Effects of ACTL6A knockdown on proliferation , apoptosis , migration and invasion of pancreatic cancer cells
10.19405/j.cnki.issn1000-1492.2022.10.015
- Author:
Zhenyu Lin
1
;
Qingtai Dong
1
;
Jianxin Zhang
2
;
Bin Zhong
1
;
Tao Zhang
2
;
Zuohong Shang
2
;
Wei Yin
2
;
Zhonghu Li
2
;
Dandan Ma
2
;
Weidong Jin
1
,
2
Author Information
1. The First School of Clinical Medicine , Southern Medical University, Guangzhou 510515
2. Dept of General Surgery, General Hospital of Central Theater Command , Wuhan 430070
- Publication Type:Journal Article
- Keywords:
actin like 6A;
pancreatic cancer;
knockdown;
proliferation;
apoptosis;
migration;
invasion
- From:
Acta Universitatis Medicinalis Anhui
2022;57(10):1589-1594
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To investigate the effects of actin like 6A (ACTL6A) knockdown on the proliferation, apop⁃ tosis, migration and invasion of SW1990 cells in pancreatic cancer.
Methods :The Oncomine database was used to analyze the expression of ACTL6A mRNA in the tissues of pancreatic cancer and normal pancreas. The plasmid of knockdown ACTL6A and siRNA negative control were established and transfected into SW1990 cell line as siRNA⁃ACTL6A group and siRNA⁃NC group. CCK⁃8, cell apoptosis experiment, Wound healing and Transwell assay were used to determine the effects of ACTL6A knockdown on the proliferation, apoptosis, migration and invasion of SW1990 cells. GSEA predicted a possible pathway regulated by ACTL6A in pancreatic cancer. T⁃test was used between the two groups.
Results :The expression of ACTL6A in pancreatic cancer tissues was higher than that in normal pancreatic tissues ( P < 0. 05 ) . The results of CCK⁃8 assay showed that the absorbance of siRNA⁃ACTL6A group at 24 and 48 h were lower than those in the siRNA⁃NC group, and the difference was statistically significant ( t = 5. 840, 8. 454, P < 0. 01) . The results of Wound healing assay and Transwell assay showed that the healing rate and the number of invasive cells in siRNA⁃ACTL6A group were both lower than those in the siRNA⁃NC group. The difference was statistically significant ( t = 3. 960,4. 464, P < 0. 05), but the apoptosis rate of siRNA⁃ACTL6A group was significantly higher than that of the siRNA⁃NC group, and the difference was statistically significant( t = 12. 192, P < 0. 001) . GSEA results showed that the group with high expression of ACTL6A mRNA was up⁃regulated in cell cycle, nucleotide excision repair, base excision repair, DNA replication, pathways in cancer, NOTCH signaling pathway and other related gene sets(P < 0. 05) . These pathways were activated when the expression of ACTL6A was up⁃regulated.
Conclusion :ACTL6A is highly expressed in pancreatic cancer tissues. ACTL6A knockdown promotes the cell apoptosis of SW1990 cells, and inhibits proliferation, invasion and migration of SW1990 cells. The mechanism of the occurrence and development of ACTL6A in pancreatic cancer is attributed to the activation of cell cycle, nucleotide excision repair, base excision repair, DNA replication, pathways in cancer, NOTCH signaling pathway.
- Full text:202408112048464590沉默肌动蛋白样6A对胰腺癌...殖、凋亡、侵袭及迁移的影响_林振宇.pdf
