Research Article

Wnt/β-catenin aids in regulating the proliferation of hepG2 cells mediated by thy-1

Published: July 07, 2014
Genet. Mol. Res. 13 (3) : 5115-5127 DOI: https://doi.org/10.4238/2014.July.7.4
Cite this Article:
B.Q. Cheng, Y. Jiang, Q. Zhu, W.G. Lin (2014). Wnt/β-catenin aids in regulating the proliferation of hepG2 cells mediated by thy-1. Genet. Mol. Res. 13(3): 5115-5127. https://doi.org/10.4238/2014.July.7.4
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Abstract

Cancer stem cells have been found to play important roles in carcinoma. Although thy-1 has been identified as a potential stem cell marker of liver cancer, whether the Wnt/β-catenin signaling pathway plays an important role in regulating hepatocarcinoma proliferation and apoptosis mediated by thy-1 remains unknown. Our results showed that high thy-1 expression caused hepG2 cells transfected with a pReceiver-M29/thy-1 eukaryotic expression vector to exhibit obvious heteromorphism, featuring double or multiple nuclei and weaker apoptosis. A high expression of β-catenin, as a critical signaling protein of Wnt/β-catenin, and its downstream transcription factor, cyclinD1, were detected in transfected hepG2 cells. We also used aspirin as an inhibitor of the Wnt signaling pathway in the treatment of hepG2 cells transfected with the pReceiver-M29/thy-1 expression vector to make detailed observations of apoptosis in hepG2 cells as well as the differential expression of β-catenin, cyclinD1, and thy-1. An increasing apoptosis rate was detected in the hepG2 cells and downregulated expression of the three proteins was detected. Hence, we suggest that thy-1 upregulation promotes the proliferation and inhibits apoptosis of hepG2 cells, and that these processes are regulated by the Wnt/β- catenin signaling pathway.

Cancer stem cells have been found to play important roles in carcinoma. Although thy-1 has been identified as a potential stem cell marker of liver cancer, whether the Wnt/β-catenin signaling pathway plays an important role in regulating hepatocarcinoma proliferation and apoptosis mediated by thy-1 remains unknown. Our results showed that high thy-1 expression caused hepG2 cells transfected with a pReceiver-M29/thy-1 eukaryotic expression vector to exhibit obvious heteromorphism, featuring double or multiple nuclei and weaker apoptosis. A high expression of β-catenin, as a critical signaling protein of Wnt/β-catenin, and its downstream transcription factor, cyclinD1, were detected in transfected hepG2 cells. We also used aspirin as an inhibitor of the Wnt signaling pathway in the treatment of hepG2 cells transfected with the pReceiver-M29/thy-1 expression vector to make detailed observations of apoptosis in hepG2 cells as well as the differential expression of β-catenin, cyclinD1, and thy-1. An increasing apoptosis rate was detected in the hepG2 cells and downregulated expression of the three proteins was detected. Hence, we suggest that thy-1 upregulation promotes the proliferation and inhibits apoptosis of hepG2 cells, and that these processes are regulated by the Wnt/β- catenin signaling pathway.

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