Expression and Role of Integrin β-like 1 in Hepatocellular Carcinoma
10.3971/j.issn.1000-8578.2022.22.0260
- VernacularTitle:整合素β样1在肝细胞癌中的表达及作用
- Author:
Liyan LIN
1
;
Jianping LU
;
Weifeng ZHU
;
Shi HE
;
Fengying PENG
;
Gang CHEN
Author Information
1. Department of Pathology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou 350014, China
- Publication Type:Research Article
- Keywords:
Hepatocellular carcinoma;
Integrin subunit β-like 1;
Proliferation;
Migration;
Invasion
- From:
Cancer Research on Prevention and Treatment
2022;49(12):1232-1239
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression of ITGBL1 in hepatocellular carcinoma (HCC) and its role in promoting the proliferation, migration, and invasion of HCC cell lines. Methods RT-qPCR and immunohistochemistry were used in investigating ITGBL1 expression in 12 pairs of fresh HCC and adjacent normal liver tissue samples and 160 paraffin HCC specimens. The relationships of ITGBL1 expression level with clinicopathological parameters and prognosis were analyzed. HUH7 cell line with the stable overexpression of ITGBL1 and LM3 cell line with stable downregulated expression of ITGBL1 were constructed. The effects of ITGBL1 on the proliferation, migration, and invasion of HCC cells were examined by CCK8 assay, wound-healing assay, and Transwell invasion assay. Results The expression levels of ITGBL1 gene and protein in tumor tissues were higher than those in surrounding liver tissues. The high expression of ITGBL1 was correlated with serum AFP level, tumor capsular invasion, vascular invasion, tumor differentiation, and clinical stage (P < 0.05). The results of Kaplan-Meier analysis showed that patients with high expression of ITGBL1 had shorter DFS. In vitro, increased ITGBL1 expression promoted HCC cell proliferation, migration, and invasion, whereas ITGBL1 knockdown inhibited these processes. Conclusion ITGBL1 expression is highly expressed in HCC tissues, and ITGBL1 can increase the proliferation, migration, and invasion of HCC cells. However, the mechanism needs further study.
