Next Article in Journal
KRAS-Driven Lung Adenocarcinoma and B Cell Infiltration: Novel Insights for Immunotherapy
Next Article in Special Issue
Reactive Oxygen Species in the Tumor Microenvironment: An Overview
Previous Article in Journal
SETDB-1: A Potential Epigenetic Regulator in Breast Cancer Metastasis
Previous Article in Special Issue
Linking Cancer Metabolic Dysfunction and Genetic Instability through the Lens of Iron Metabolism
Open AccessReview

Cancer Metabolism and the Evasion of Apoptotic Cell Death

Department of Hematology and Medical Oncology, Winship Cancer Institute, School of Medicine, Emory University, Atlanta, GA 30322, USA
*
Author to whom correspondence should be addressed.
Cancers 2019, 11(8), 1144; https://doi.org/10.3390/cancers11081144
Received: 1 July 2019 / Revised: 29 July 2019 / Accepted: 8 August 2019 / Published: 9 August 2019
(This article belongs to the Special Issue Metabolic Reprogramming and Vulnerabilities in Cancer)
  |  
PDF [1349 KB, uploaded 9 August 2019]
  |  

Abstract

Cellular growth and proliferation depend upon the acquisition and synthesis of specific metabolites. These metabolites fuel the bioenergy, biosynthesis, and redox potential required for duplication of cellular biomass. Multicellular organisms maintain tissue homeostasis by balancing signals promoting proliferation and removal of cells via apoptosis. While apoptosis is in itself an energy dependent process activated by intrinsic and extrinsic signals, whether specific nutrient acquisition (elevated or suppressed) and their metabolism regulates apoptosis is less well investigated. Normal cellular metabolism is regulated by lineage specific intrinsic features and microenvironment driven extrinsic features. In the context of cancer, genetic abnormalities, unconventional microenvironments and/or therapy engage constitutive pro-survival signaling to re-program and rewire metabolism to maintain survival, growth, and proliferation. It thus becomes particularly relevant to understand whether altered nutrient acquisition and metabolism in cancer can also contribute to the evasion of apoptosis and consequently therapy resistance. Our review attempts to dissect a causal relationship between two cancer hallmarks, i.e., deregulated cellular energetics and the evasion of programmed cell death with primary focus on the intrinsic pathway of apoptosis. View Full-Text
Keywords: apoptosis; BCL-2; metabolism apoptosis; BCL-2; metabolism
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Sharma, A.; Boise, L.H.; Shanmugam, M. Cancer Metabolism and the Evasion of Apoptotic Cell Death. Cancers 2019, 11, 1144.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Cancers EISSN 2072-6694 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top