Published online Dec 28, 2015. doi: 10.3748/wjg.v21.i48.13447
Peer-review started: May 27, 2015
First decision: August 26, 2015
Revised: September 12, 2015
Accepted: October 17, 2015
Article in press: October 20, 2015
Published online: December 28, 2015
Processing time: 212 Days and 12.9 Hours
AIM: To investigate the roles and interactions of mutT homolog (MTH)-1 and hypoxia-inducible factor (HIF)-1α in human colorectal cancer (CRC).
METHODS: The expression and distribution of HIF-1α and MTH-1 proteins were detected in human CRC tissues by immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR). SW480 and HT-29 cells were exposed to normoxia or hypoxia. Protein and mRNA levels of HIF-1α and MTH-1 were analyzed by western blotting and qRT-PCR, respectively. In order to determine the effect of HIF-1α on the expression of MTH-1 and the amount of 8-oxo-deoxyguanosine triphosphate (dGTP) in SW480 and HT-29 cells, HIF-1α was silenced with small interfering RNA (siRNA). Growth studies were conducted on cells with HIF-1α inhibition using a xenograft tumor model. Finally, MTH-1 protein was detected by western blotting in vivo.
RESULTS: High MTH-1 mRNA expression was detected in 64.2% of cases (54/84), and this was significantly correlated with tumor stage (P = 0.023) and size (P = 0.043). HIF-1α protein expression was correlated significantly with MTH-1 expression (R = 0.640; P < 0.01) in human CRC tissues. Hypoxic stress induced mRNA and protein expression of MTH-1 in SW480 and HT-29 cells. Inhibition of HIF-1α by siRNA decreased the expression of MTH-1 and led to the accumulation of 8-oxo-dGTP in SW480 and HT-29 cells. In the in vivo xenograft tumor model, expression of MTH-1 was decreased in the HIF-1α siRNA group, and the tumor volume was much smaller than that in the mock siRNA group.
CONCLUSION: MTH-1 expression in CRC cells was upregulated via HIF-1α in response to hypoxic stress, emphasizing the crucial role of HIF-1α-induced MTH-1 in tumor growth.
Core tip: Hypoxia is a common characteristic of solid tumors. However, the relationship between hypoxia-inducible factor (HIF)-1α and the human mutT homolog (MTH)-1 had not been clearly investigated. The present study revealed a new mechanism through which HIF-1α upregulates MTH-1 expression in colorectal cancer and provided evidence that hypoxia enhances the expression of MTH-1, likely by modulating HIF-1α protein level. These results emphasize the important role of HIF-1α-induced MTH-1 in tumor progression.