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MicroRNA-592 inhibits the progression of breast cancer through targeting CYP20A1

ABSTRACT: MicroRNA-592 inhibits the progression of breast cancer through targeting CYP20A1

PROVIDER: PRJNA763812 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15913263_1.fastq.gz	Fastqsanger.gz
	SRR15913263_2.fastq.gz	Fastqsanger.gz
	SRR15913264_1.fastq.gz	Fastqsanger.gz
	SRR15913264_2.fastq.gz	Fastqsanger.gz
	SRR15913265_1.fastq.gz	Fastqsanger.gz

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MicroRNA-592 inhibits the progression of breast cancer through targeting CYP20A1

Project description:Previous studies have shown that miR-592 may play an important role in the development of various cancer types. However, the mechanism of miR-592 in breast cancer progression remains unclear. Functional analysis showed that overexpression of miR-592 significantly inhibited the cell proliferation, clonal formation, and migration and invasion of MCF-7 cells in vitro. RNA sequencing (RNA-seq) was then used to identify the significantly dysregulated genes and enriched pathways in response to miR-592 overexpression in MCF-7 cells.

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MicroRNA-592 Inhibits the Growth of Ovarian Cancer Cells by Targeting ERBB3.

Project description:Objectives: Ovarian cancer is the most lethal gynecologic malignancy, and targeted therapy for different pathological types and molecular phenotypes is urgent to be studied. Studies have shown that MicroRNA-592 (miR-592) plays an important negative regulatory role in the occurrence of gastrointestinal malignancies, breast cancer, non-small cell lung cancer, and glioma, but the expression of miR-592 in ovarian cancer and the mechanism of action are still unclear. Methods: The expressions of miR-592 were examined by RT-PCR and Western Blot. Cell viability and migratory capacity were detected by CCK-8 and transwell assay. TargetScan (http://www.targetscan.org) was analyzed to predict potential targets of miR-592. Then Dual-luciferase reporter gene assay was performed to verify the targeting relationship between miR-592 and ERBB3. A mouse xenograft model was applied to confirm the effect of miR-592. Results: In our study, we found that the expression of miR-592 is reduced in epithelial ovarian cancer tissues. The exogenous expression of miR-592 inhibits the proliferation, migration, and invasion in epithelial ovarian cancer tumor cells. Furthermore, the exogenous expression of miR-592 inhibits tumor growth in the nude mouse xenograft model. Therefore, miR-592 may play a role of tumor suppressor miRNA in the occurrence and development of ovarian cancer. Further experiments demonstrated that tumor-related ERBB3 is a target gene mediated by miRNA-592. The dual-luciferase reporter system was used to identify miRNA-592 target genes; qPCR and Western Blot were used to detect the expression of ERBB3. Mechanical experiments confirmed that miRNA-592 negatively regulated ERBB3.Conclusion: Together, these findings identify a heretofore unrecognized link between miR-592 and ERBB3 and suggest that targeting on miR-592 warrants attention as a novel and potential therapeutic strategy for ovarian cancer.

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