MicroRNA‑26a inhibits cell proliferation and invasion by targeting FAM98A in breast cancer
- Tan Liu
- Ziming Wang
- Menghao Dong
- Jingjing Wei
- Yueyin Pan
Affiliations: Department of Oncology, Provincial Hospital Affiliated to Anhui Medical University, Hefei, Anhui 230032, P.R. China
- Published online on: March 10, 2021 https://doi.org/10.3892/ol.2021.12628
Copyright: © Liu
et al. This is an open access article distributed under the
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MicroRNAs (miRNAs/miRs) play key roles in cancer progression. Extensive research has revealed that miR‑26a is abnormally expressed and functions as a tumor suppressor in numerous types of cancer. Thus, the present study was undertaken to investigate the regulatory role and potential mechanism of action of miR‑26a in breast cancer. Furthermore, the present study aimed to examine the alterations in miR‑26a expression and its effects on human breast cancer cells. Reverse transcription‑quantitative PCR was conducted to assess the differences in miR‑26a expression between human breast cancer and normal breast specimens. A Cell Counting Kit‑8 assay and cloning experiments were used to detect cell proliferation and clone formation. Wound healing and Transwell assays were performed to examine cell migration and invasion. A luciferase activity experiment was utilized to validate the association between miR‑26a and family with sequence similarity 98 member A (FAM98A). Western blotting was conducted to detect the protein expression levels of FAM98A, sonic hedgehog signaling molecule (SHH), smoothened, frizzled class receptor (SMO) and GLI family zinc finger 1 (GLI1). The results indicated that miR‑26a expression was decreased in breast carcinoma tissues and cell lines. Moreover, overexpression of miR‑26a significantly suppressed cell proliferation, clone formation ability and metastasis, and it sensitized breast cancer cells to docetaxel. It was demonstrated that miR‑26a directly targeted FAM98A, and that FAM98A, SHH, SMO and GLI1 expression levels were decreased in cells transfected with miR‑26a mimics. Collectively, the results of the present study suggested that miR‑26a negatively regulated the expression of FAM98A, indicating that it may play a key role in the suppression of breast carcinogenesis.