Oncogenic microRNA‐765 promotes the growth and metastasis of breast carcinoma by directly targeting ING4

Abstract

Previous investigations have proved that microRNA (miR)‐765 is significantly overexpressed in multiple tumor types. Nevertheless, the underlying molecular mechanism of miR‐765 in mediating breast carcinoma cell growth and metastasis remains unclear. Quantitative real‐time polymerase chain reaction was used to determine the levels of miR‐765 and inhibitor of growth 4 (ING4) in breast carcinoma tissues and breast carcinoma cells. Cell proliferation, colony formation, wound healing, and Transwell invasion assays were used to analysis the role of miR‐765 on breast carcinoma cell growth and aggressiveness. The expressions of ING4 were determined using Western blot analysis and immunohistochemical staining. The direct target of ING4 and miR‐765 was confirmed using the luciferase reporter assay. Nude mice were subcutaneously implanted with miR‐765 inhibitor transfected MDA‐MB‐231 cells to determine the potential role of miR‐765 in tumor growth in vivo. We observed that miR‐765 is overexpressed in breast carcinoma tissue and breast cancer cells. By using luciferase reporter gene bioassay, we find that ING4 is the direct target of miR‐765 in breast carcinoma. The level of ING4 is inversely associated with the level of miR‐765. The gain‐of‐function and loss‐of‐function experiments in vitro indicate that the downregulation of miR‐765 suppresses the growth, mobility, and invasion abilities of breast cancer cells by inhibiting ING4. In addition, overexpression of ING4 suppresses the aggressiveness of the MDA‐BA‐231 cell that is induced by miR‐761 in vitro. In this study, we prove that miR‐765 regulates the growth and metastasis of breast cancer via modulating miR‐765‐ING4‐negative feedback loop.

<p>Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma</p>

“…21,22 Besides, miR-765 plays oncogenic or anti-cancer roles in gastric cancer and breast cancer. 23,24 Its role in glioma remains unclear. Our results suggested that miR-765 was a tumor suppressor in glioma.…”

miR-765 Acts as a Tumor Promoter and Indicates Poor Prognosis in Non-Small Cell Lung Cancer

“…14 It also has been reported that miR-765 was dysregulated and participated in the progression of many other cancers, including esophageal squamous cell carcinoma, breast cancer, prostate cancer, and renal cell carcinoma, etc. [15][16][17][18] In the previously reported miRNA expression file in NSCLC, miR-765 was found to be upregulated but its role in the progression of NSCLC was unclear. This study focused on the role of miR-765 in the prognosis and progression of NSCLC by qRT-PCR, CCK8, and Transwell assay aimed to provide a novel insight into the therapy and management of NSCLC.…”

Prognostic model and immunomicroenvironment analysis of combined thyroid and breast cancer in females based on cuproptosis related miRNA

“…miR-466 declined the growth and metastasis of prostate cancer by directly targeting the bone-associated transcription factor RUNX2 [41] . miR-765 regulated the growth and metastasis of breast cancer by regulating the Mir-765-ING4 negative feedback loop [42] . These literature studies suggested that miRNA markers associated with cuproptosis may be associated with the progression of TC and BC, and reveal expected targets for the treatment of TC and BC.…”