Am J Cancer Res 2013;3(3):251-265
Review Article
Autophagy in breast cancer and its implications for therapy
Kirti Jain, Krishna S Paranandi, Savitha Sridharan, Alakananda Basu
Department of Molecular Biology & Immunology, University of North Texas Health Science Center and Institutes for Cancer
Research and Focused on Resources for her Health Education and Research, Fort Worth, Texas, 76107, USA
Received March 25, 2013; Accepted May 1, 2013; Epub June 20, 2013; Published June 30, 2013
Abstract: Autophagy is an evolutionarily conserved process of cellular self-digestion that serves as a mechanism to clear
damaged organelles and recycle nutrients. Since autophagy can promote cell survival as well as cell death, it has been linked to
different human pathologies, including cancer. Although mono-allelic deletion of autophagy-related gene BECN1 in breast
tumors originally indicated a tumor suppressive role for autophagy in breast cancer, the intense research during the last decade
suggests a role for autophagy in tumor progression. It is now recognized that tumor cells often utilize autophagy to survive
various stresses, such as oncogene-induced transformation, hypoxia, endoplasmic reticulum (ER) stress and extracellular
matrix detachment. Induction of autophagy by tumor cells may also contribute to tumor dormancy and resistance to anticancer
therapies, thus making autophagy inhibitors promising drug candidates for breast cancer treatment. The scientific endeavors
continue to define a precise role for autophagy in breast cancer. In this article, we review the current literature on the role of
autophagy during the development and progression of breast cancer, and discuss the potential of autophagy modulators for
breast cancer treatment. (ajcr0000191).
Keywords: Autophagy, breast cancer, transformation, hypoxia, ER stress, tumor microenvironment, metabolism, metastasis,
apoptosis, cancer therapy
Address correspondence to: Dr. Alakananda Basu, Department of Molecular Biology & Immunology, University of North Texas
Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107. Tel: 817-735-2487; Fax: 817-735-2118; E-mail:
alakananda.basu@unthsc.edu
Review Article
Autophagy in breast cancer and its implications for therapy
Kirti Jain, Krishna S Paranandi, Savitha Sridharan, Alakananda Basu
Department of Molecular Biology & Immunology, University of North Texas Health Science Center and Institutes for Cancer
Research and Focused on Resources for her Health Education and Research, Fort Worth, Texas, 76107, USA
Received March 25, 2013; Accepted May 1, 2013; Epub June 20, 2013; Published June 30, 2013
Abstract: Autophagy is an evolutionarily conserved process of cellular self-digestion that serves as a mechanism to clear
damaged organelles and recycle nutrients. Since autophagy can promote cell survival as well as cell death, it has been linked to
different human pathologies, including cancer. Although mono-allelic deletion of autophagy-related gene BECN1 in breast
tumors originally indicated a tumor suppressive role for autophagy in breast cancer, the intense research during the last decade
suggests a role for autophagy in tumor progression. It is now recognized that tumor cells often utilize autophagy to survive
various stresses, such as oncogene-induced transformation, hypoxia, endoplasmic reticulum (ER) stress and extracellular
matrix detachment. Induction of autophagy by tumor cells may also contribute to tumor dormancy and resistance to anticancer
therapies, thus making autophagy inhibitors promising drug candidates for breast cancer treatment. The scientific endeavors
continue to define a precise role for autophagy in breast cancer. In this article, we review the current literature on the role of
autophagy during the development and progression of breast cancer, and discuss the potential of autophagy modulators for
breast cancer treatment. (ajcr0000191).
Keywords: Autophagy, breast cancer, transformation, hypoxia, ER stress, tumor microenvironment, metabolism, metastasis,
apoptosis, cancer therapy
Address correspondence to: Dr. Alakananda Basu, Department of Molecular Biology & Immunology, University of North Texas
Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107. Tel: 817-735-2487; Fax: 817-735-2118; E-mail:
alakananda.basu@unthsc.edu
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American Journal of Cancer Research
| ISSN: 2156-6976 |