This report demonstrates that DLC-1 is negatively associated with NPC carcinogenesis, and promoter hypermethylation along with loss of heterozygosity, but not mutation, contributes to inactivation of DLC-1 in NPC.
Collectively, our observations suggest that hypermethylation is responsible for abrogating the function of the DLC‑1 gene in colon cancer and indicate a role of DLC‑1 in colon carcinogenesis.
Here we review the pathways governing DNA replication fidelity and discuss evidence implicating replication errors (point mutation instability or PIN) in carcinogenesis.
Taken together, these results suggest that DLC-1 plays a crucial role in signal transduction pathway regulating the cell proliferation, migration, and carcinogenesis of human RCC.
In conclusion, our results demonstrate that transcriptional silencing of DLC-1 through promoter hypermethylation may contribute to tumorigenesis in a subset of SPNETs, and that loss of DLC-1 expression in MBs may be related to mechanisms other than promoter hypermethylation, genomic deletion, and mutation.
Taken together, the results of our study suggest that the transcriptional silencing of DLC-1, by epigenetic mechanism, may be involved in gastric carcinogenesis.
PIN is associated with progressive abnormalities of phenotype and genotype intermediate between normal prostatic epithelium and cancer, indicating impairment of cell differentiation and regulatory control with advancing stages of prostatic carcinogenesis.