NDLI: CDKN2A-p53 mediated antitumor effect of Lupeol in head and neck cancer

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Cellular Oncology : Volume 40, Issue 1, February 2017

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Cellular Oncology : Volume 37

Cellular Oncology : Volume 36

Cellular Oncology : Volume 35

Cellular Oncology : Volume 34

CDKN2A-p53 mediated antitumor effect of Lupeol in head and neck cancer

Content Provider	Springer Nature Link
Author	Bhattacharyya, Sayantan Sekar, Vasanthakumar Majumder, Biswanath Mehrotra, Debapriya G Banerjee, Samir Bhowmick, Anup K Alam, Neyaz Mandal, Gautam K Biswas, Jaydip Majumder, Pradip K Murmu, Nabendu
Copyright Year	2016
Abstract	The tumor suppressor protein p53 is known to control cell cycle arrest and apoptosis. Lupeol is a phytochemical that has been found to induce apoptosis in different cancer types through the extrinsic pathway. As yet, however, its role in the induction of cell cycle arrest and apoptosis through the intrinsic pathway in head and neck cancer has not been investigated. Here, we aimed at understanding the mechanism underlying the antitumor effect of Lupeol in head and neck cancer.The antitumor effect of Lupeol on oral and laryngeal carcinomas was assessed using two in vitro 2D cell line models (HEp-2, UPCI:SCC-131) and, subsequently, an ex vivo 3D tumor explant culture platform that maintains key features of the native tumor microenvironment. The mechanism underlying Lupeol-mediated antitumor responses was delineated using MTT, colony formation, flow cytometry, immunofluorescence, Western blotting and immunohistochemistry assays.We found that Lupeol induced an enhanced expression of p53 in both cell line models tested and, subsequently, cell cycle arrest at the G1 phase. In addition we found that, following Lupeol treatment, p53 induced Bax expression and activated the intrinsic apoptotic pathway (as measured by Caspase-3 cleavage). Interestingly, Lupeol was also found to trigger G1 cell cycle arrest through up-regulation of the expression of CDKN2A, but not p21, resulting in inhibition of CyclinD1. In an ex vivo platform Lupeol was found to impart a potent antitumor response as defined by inhibition of Ki67 expression, decreased cell viability and concomitant activation (cleavage) of Caspase-3. Finally, we found that Lupeol can re-sensitize primary head and neck squamous cell carcinoma (HNSCC) tumor samples that had clinically progressed under a Cisplatin treatment regimen.Together, our data indicate that Lupeol may orchestrate a bifurcated regulation of neoplastic growth and apoptosis in head and neck cancers and may serve as a promising agent for the management of tumors that have progressed on a platinum-based treatment regimen.
Starting Page	145
Ending Page	155
Page Count	11
File Format	PDF
ISSN	22113428
Journal	Cellular Oncology
Volume Number	40
Issue Number	2
e-ISSN	22113436
Language	English
Publisher	Springer Netherlands
Publisher Date	2016-12-30
Publisher Institution	International Society for Cellular Oncology
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Lupeol p53 Cell cycle arrest Apoptosis Head and neck cancer Cancer Research Biomedicine Pathology Oncology
Content Type	Text
Resource Type	Article
Subject	Cancer Research Molecular Medicine Oncology

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CDKN2A-p53 mediated antitumor effect of Lupeol in head and neck cancer

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CDKN2A-p53 mediated antitumor effect of Lupeol in head and neck cancer