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MicroRNA-10a suppresses breast cancer progression via PI3K/Akt/mTOR pathway

Kongliang Ke¹, Tingting Lou²

¹Department of General Surgery, Ningbo First Hospital, Ningbo, Zhejiang 315010, P.R. China.

Oncology Letters

|November 9, 2017

Abstract:

Previous studies have demonstrated that microRNA-10a (miR-10a) regulates various opposing biological functions in breast cancer. The aim of the present study was to investigate the exact functions of miR-10a in the pathogenesis of breast cancer. miR-10a expression was initially detected in two human breast cancer cell lines, MCF-7 and MDA-MB-231 and a normal human mammary epithelial cell line MCF-10A. The proliferation, migration and apoptosis of breast cancer cells were analyzed using MTT assays, Transwell assays and flow cytometry, respectively, following transfection of MCF-7 and MDA-MB-231 cells with an miR-10a mimic or anti-miR-10a. The expression of phosphorylated (p-)protein kinase B (Akt), p-mammalian target of rapamycin (p-mTOR), p-ribosomal protein S6 kinase β-1 (p-p70S6K), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (PIK3CA), Cytochrome C (Cyt C), B-cell lymphoma 2 (Bcl-2), BCL-2 associated X, apoptosis regulator (Bax), and cleaved caspase-3 were analyzed by western blotting. The migration of MCF-7 cells pretreated with an mTOR inhibitor CCI-779, was detected using a Transwell assay. Relative miR-10a expression was significantly elevated in MDA-MB-231 breast cancer cells and was at its highest levels in MCF-7 cells. Transfection with the miR-10a mimic significantly inhibited proliferation and migration, and promoted the apoptosis of breast cancer cells. Furthermore, upregulation of miR-10a markedly suppressed the levels of p-Akt, p-mTOR, p-p70S6K, and PIK3CA, and increased the expression of Cyt C, cleaved caspase-3, and the ratio of Bax/Bcl-2. Anti-miR-10a had the opposite effects. In addition, CCI-779 reversed the effect of anti-miR-10a on the migration of MCF-7 cells in a dose-dependent manner. In conclusion, miR-10a is downregulated in high aggressive breast cancer cells. miR-10a inhibited the proliferation and migration, and promoted apoptosis of breast cancer cells via phosphoinositide/Akt/mTOR signaling, and the mitochondrial apoptotic pathway.

Insights

MicroRNA-10a (miR-10a) plays a crucial role in breast cancer pathogenesis. This study found that miR-10a suppresses tumor growth and metastasis by inhibiting the Akt/mTOR pathway and promoting apoptosis.

Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

MicroRNA-10a (miR-10a) exhibits complex roles in breast cancer, influencing diverse cellular functions.
Understanding the precise mechanisms of miR-10a in breast cancer pathogenesis is critical for therapeutic development.

Purpose of the Study:

To elucidate the specific functions of miR-10a in breast cancer progression.
To investigate the molecular pathways regulated by miR-10a in breast cancer cells.

Main Methods:

Assessed miR-10a expression in human breast cancer cell lines (MCF-7, MDA-MB-231) and a normal cell line (MCF-10A).
Utilized MTT, Transwell, and flow cytometry assays to evaluate proliferation, migration, and apoptosis following miR-10a mimic or anti-miR-10a transfection.
Analyzed key protein expression (p-Akt, p-mTOR, PIK3CA, Cyt C, Bcl-2, Bax, cleaved caspase-3) via Western blotting.

Main Results:

miR-10a expression was significantly altered in breast cancer cells, notably higher in MCF-7 cells.
miR-10a mimic transfection inhibited proliferation and migration while promoting apoptosis in breast cancer cells.
Upregulation of miR-10a suppressed the Akt/mTOR signaling pathway and induced mitochondrial apoptosis.

Conclusions:

miR-10a is downregulated in highly aggressive breast cancer cells.
miR-10a acts as a tumor suppressor by inhibiting proliferation and migration and promoting apoptosis.
The miR-10a-mediated effects involve the phosphoinositide/Akt/mTOR signaling and mitochondrial apoptotic pathways.

Read full analysis

Keywords:

breast cancer microRNA-10a mitochondrial apoptotic pathway phosphoinositide-3/protein kinase B/mammalian target of rapamycin

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