Retracted: SiRNA‐Mediated Down‐Regulation of CLIC4 Gene Inhibits Cell Proliferation and Accelerates Cell Apoptosis of Mouse Liver Cancer Hca‐F and Hca‐P Cells

Abstract

This study explored the effects involved in silencing CLIC4 on apoptosis and proliferation of mouse liver cancer Hca-F and Hca-P cells. A CLIC4-target small interfering RNA (siRNA) was designed to compound into two individual complementary oligonucleotide chains. A process of annealing and connection to a pSilencer vector was followed by transfection with Hca-F and Hca-P cells. Quantitative real-time polymerase chain reaction and Western blotting techniques were used to determine CLIC4 mRNA and protein expressions. CCK8 assay and flow cytometry were employed for analysis of the survival and apoptosis rate as well as the cell cycle in an octreotide-induced apoptosis model. Expressions of caspase 3, caspase 9, and cleaved PARP were measured using Western blotting. The CLIC4 mRNA and protein expressions in Hca-F and Hca-P cells transfected by pSilencer-CLIC4 siRNA plasmid in the blank group displayed remarkably decreased levels of expression, when compared with both the control and negative control (NC) groups. Decreased survival rates and cleaved PARP expression, increased cell apoptosis rate, expressions of caspase 3 and caspase 9 in Hca-F and Hca-P cells were detected in groups that had been cultured in a medium containing octreotide. The pSilencer-CLIC4 siRNA-2 group when compared with the control and NC groups exhibited decreased survival rates, cleaved PARP expression, increased cell apoptosis rates, and increased expressions of caspase 3 and caspase 9 of Hca-F and Hca-P cells. The results demonstrated that siRNA-induced down-regulation of CLIC4 could proliferation, while in turn promoting apoptosis of mouse liver cancer Hca-F and Hca-P cells.

Sig1R activates extracellular matrix-induced bladder cancer cell proliferation and angiogenesis by combing β-integrin

“…Due to the deep remodeling of the tumor cell microenvironment, the characterization of molecular participants that act between cancer cells and the tumor microenvironment is critical [45]. The ion channels expressed on the surface of tumor cells, like microbial sensors, transmit changes in the structure and function of the microenvironment, allowing the cells to respond accordingly [21,46], and CLIC4 may be strongly involved in this mechanism and has been characterized as biomarker for many tumors [47,48]. By building membrane protein platforms with tumor microenvironment receptors, such as β-integrin, CLIC4 was observed to profoundly affect the conduction of tumor metastasis-associated pathways, thereby altering the tumor microenvironment to promote tumor invasion and metastasis [39][40][41][42].…”