AI Article Synopsis
- - The study investigates how S-adenosylmethionine (SAM) affects the growth of gastric cancer by altering the methylation of the VEGF-C gene promoter.
- - Researchers used MTT analyses and a nude mouse model to show that SAM significantly increases the methylation of the VEGF-C promoter, leading to decreased protein levels of VEGF-C, which is linked to cancer growth.
- - The findings suggest that SAM can reverse DNA hypomethylation of VEGF-C, effectively inhibiting gastric cancer growth both in lab experiments and in live subjects.
Article Abstract
Objective: To explore inhibitory effects of S-adenosylmethionine on vascular endothelial growth factor-C (VEGF-C) protein and cellular proliferation in gastric cancer by regulating methylation status of VEGF-C promoter.
Methods: MTT analyses and nude mice model were employed to examine the effects of S- adenosylmethionine on inhibiting gastric cancer growth in vitro and in vivo. The protein expression of VEGF-C in gastric cancer cells was assessed by Western blot. The methylation status of VEGF-C promoter was assessed by bisulfite genomic DNA sequencing analysis.
Results: VEGF-C promoter was hypomethylated in MGC803 and SGC7901. The treatment of S-adenosylmethionine resulted in a heavy hypermethylation of VEGF-C promoter, which consequently down regulated protein level of VEGF-C. S-adenosylmethionine effectively inhibited the growth of gastric cancer cells in vitro and in vivo (P<0. 05).
Conclusion: S-adenosylmethionine can effectively reverse DNA hypomethylation on VEGF-C promoter which down-regulates VEGF-C protein expression and inhibit gastric cancer growth.
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