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Research Paper

MicroRNA-30c-2-3p represses malignant progression of gastric adenocarcinoma cells via targeting ARHGAP11A

, , , , , , & show all
Pages 14534-14544 | Received 03 Feb 2022, Accepted 10 Jun 2022, Published online: 27 Jun 2022
 

ABSTRACT

MicroRNAs are crucial tumor regulators to tumor development and progression. MiR-30c-2-3p can suppress malignant progression of tumor cells, but no study has reported the modulatory process of miR-30c-2-3p in gastric adenocarcinoma (GA). We herein investigated role of miR-30c-2-3p in GA cells. Here, we evaluated gene level in cancer cells by qRT-PCR. CCK-8, colony formation, flow cytometry, and transwell assays revealed biological functions of miR-30c-2-3p and ARHGAP11A. Genes downstream of miR-30c-2-3p were acquired through bioinformatics analysis. Our results suggested a low level of miR-30c-2-3p in GA tissue and cells, while its high expression could repress the malignant progression and promote cell cycle arrest and apoptosis of GA cells. Besides, ARHGAP11A was downstream of miR-30c-2-3p, with up-regulated ARHGAP11A facilitating malignant progression and repressing cell cycle arrest and apoptosis of GA cells. In addition, changes in GA cell functions caused by high ARHGAP11A expression could be partially offset by enhancing miR-30c-2-3p. Thus, our observations indicated that miR-30c-2-3p was a tumor repressor that could inhibit GA progression via modulating ARHGAP11A.

Disclosure statement

All authors declare that they have no potential conflicts of interest.

Data availability statements

The data used to support the findings of this study are available from the corresponding author upon request.https://portal.gdc.cancer.gov/

Authors’ contributions

LZ: Conceptualization, Methodology, Writing - Original Draft

XC: Validation, Methodology

JS: Formal analysis, Visualization

HS: Resources

JZ: Investigation, Writing - Original Draft

XK: Data Curation

HL: Supervision, Writing - Review & Editing

YC: Project administration, Writing - Review & Editing

Supplementary material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/21655979.2022.2090222

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.