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LINC01296 Regulates Wnt/β-catenin Signaling Pathway and Affects SK-N-SH Cell Proliferation, Apoptosis, Migration and Invasion


WANG Qingsong, XIA Ying*, CHEN Huanxiong

(Department of Neurosurgery, Haikou People’s Hospital, Haikou 570000, China)
Abstract:

This study was to investigate whether lncRNA LINC01296 could regulate the proliferation, apoptosis, migration and invasion of human neuroblastoma cell SK-N-SH by regulating Wnt/β-catenin signaling pathway. The qRT-PCR method was used to detect the expression level of LINC01296 in neuroblastoma tissues and adjacent tissues. SK-N-SH cells were cultured in vitro and randomly divided into Control group (normally cultured SK-N-SH cells), si-NC group (si-NC transfected to SK-N-SH cells), si-LINC01296 group (si-LINC01296 transfected into SK-N-SH cells), LiCl group (Wnt/β-catenin signaling pathway activator treated SK-N-SH cells), si- LINC01296+LiCl group (si-LINC01296 and LiCl co-treated SK-N-SH cells). MTT and clone formation experiments were used to detect the cell proliferation ability. Transwell cell test was used to detect cell migration and invasion abilities. Flow cytometry was used to detect the apoptosis rate. Western blot was used to detect the expression of Ki67, Ncadherin, E-cadherin, cleaved-caspase3, Wnt1, β-catenin protein. Compared with adjacent tissues, the expression level of LINC01296 in neuroblastoma tissues was reduced (P<0.05). Compared with the si-NC group, the cell viability of the si-LINC01296 group was significantly reduced (P<0.05); the number of clone formation, the number of migrated cells, and the number of invasive cells were significantly reduced (P<0.05), and the apoptosis rate was significantly increased (P<0.05 ); the levels of Wnt1, β-catenin, Ki67, N-cadherin proteins were significantly reduced (P<0.05); the levels of E-cadherin, cleaved-caspase3 proteins were significantly increased (P<0.05). Activation of the Wnt/β-catenin signaling pathway could partially reverse the effect of interfering with the expression of LINC01296 on the proliferation, migration, invasion and apoptosis of SK-N-SH cells (P<0.05). Compared with the LiCl group, the cell viability of the si-LINC01296+LiCl group was significantly reduced (P<0.05); the number of clone formation, migrated cells, and invasion cells were significantly reduced (P<0.05), and the apoptosis rate was significantly increased (P<0.05 ); the levels of Wnt1, β-catenin, Ki67, N-cadherin proteins were significantly reduced (P<0.05); the levels of E-cadherin and cleaved-caspase3 proteins were significantly increased (P<0.05). Interference with the expression of LINC01296 could inhibit the proliferation, migration, invasion and apoptosis of SK-N-SH cells, and its mechanism might be related to inhibiting the activation of Wnt/β-catenin signaling pathway.



CSTR: 32200.14.cjcb.2020.12.0002