HK2 Promotes Proliferation and Migration of Cervical Cancer Cells by Up-regulating Cyclin D1 and MMP7 Expression Through Wnt/β-catenin Signaling Pathway

Abstract

Objective To investigate the effect of HK2 on the proliferation and migration of cervical cancer cell lines HeLa and related mechanism. Methods HeLa cells with stable HK2 expression were screened. Cell proliferation, viability and cell cycle were detected by cell growth curves, MTT assay and flow cytometry, respectively. Wound-healing assay and Transwell cell invasion assay were used to detect the effect of HK2 on the migration and invasion potential of HeLa cells. The expression of β-catenin, Cyclin D1, MMP7 and Slug were detected by Western blot and immunocytochemistry. The activity of Wnt/β-catenin signalling pathway was detected by TOP/FOP assay. Cell growth, migration and invasion were detected in HeLa-HK2 cells treated with Wnt/β-catenin inhibitor (XAV-939). Results HeLa cells lines that stably expressing HK2 were successfully constructed. HK2 overexpression promoted the proliferation, migration, invasion and viability of HeLa cells, accelerated the transition of cell cycle from G0/G1 phase to S phase, enhanced the activity of Wnt/β-catenin signalling pathway and up-regulated the protein expression of downstream factors, such as Cyclin D1, MMP7 and Slug. The promoted growth, migration and invasion of HeLa-HK2 cells were inhibited by Wnt/β-catenin inhibitor XAV-939. Conclusion HK2 could promote the proliferation, migration and invasion of HeLa cells by up-regulating the expression of Cyclin D1, MMP7 and Slug via Wnt/β-catenin signaling pathway.

Keywords

• hk2
• β-catenin
• cyclin d1
• slug
• mmp7
• cervical cancer