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Musa paradisiaca inflorescence induces human colon cancer cell death by modulating cascades of transcriptional events

Abstract

Colorectal cancer (CRC) is one of the leading causes of cancer death with diet playing an important role in etiology of CRC. Traditional medical practitioners in many of the South Asian Countries use plantain inflorescence for the treatment of various gastro-intestinal ailments. The aim of the present study is to investigate the anticancer effect of extracts of inflorescence of Musa paradisiaca against HT29 human colon cancer cells and elucidate the mechanism by studying the modulation of cascades of transcriptional events. In vitro assays depicted that methanol extract of Musa paradisiaca inflorescence (PIMET) were cytotoxic to HT29 cells. PIMET induced DNA damage and arrested the cell cycle at G2/M phase. Expression studies show that PIMET pretreatment up regulates pro-apoptotic Bcl2 and down regulates anti-apoptotic Bax proteins. Different assays showed that the deregulation of pro/antiapoptotic proteins reduces mitochondrial membrane potential and ATP production; further enhances Cytochrome C release which triggers apoptotic pathway and further cleaves Caspase 3 and PARP proteins resulting in apoptosis. Changes in protein expression profile of HT29 cells after PIMET treatment were analyzed using mass-spectrometry-based proteomics. PIMET treatment significantly altered the HT29 protein expression and interestingly the X-linked inhibitor of apoptosis protein was down regulated. The alteration in expression of this protein has significant effect leading to HT29 cell death.

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Publication details

The article was received on 19 Sep 2017, accepted on 28 Nov 2017 and first published on 29 Nov 2017


Article type: Paper
DOI: 10.1039/C7FO01454F
Citation: Food Funct., 2017, Accepted Manuscript
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    Musa paradisiaca inflorescence induces human colon cancer cell death by modulating cascades of transcriptional events

    A. K. Babu, A. Madhavan, R. T. R. , S. Thomas and N. P, Food Funct., 2017, Accepted Manuscript , DOI: 10.1039/C7FO01454F

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