Linc00707 promotes cell proliferation, invasion, and migration via the miR-30c/CTHRC1 regulatory loop in breast cancer.

OBJECTIVE:Breast cancer (BC) is the most common malignant tumor in women. We aimed at investigating the function of long non-coding RNA LINC00707 in BC and the potential mechanism. PATIENTS AND METHODS:The expression level of linc00707 was determined using the quantitative Real (qRT-PCR) in BC tissues and cell lines. The Cell Counting Kit-8 (CCK-8) and colony formation assays were performed to detect the potential influence of LINC0070 on the proliferation ability of the BC cells. Also, the invasion and migration abilities were assessed by the transwell assay. Furthermore, with the bioinformatic analysis and the Dual-Luciferase Assay, we analyzed the interaction in LINC00707/miR-30c/CTHRC1 regulatory loop. The regulatory effects of LINC00707/miR-30c/CTHRC1 on BC were finally determined. RESULTS:LINC00707 was significantly upregulated in BC tissues and cell lines. The knockdown of LINC00707 inhibited proliferation, invasion, and migration in MDA-MB-231 cells, while the overexpression of LINC00707 achieved the opposite results in MDA-MB-468 cells. LINC00707, acting as a competing endogenous RNA (ceRNA), could sponge miR-30c to upregulate CTHRC1, thus promoting BC progression. CONCLUSIONS:LINC00707 was highly expressed in BC tissues and cells. It promoted cell proliferation, invasion, and migration via miR-30c/CTHRC1 regulatory loop. This might provide a novel target for the diagnosis, treatment, and prognosis for BC.

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