Knockdown of miR-629 Inhibits Ovarian Cancer Malignant Behaviors by Targeting Testis-Specific Y-Like Protein 5

Shao, Liping; Shen, Zhi‐Liang; Hua, Qian; Zhou, Sufang; Chen, Youguo

doi:10.1089/dna.2017.3904

Cited by 19 publications

(22 citation statements)

References 25 publications

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“…In our results, we showed that miR‐629 was up‐regulated in hypoxia‐induced HPASMCs. Previous studies also showed the up‐regulation of miR‐629 in several types of cancers, and overexpression of miR‐629 showed enhanced effects on the cancer cells including cervical cancer, colorectal cancer, breast cancer and ovarian cancer . Consistently, our data showed that overexpression of miR‐629 promoted cell proliferation and inhibited cell apoptosis of HPASMCs, while knockdown of miR‐629 exerted the opposite effects in HPASMCs during hypoxia.…”

Section: Discussionsupporting

confidence: 88%

“…In addition, down‐regulation of miR‐126 contributed to the right ventricle failure in PAH and restoration miR‐129 expression in the right ventricle improved micro‐vessel density and right ventricle function in experimental PAH . miR‐629 was a newly identified miRNA and plays an oncogenic role in several types of cancers including cervical cancer, colorectal cancer, breast cancer and ovarian cancer . Despite the role of miR‐629 in cancer, the role of miR‐629 in PAH has not been investigated so far.…”

Section: Introductionmentioning

confidence: 99%

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MiR‐629 regulates hypoxic pulmonary vascular remodelling by targeting FOXO3 and PERP

Zhao

Chen

et al. 2019

J Cellular Molecular Medi

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Pulmonary arterial hypertension (PAH) is featured by the increase in pulmonary vascular resistance and pulmonary arterial pressure. Despite that abnormal proliferation and phenotypic changes in human pulmonary artery smooth muscle cells (HPASMCs) contributing to the pathophysiology of PAH, the underlying molecular mechanisms remain unclear. In the present study, we detected the expression of miR‐629 in hypoxia‐treated HPASMCs and explored the mechanistic role of miR‐629 in regulating HPASMC proliferation, migration and apoptosis. Hypoxia time‐dependently induced up‐regulation of miR‐629 and promoted cell viability and proliferation in HPASMCs. Treatment with miR‐629 mimics promoted HPASMCs proliferation and migration, but inhibited cell apoptosis; while knockdown of miR‐629 suppressed the cell proliferation and migration but promoted cell apoptosis in HPASMCs. The bioinformatics prediction revealed FOXO3 and PERP as downstream targets of miR‐629, and miR‐629 negatively regulated the expression of FOXO3 and PERP via targeting the 3’ untranslated regions. Enforced expression of FOXO3 or PERP attenuated the miR‐629 overexpression or hypoxia‐induced enhanced effects on HPASMC proliferation and proliferation, and the suppressive effects on HPASMC apoptosis. Furthermore, the expression of miR‐629 was up‐regulated, and the expression of FOXO3 and PERP mRNA was down‐regulated in the plasma from PAH patients when compared to healthy controls. In conclusion, the present study provided evidence regarding the novel role of miR‐629 in regulating cell proliferation, migration and apoptosis of HPASMCs during hypoxia.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

MiR‐629 regulates hypoxic pulmonary vascular remodelling by targeting FOXO3 and PERP

Zhao

Chen

et al. 2019

J Cellular Molecular Medi

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“…Here, we found that miR-629-5p was up-regulated both in colorectal cancer tissues and cell lines. However, its extent of up-regulation in colorectal cancer is significantly lower than that in other cancer types [ 12 , 24 ], indicating a potential varied regulation of miR-629-5p in different types of cancer. Additionally, there was no significant correlation between the metastasis of tested cell lines and the expression level of miR-629-5p .…”

