lncRNA MALAT1/miR‑26a/26b/ST8SIA4 axis mediates cell invasion and migration in breast cancer cell lines.

Metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1) is a long non‑coding RNA that is overexpressed in various human cancers, including breast cancer. Evidence has associated the function of the α‑2,8‑sialyltransferase (ST8SIA) family with breast cancer. The present study aimed to investigate the potential roles of MALAT1 in breast cancer development and progression using analyses of both breast cancer tissues and cell lines. The mRNA levels of MALAT1, microRNA (miR)‑26a/26b and ST8SIA4 were detected by reverse transcription‑quantitative PCR (RT‑qPCR) and the protein level of ST8SIA4 was assessed by western blot analysis. Cell proliferation, invasion and migration were detected by CCK‑8, wound healing and Transwell assays, respectively. Interactions between MALAT1 and miR‑26a/26b were assessed using fluorescence in situ hybridization, RNA immunoprecipitation and luciferase reporter assays. Herein, different levels of MALAT1 were primarily observed in human breast cancer samples and cells. Upregulated MALAT1 was a crucial predictor of poor breast cancer prognosis. Altered MALAT1 modulated cell progression in breast cancer. Moreover, miR‑26a/26b was confirmed as a direct regulator of MALAT1, and ST8SIA4 was predicted as a target of miR‑26a/26b. Functional analysis in human breast cancer cell lines demonstrated that MALAT1 modulated breast cancer cell tumorigenicity by acting as a competing endogenous lncRNA (ceRNA) to regulate ST8SIA4 levels by sponging miR‑26a/26b. The identification of the MALAT1/miR‑26a/26b/ST8SIA4 axis which contributes to breast cancer progression may constitute a potential new therapeutic target.