Research Paper Volume 15, Issue 12 pp 5734—5750

lncSNHG3 drives breast cancer progression by epigenetically increasing CSNK2A1 expression level


Figure 7. Tumor-promoting functions of SNHG3 is dependent on CSNK2A1. (A) CCK-8 assays demonstrated that overexpression of SNHG3 promoted cancer cell growth. CSNK2A1 knockdown could abolish growth promotion caused by SNHG3. (B) EdU assays showed that CSNK2A1 knockdown abolished the increased proliferation rates of MDA-MB-231 cells caused by SNHG3. (C) Transwell assays demonstrated that CSNK2A1 knockdown abolished the increased abilities of migration and invasion caused by SNHG3. (D) The CSNK2A1, cell cycle-related proteins, and metastasis-related proteins were detected by western blotting with indicated treatment. (E) Schematic of the proposed mechanism of SNHG3 in breast cancer cells.