Section: Discussionmentioning

confidence: 99%

MiR-629-5p promotes colorectal cancer progression through targetting CXXC finger protein 4

et al. 2018

Bioscience Reports

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MiR-629-5p has been shown to function as a tumor promoter in some types of cancer. However, the role of miR-629-5p in colorectal cancer remains unclear. Here, the significant up-regulation of miR-629-5p in colorectal cancer tissues and cell lines was observed. Overexpression of miR-629-5p showed a positive effect on cell proliferation and migration. The enhanced miR-629-5p level also suppressed cell apoptosis and resulted in a low Bax level and a high Bcl-2 level. Further down-regulating miR-629-5p demonstrated opposite effects. CXXC finger protein 4 (CXXC4) was predicted as a direct target of miR-629-5p. Dual-luciferase reporter and Western blotting assays exhibited miR-629-5p directly bound to the 3′UTR of CXXC4 and then down-regulated its expression at post-transcriptional level. CXXC4 knockdown rescued the decreased cell proliferation and migration and the enhanced cell apoptosis induced by inhibiting miR-629-5p expression. Notably, overexpression of miR-629-5p also conferred 5-fluorouracil sensitivity, which was partly abrogated by coexpression of CXXC4. Overall, the results presented here suggest that miR-629-5p functions as a tumor promoter by improving proliferation and migration and repressing apoptosis and 5-FU sensitivity in colorectal cancer progression by directly down-regulating CXXC4.

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“…Moreover, another research highlighted TSPYL5 as a tumor inhibitor gene and was poorly expressed in PCa [17]. Similarly, previous research has demonstrated that decreasing TSPYL5 expression may influence ovarian cancer cell invasion and proliferation in a suppressive way [33].…”

Section: Discussionmentioning

confidence: 88%

LINC00908 negatively regulates microRNA-483-5p to increase TSPYL5 expression and inhibit the development of prostate cancer

Фан

Zhang

2020

Cancer Cell Int

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Background: Accumulating evidence has associated aberrant long non-coding RNAs (lncRNAs) with various human cancers. This study aimed to explore the role of LINC00908 in prostate cancer (PCa) and its possible underlying mechanisms. Methods: Microarray data associated with PCa were obtained from the Gene Expression Omnibus (GEO) to screen the differentially expressed genes or lncRNAs. Then, the expression of LINC00908 in PCa tissues and cell lines was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The localization of LINC00908 in PCa cells was examined by fluorescence in situ hybridization (FISH). The relationship among LINC00908, microRNA (miR)-483-5p, and TSPYL5 was detected by bioinformatics analysis, dual-luciferase reporter assay, RNA pull-down, RNA binding protein immunoprecipitation (RIP), and FISH assays. Cell biological behaviors were assessed after the expression of LINC00908, miR-483-5p, and TSPYL5 was altered in PCa cells. Lastly, tumor growth in nude mice was evaluated. Results: Poorly expressed LINC00908 was witnessed in PCa tissues and cells. LINC00908 competitively bound to miR-483-5p to up-regulate the TSPYL5 expression. Overexpression of LINC00908 resulted in reduced PCa cell proliferation, migration and invasion, and promoted apoptosis. Additionally, the suppression on PCa cell proliferation, migration and invasion was induced by up-regulation of TSPYL5 or inhibition of miR-483-5p. In addition, in vivo experiments showed that overexpression of LINC00908 inhibited tumor growth of PCa. Conclusion: Overall, LINC00908 could competitively bind to miR-483-5p to increase the expression of TSPYL5, thereby inhibiting the progression of PCa. Therefore, LINC00908 may serve as a novel target for the treatment of PCa.

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Knockdown of miR-629 Inhibits Ovarian Cancer Malignant Behaviors by Targeting Testis-Specific Y-Like Protein 5

Cited by 19 publications

References 25 publications

MiR‐629 regulates hypoxic pulmonary vascular remodelling by targeting FOXO3 and PERP

MiR‐629 regulates hypoxic pulmonary vascular remodelling by targeting FOXO3 and PERP

MiR-629-5p promotes colorectal cancer progression through targetting CXXC finger protein 4

LINC00908 negatively regulates microRNA-483-5p to increase TSPYL5 expression and inhibit the development of prostate cancer

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