Zhongguo aizheng zazhi (Sep 2022)
LINC02163 targeting miR-338-3p affects proliferation, invasion and migration of breast cancer cells
Abstract
Background and purpose: Long non-coding RNA (lncRNA) has been found to be dysregulated in breast cancer and is closely related to the malignant behavior of tumors. This study aimed to explore the effects of LINC02163 targeting miR-338-3p on the proliferation, invasion and migration of breast cancer cells. Methods: Breast cancer tissue samples and the adjacent tissue samples (2 cm to cancer tissue) were collected from 9 female breast cancer patients admitted to People’s Hospital of Zhengzhou from January 2020 to September 2021. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the expression of LINC02163 in tissue samples, human normal breast epithelial cell line (MCF-10A) and breast cancer cell lines (MCF-7, BT-20, MDA-MB-231, T47D). MDA-MB-231 was divided into control group, sh-NC group, sh-LINC02163 group, sh-LINC02163+inhibitor-NC group and sh-LINC02163+miR-338-3p inhibitor group. MTT method, transwell test and scratch test were used to detect the MDA-MB-231 cell viability, invasion and migration ability. Western blot was used to detect the protein expression of c-Myc, matrix metalloproteinase (MMP) 2, MMP9, E-cadherin and N-cadherin in MDA-MB-231 cells. Dual luciferase reporter gene was used to detect the targeting relationship between LINC02163 and miR-338-3p. In vivo tumor formation experiment was used to detect tumor volume and weight in nude mice. Immunohistochemical method was used to detect the Ki-67 proliferation index in tumor tissues of BALB/c nude mice. Results: Compared with adjacent tissues, the expression of LINC02163 in breast cancer tissues was significantly higher (P<0.05). Compared with MCF-10A cells, the expression of LINC02163 in MCF-7, BT-20, MDA-MB-231 and T47D cells was significantly higher, and it increased most significantly in MDA-MB-231 cells (P<0.05). Compared with the control group, the LINC02163 expression, cell survival rate, number of invasive cells, migration rate, expressions of c-Myc, MMP2, MMP9 and N-cadherin, tumor volume and weight, and Ki-67 proliferation index were significantly reduced in the sh-LINC02163 group, while the expressions of miR-338-3p and E-cadherin were significantly increased (P<0.05). Compared with the sh-LINC02163 group, the expression of LINC02163 in the sh-LINC02163+miR-338-3p inhibitor group did not change significantly (P>0.05), the cell survival rate, number of invasive cells, migration rate, expressions of c-Myc, MMP2, MMP9 and N-cadherin, tumor volume and weight, and Ki-67 proliferation index were significantly increased, while the expressions of miR-338-3p and E-cadherin were significantly reduced (P<0.05). LINC02163 had a potential targeting relationship with miR-338-3p in breast cancer. Conclusion: Silencing the expression of LINC02163 can inhibit the proliferation, invasion and migration of breast cancer cells by promoting the expression of miR-338-3p.
Keywords
