SGOLl Promotes Proliferation and Invasion of Lung Cancer Cells Through PKM2
10.13865/j.cnki.cjbmb.2021.08.1059
- Author:
Bo-Yun DENG
1
;
Wen-Fan FU
1
;
Ze-Yong JIANG
1
;
Lu DAI
1
;
Sheng-Peng ZHONG
1
;
Jian ZHAO
1
Author Information
1. Department of Chest Surgery, Affiliated Cancer Hospital, Institute of Cuangzhou Medical University
- Publication Type:Journal Article
- Keywords:
Key words shugoshin-l(SGOLl);
lung cancer;
pyruvate kinase muscle isoenzyme 2(PKM2)
- From:
Chinese Journal of Biochemistry and Molecular Biology
2021;37(10):1394-1400
- CountryChina
- Language:Chinese
-
Abstract:
Shugoshin-1 (SGOLl) is one of the human homologues of yeast Shugoshin that locates in the centromeric region. It prevents premature division of the eentromerie cohesin complex and maintaining chromosome stability. Very recently, the role of SGOLl in tumors has emerged, but its role in lung cancer is unclear. In this study, we identify that SGOLl was upregulated in lung cancer samples from the TCGA database (n=529, P< 0.00001), which was correlated to the overall survival time of lung cancer patients (P = 0.0049). Detected by qRT-PCR and Western blotting, we demonstrate that SGOLl was consistently upregulated in lung cancer cell lines than normal epithelial cell line. Regulatory effects of SGOLl on cell viability, clonality, migration and invasion of lung cancer cells A549 and NCI-H2405 were examined by Cell Counting Kit-8 (CCK8), Colony formation, Scratch and Transwell assays, respectively. Compared with the control group, knockdown of SGOLl significantly inhibited proliferation, migration and invasion in A549 and NCI-H2405 cells (P<0. 05). A positive correlation was identified between expression levels of pyruvate kinase muscle isoenzyme 2 (PKM2) and SGOLl in the TCGA data-base (r=0. 38, P = 0). Western blotting results showed that knockdown of SGOLl in A549 and NCI-H2405 cells down-regulated PKM2 as well. In addition, co-interventions of SGOLl and PKM2 were performed in A549 and NCI-H2405 cells to clarify the interaction mechanism between them. The results showed that overexpression of PKM2 in lung cancer cells could partially reverse the regulatory effects of SGOLl knockdown on proliferation, migration and invasion (P<0. 05). Therefore, our study showed that SGOLl promoted the proliferation, migration and invasion of lung cancer cells by regulating PKM2. This study provided a theoretical basis for the mechanism of SGOLl in lung cancer.
