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

Colorectal cancer (CRC) is one of the leading causes of cancer death, and diet plays an important role in the etiology of CRC. Traditional medical practitioners in many South Asian countries use plantain inflorescence to treat various gastro-intestinal ailments. The aim of the present study was to i...

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Bibliographic Details
Published in:Food & function 2018-01, Vol.9 (1), p.511-524
Main Authors: K B, Arun, Madhavan, Aravind, T R, Reshmitha, Thomas, Sithara, Nisha, P
Format: Article
Language:English
Subjects:
Anticancer properties
Apoptosis
Bax protein
Cancer
Cascades
Caspase
Caspase-3
Cell cycle
Cell death
Colon
Colon cancer
Colorectal cancer
Colorectal carcinoma
Cytochrome
Cytochrome c
Cytotoxicity
Deoxyribonucleic acid
Deregulation
DNA
DNA damage
Etiology
Intestine
Membrane potential
Mitochondria
Mortality
Musa paradisiaca
Poly(ADP-ribose) polymerase
Pretreatment
Proteins
Proteomics
Spectrometry
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Summary:Colorectal cancer (CRC) is one of the leading causes of cancer death, and diet plays an important role in the etiology of CRC. Traditional medical practitioners in many South Asian countries use plantain inflorescence to treat various gastro-intestinal ailments. The aim of the present study was to investigate the anticancer effects of extracts of inflorescence of Musa paradisiaca against HT29 human colon cancer cells and elucidate the mechanism of these effects by studying the modulation of cascades of transcriptional events. In vitro assays depicted that methanol extract of Musa paradisiaca inflorescence (PIMET) was cytotoxic to HT29 cells. PIMET induced DNA damage and arrested the cell cycle at the G2/M phase. Expression studies showed that PIMET pretreatment upregulates pro-apoptotic Bcl2 and downregulates anti-apoptotic Bax proteins. Different assays showed that the deregulation of pro/antiapoptotic proteins reduces the mitochondrial membrane potential and ATP production; moreover, it enhances cytochrome c release, which triggers the apoptotic pathway, and further cleaves caspase 3 and PARP proteins, resulting in apoptosis. Changes in the protein expression profile of HT29 cells after PIMET treatment were analyzed using mass-spectrometry-based proteomics. PIMET treatment significantly altered the expression of HT29 protein; interestingly, X-linked inhibitor of apoptosis protein was also downregulated. Alteration in the expression of this protein has significant effects, leading to HT29 cell death.
ISSN:2042-6496
2042-650X
DOI:10.1039/c7fo01454f