lncRNA located on chromosome 19p13. 2. ILF3-AS1 played a key role in the occurrence and development of a variety of tumors, but its role in cervical cancer had not been explored yet. Therefore, we first used TCGA and GTEx database to conduct bioinformatics analysis. The results suggested that ILF3-AS1 was down-regulated in cervical cancer tissues (P < 0. 001) and was associated with a good prognosis (P = 0. 045). The qRT-PCR experiment showed that expression of ILF3-AS1 in cervical cancer tissues and SiHa, HeLa, CaSki cervical cancer cell lines was lower than that in control groups. Subsequently, overexpressing of ILF3-AS1 can significantly inhibit the cancer cell viability and stimulate apoptosis (P<0. 001). Analysis using the Star Base v3. 0 database suggested that ILF3-AS1 can target miR-130a-3p; while miR-130a-3p may target PTEN. The qRT-PCR test showed that the expression of miR-130a-3p in cervical cancer was significantly higher than that in normal cervical tissues (P < 0. 01). The results of the luciferase reporter assay showed that ILF3-AS1 can specifically bind to miR-130a-3p (P<0. 01). After overexpression of ILF3-AS1 in HeLa cells, the expression of miR-130a-3p was significantly down-regulated (P < 0. 01). Co-transfection with pcDNA3. 1-ILF3-AS1 and miR-130a-3p mimics, the inhibitory effect of LF3-AS1 on cell proliferation can partially be reversed (P<0. 001). After HeLa cells overexpressed ILF3-AS1, the expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN) mRNA (P < 0. 001) and proteins (P < 0. 001) significantly increased; when miR-130a-3p mimics was simultaneously used in HeLa cell, the increased expression of PTEN mRNA (P <0. 001) and proteins (P < 0. 001) was notably inhibited. In summary, ILF3-AS1 inhibited the proliferation of cervical cancer cells by sponging miR-130a-3p to regulate the expression of PTEN.

Overexpression of miR-130a-3p attenuates cardiomyocyte hypertrophy / 生物医学工程学杂志

This study aimed to explore the role of miR-130a-3p in cardiomyocyte hypertrophy and its underlying mechanisms. Pressure-overload induced myocardial hypertrophy mice model was constructed by thoracic aortic constriction (TAC). , norepinephrine (NE) was used to stimulate neonatal rat cardiomyocytes (NRCMs) and H9c2 rat cardiomyocytes to induce hypertrophic phenotypes. The expression of miR-130a-3p was detected in mice hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. The mimics and inhibitors of miR-130a-3p were transfected into H9c2 cells to observe the role of miR-130a-3p on the hypertrophic phenotype change of cardiomyocytes separately. Furthermore, whether miR-130a-3p regulated hypertrophic related signaling pathways was explored. The results showed that the expression of miR-130a-3p was significantly decreased in hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. After transfection of miR-130a-3p mimics, the expression of hypertrophic marker genes, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), and the cell surface area were notably down-regulated compared with the control group (mimics N.C. + NE group). But after transfection of miR-130a-3p inhibitor, the expression of ANP, BNP and β-MHC in H9c2 cells increased significantly, and the cell area increased further. By Western blot, it was found that the protein phosphorylation level of Akt and mTOR were down-regulated after over-expression of miR-130a-3p. These results suggest that miR-130a-3p mimics may alleviate the degree of cardiomyocyte hypertrophy, meanwhile its inhibitor can further aggravate cardiomyocyte hypertrophy. Over-expression of miR-130a-3p may attenuate cardiomyocytes hypertrophy by affecting the Akt pathway.

miR-130a-3p inhibits invasion of breast cancer MCF-7 cells through HGF/MET pathway / 中国肿瘤生物治疗杂志

@# Objective: To explore the molecular mechanism of miR-130a-3p regulating epithelial mesenchymal transition (EMT) to affect the invasion and metastasis of breast cancer cells through HGF/MET pathway. Methods: A total of 22 pairs of cancer tissues and adjacent normal tissues from breast cancer patients, who were admitted to Affiliated Hospital of Chengde Medical College from January 2018 to October 2018, were collected for this study; in addition, breast cancer cell lines (MCF-7, MDA-MB-231 and MDA-MB453) and normal breast epithelial cells MCF10A were obtained from the Institute of Basic Sciences, Chengde Medical College. And then, the expression of miR-130a-3p in tissues and cell lines were detected by qRT-PCR. The experiment cells were divided into control group, miR-130a-3p mimics group, miR-130a-3p inhibitor group, PHA665752 (a small-molecule MET inhibitor) transfection group and PHA665752+miR-130a-3p inhibitor co-transfection group. CCK-8 assay and Transwell assay were performed to detect the proliferation, invasion and migration of MCF-7 cells, respectively. The expressions of EMT and HGF/MET signaling pathway related proteins in MCF-7 cells were detected by WB. In addition, the targeted relationship between miR-130a-3p and MET was verified by Dual luciferase reporter gene assay. Results: miR-130a-3p was down-regulated in breast cancer tissues and cell lines. Over-expression of miR130a-3p could suppress the proliferation, invasion, migration and EMT of MCF-7 cells, while knockdown of miR-130a-3p had the opposite results. The results of Dual luciferase reporter gene assay indicated that miR-130a-3p targetedly down-regulated the expression of MET, and miR-130a-3p negatively regulated the expression of HGF/MET signaling pathway. Further experiments confirmed that miR-130a-3p inhibited the proliferation, invasion, migration and EMT of MCF-7 cells by blocking HGF/MET signaling pathway. Conclusion: miR-130a-3p suppresses the EMT of MCF-7 cells via blocking HGF/MET signaling pathway, thereby repressing the invasion and metastasis of MCF-7 cells.