Long-Chain Non-Coding SOX21-AS1 Promotes Proliferation and Migration of Breast Cancer Cells Through the PI3K/AKT Signaling Pathway.

Aim This study aimed to investigate the effect of long-chain non-coding SOX21-AS1 on the proliferation and migration of breast cancer (BC) cells through the PI3K/AKT signaling pathway. Methods Eighty-eight BC and adjacent tissues were collected, and BC cells and normal breast epithelial cells were purchased. LncRNA SOX21-AS1 expression in tissues and cells was detected by RT-PCR. miR-NC, si-SOX21-AS1, and Sh-SOX21-AS1 were transfected into BC cells. The PI3K/AKT signaling pathway was interfered with L740Y-P (activator of the PI3K/AKT pathway) and LY294002 (inhibitor of the PI3K/AKT pathway) in BC cells. The SOX21-AS1 expression in BC tissues and cells was tested by qRT-PCR, and the expression levels of p-PI3K, p-AKT, N-cadherin, E-cadherin, and vimentin were detected by WB. Results SOX21-AS1 was highly expressed in BC, and the p-PI3K and p-AKT levels were also high. Cell experiments showed that inhibiting SOX21-AS1 expression could inhibit the proliferation, invasion, migration, and EMT of BC cells, and up-regulating its expression could promote the proliferation, invasion, migration, and EMT of ovarian cancer cells. The tumor-forming experiment in nude mice was consistent with the results in vitro. 740Y-P intervention could reverse the inhibition effect of Si-SOX21-AS1 on BC cell proliferation, invasion, migration, and EMT, while LY294002 intervention could reverse the promotion effect of Sh-SOX21-AS1 on BC cell proliferation, invasion, migration, and EMT. Conclusion SOX21-AS1 is highly expressed in BC tissues. Silencing BC expression can inhibit the proliferation, invasion, migration, and EMT of cells by inhibiting the PI3K/AKT signaling pathway, which may be a new target for diagnosis and treatment.