RESUMO
Objective:To investigate the effect and mechanism of long non-coding RNA (lncRNA) TTN-AS1 on the radiosensitivity of breast cancer cells. Methods:The expression of TTN-AS1 in breast cancer cells was detected by real-time reverse transcription PCR (qRT-PCR). MDA-MB-231 cells were divided into the 0 Gy group, 4 Gy group, negative control (NC) +4 Gy group, si- TTN-AS1+4 Gy group, si- TTN-AS1+ miR-107 inhibitor+4 Gy group, and si- TTN-AS1+ miR-107 inhibitor+si- HMGA1+4 Gy group. CCK-8 assay and flow cytometry were used to detect the proliferation and apoptosis rates in each group. Results:Compared with breast epithelial cells, TTN-AS1 was significantly highly expressed in breast cancer cell lines ( P<0.001). Compared with the NC+4 Gy group, the cell proliferation ability was significantly decreased ( P<0.05) and cell apoptosis was significantly increased ( P<0.001) in the si- TTN-AS1+4 Gy group. Compared with the 0 Gy group, the expression levels of TTN-AS1 and HMGA1 from 8 h to 24 h after radiotherapy were significantly up-regulated (both P<0.01), whereas the expression of miR-107 was significantly down-regulated from 8 h to 24 h after radiotherapy in the 4 Gy group ( P<0.001). The cell proliferation ability in the si- TTN-AS1+ miR-107 inhibitor+4 Gy group was significantly higher than that in the si- TTN-AS1+4 Gy group ( P<0.001), and cell apoptosis was significantly lower than that in the si- TTN-AS1+4 Gy group ( P<0.001). Compared with the si- TTN-AS1+ miR-107 inhibitor+4 Gy group, cell proliferation ability was significantly decreased ( P<0.001), whereas cell apoptosis was significantly increased in the si- TTN-AS1+ miR-107 inhibitor+si- HMGA1+4 Gy group ( P<0.001). Conclusion:TTN-AS1 can promote the radiosensitivity of breast cancer cells by regulating the miR-107/ HMGA1 signaling axis.