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Research ArticleExperimental Studies

Pongamol Inhibits Epithelial to Mesenchymal Transition Through Suppression of FAK/Akt-mTOR Signaling

HARDYANTI EKA PUTRI, BOONCHOO SRITULARAK and PITHI CHANVORACHOTE
Anticancer Research December 2021, 41 (12) 6147-6154; DOI: https://doi.org/10.21873/anticanres.15434
HARDYANTI EKA PUTRI
1Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand;
2Cell-Based Drug and Health Product Development Research Unit, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand;
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BOONCHOO SRITULARAK
3Department of Pharmacognosy and Pharmaceutical Botany, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand
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PITHI CHANVORACHOTE
1Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand;
2Cell-Based Drug and Health Product Development Research Unit, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand;
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  • For correspondence: pithi.c@chula.ac.th
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Abstract

Background/Aim: Cancer metastasis is the main cause of mortality in cancer patients. As lung cancer patients are mostly detected at metastatic stages, strategies that inhibit cancer metastasis may offer effective therapies. Activation of FAK and Akt/mTOR pathways promotes the highly metastatic phenotypes of epithelial to mesenchymal transition (EMT). We unraveled EMT inhibitory action of pongamol and the mechanism controlling cell dissemination in lung cancer cells. Materials and Methods: Cytotoxic and antiproliferative effects of pongamol were determined by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis and necrosis induction in response to pongamol treatment was observed and visualized by nuclei staining assay. Wound healing migration, invasion, and anchorage-dependent growth assay were conducted to evaluate metastatic behaviors. EMT protein expression and FAK pathway were detected by western blot analysis. Results: Pongamol at 0-100 μM exhibited significant inhibition on migration, and invasion of cancer cells. Regarding anoikis resistance potential, the compound significantly inhibited survival and growth of cancer cells in an anchorage-independent manner, as indicated by the depletion of growing colonies in pongamol-pretreated cells. Protein level analysis further showed that pongamol exerted its anti-metastasis effect by inhibiting EMT, as indicated by a decrease of several mesenchymal proteins (N-cadherin, vimentin, Snail, and Slug). Regarding the up-stream mechanisms, we found that pongamol inhibited activation of FAK and Akt/mTOR signaling pathways. Conclusion: Pongamol exhibits potent anti-metastatic activity through suppressing key potentiating factors of cancer metastasis EMT and FAK.

Key Words:
  • Pongamol
  • EMT
  • non-small cell lung cancer
  • FAK
  • Received September 20, 2021.
  • Revision received October 15, 2021.
  • Accepted November 2, 2021.
  • Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.
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Anticancer Research: 41 (12)
Anticancer Research
Vol. 41, Issue 12
December 2021
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Pongamol Inhibits Epithelial to Mesenchymal Transition Through Suppression of FAK/Akt-mTOR Signaling
HARDYANTI EKA PUTRI, BOONCHOO SRITULARAK, PITHI CHANVORACHOTE
Anticancer Research Dec 2021, 41 (12) 6147-6154; DOI: 10.21873/anticanres.15434

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Pongamol Inhibits Epithelial to Mesenchymal Transition Through Suppression of FAK/Akt-mTOR Signaling
HARDYANTI EKA PUTRI, BOONCHOO SRITULARAK, PITHI CHANVORACHOTE
Anticancer Research Dec 2021, 41 (12) 6147-6154; DOI: 10.21873/anticanres.15434
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Keywords

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