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Effect of long noncoding RNA CCAT2 on drug sensitivity to 5‐fluorouracil of breast cancer cells through microRNA‐145 meditated by p53

The current study was set out to investigate the mechanism by which silenced long noncoding RNA (lncRNA) colon cancer‐associated transcript 2 (CCAT2) modulates the cell growth, migration, invasion, and drug sensitivity of breast cancer (BC) cells to 5‐fluorouracil (5‐Fu) with the involvement of miR‐145 and p53. First, high CCAT2 expression was presented in BC cells and tissues. Subsequently, the links between CCAT2 expression and BC clinicopathological features were analyzed. Highly‐expressed CCAT2 was linked to lymph node metastasis, positive progesterone receptor, estrogen receptor, and Ki‐67 of BC cells. Then, the gain‐ and loss‐of‐function approaches were performed to measure the regulatory role of CCAT2 in the biological processes of BC cells. Silencing of CCAT2 suppressed in vitro cell growth, proliferation, invasion, migration abilities, and epithelial‐mesenchymal transformation, increased cell apoptosis, and enhanced drug sensitivity of BC cells. Silencing of CCAT2 upregulated miR‐145, which was poorly expressed in drug‐resistant BC cells. p53 can bind to the miR‐145 promoter region and increase miR‐145 expression. Upregulation of miR‐145 induced by silencing of CCAT2 can be invalidated by p53‐siRNA. To conclude, p53‐induced activation of miR‐145 could be inhibited by CCAT2, while overexpression of CCAT2 could improve the drug resistance of BC cells to 5‐Fu.