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Article

AMPK Is the Crucial Target for the CDK4/6 Inhibitors Mediated Therapeutic Responses in PANC-1 and MIA PaCa-2 Pancreatic Cancer Cell Lines

1
Department of Molecular Biology and Genetics, Atakoy Campus, Istanbul Kultur University, 34156 Istanbul, Turkey
2
Department of Molecular Biology and Genetics, Biruni University, 34010 Istanbul, Turkey
3
Cancer Research Group, School of Life Sciences, College of Liberal Arts and Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK
4
Institute of Biotechnology, Gebze Technical University, 41400 Gebze, Turkey
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Stresses 2021, 1(1), 48-68; https://doi.org/10.3390/stresses1010005
Received: 19 January 2021 / Revised: 21 February 2021 / Accepted: 23 February 2021 / Published: 18 March 2021
(This article belongs to the Special Issue Cancer and Stresses)
The survival rate of pancreatic ductal adenocarcinoma (PDAC) patients is short, and PDAC is a cancer type that ranks fourth in the statistics regarding death due to cancer. Mutation in the KRAS gene, which plays a role in pancreatic cancer development, activates the PI3K/AKT/mTOR signaling pathway. The activity of the AMPK as a cellular energy sensor is one of the fundamental mechanisms that can induce effective therapeutic responses against CDK4/6 inhibitors via adjusting the cellular and tumor microenvironment stress management. The phosphorylation of AMPKα at the different phosphorylation residues such as Thr172 and Ser 377 causes metabolic differentiation in the cells following CDK4/6 inhibitor treatment in accordance with an increased cell cycle arrest and senescence under the control of different cellular players. In this study, we examined the competencies of the CDK4/6 inhibitors LY2835219 and PD-0332991 on the mechanism of cell survival and death based on AMPK signaling. Both CDK4/6 inhibitors LY2835219 and PD-0332991 modulated different molecular players on the PI3K/AKT/mTOR and AMPK signaling axis in different ways to reduce cell survival in a cell type dependent manner. These drugs are potential inducers of apoptosis and senescence that can alter the therapeutic efficacy cells. View Full-Text
Keywords: pancreatic ductal adenocarcinoma; PD-0332991; LY2835219; PI3K/AKT/mTOR and AMPK signaling axis; cell cycle pancreatic ductal adenocarcinoma; PD-0332991; LY2835219; PI3K/AKT/mTOR and AMPK signaling axis; cell cycle
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MDPI and ACS Style

Sevgin, B.; Coban, M.N.; Rencuzogullari, Ö.; Coker-Gurkan, A.; Obakan-Yerlikaya, P.; Uysal Onganer, P.; Arisan, E.D. AMPK Is the Crucial Target for the CDK4/6 Inhibitors Mediated Therapeutic Responses in PANC-1 and MIA PaCa-2 Pancreatic Cancer Cell Lines. Stresses 2021, 1, 48-68. https://doi.org/10.3390/stresses1010005

AMA Style

Sevgin B, Coban MN, Rencuzogullari Ö, Coker-Gurkan A, Obakan-Yerlikaya P, Uysal Onganer P, Arisan ED. AMPK Is the Crucial Target for the CDK4/6 Inhibitors Mediated Therapeutic Responses in PANC-1 and MIA PaCa-2 Pancreatic Cancer Cell Lines. Stresses. 2021; 1(1):48-68. https://doi.org/10.3390/stresses1010005

Chicago/Turabian Style

Sevgin, Bortecine, Merve N. Coban, Özge Rencuzogullari, Ajda Coker-Gurkan, Pinar Obakan-Yerlikaya, Pinar Uysal Onganer, and Elif D. Arisan. 2021. "AMPK Is the Crucial Target for the CDK4/6 Inhibitors Mediated Therapeutic Responses in PANC-1 and MIA PaCa-2 Pancreatic Cancer Cell Lines" Stresses 1, no. 1: 48-68. https://doi.org/10.3390/stresses1010005

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