• SUVRA MANDAL

      Articles written in Journal of Biosciences

    • Hypomethylation of LIMD1 and P16 by downregulation of DNMT1 results in restriction of liver carcinogenesis by amarogentin treatment

      DEBOLINA PAL SUBHAYAN SUR RITUPARNA ROY SUVRA MANDAL CHINMAY KUMAR PANDA

      More Details Abstract Fulltext PDF

      Amarogentin (active component of Chirata) was found to prevent CCl4/NDEA-induced liver carcinogenesis atmild dysplastic stage through modulation of cell cycle, apoptosis, self-renewal pathways. The cell cycleregulatory genes LIMD1, P16 and RBSP3 were found to be upregulated in restricted liver lesions. Tounderstand the mechanism of upregulation during restriction of cacinogenesis, the effect of amarogentin onepigenetic modification was evaluated in this study. It was also validated in vitro. Hypermethylation of LIMD1and P16 was seen in mouse hepatocellular carcinoma (30th week carcinogen control mice); however,hypomethylation of these genes was seen in amarogentin-treated liver. In the case of RBSP3, no such changewas seen. DNMT1 expression (mRNA/protein) was significantly increased in later stages of carcinogenesis,whereas its expression was comparable to normal liver in the case of amarogentin treatment. No significantchange in expression (mRNA/protein) of HDAC1/2 was observed irrespective of treatment. Amarogentintreatment upregulated the expression (mRNA/protein) of LIMD1, P16 and RBSP3 in the HepG2 cell line. Herealso treated cells showed LIMD1 and P16 hypomethylation with DNMT1 downregulation. Increased expressionof LIMD1, P16 and RBSP3 after treating cells with demethylating agent 5-aza-2-deoxycytidine indicatedepigenetic modulation by amarogentin treatment.

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