Targeting autophagy to overcome drug resistance in cancer therapy.
Autophagy, a catabolic process, is activated by conditions of stress and nutrient deprivation, which occurs to maintain metabolic homeostasis by performing catabolic lysis of excessive or unnecessary proteins, and injured or aged organelles. Autophagy is regulated by various signaling pathways. Main regulators of autophagy are the PI3K-Akt-mTOR pathway, Beclin1, Bcl-2, Ras and p53. Autophagy plays dual role in cancer, shows both tumor suppressive and oncogenic activity. It is accepted that drug resistance in cancer cells can be overcome by inhibition of autophagy. Herein, we summarize autophagy as a potential target of anticancer drugs and targeting autophagy provides a promising therapeutic strategy to circumvent resistance and enhance the effect of anticancer therapies for cancer patients.
Kharvel Subharti College of Pharmacy, Swami Vivekanand Subharti University, NH-58, Meerut - 250005, India.
Ankit
A
Kumar
Kharvel Subharti College of Pharmacy, Swami Vivekanand Subharti University, NH-58, Meerut - 250005, India.
Umesh Kumar
UK
Singh
Meerut Institute of Engineering & Technology, NH-58, Meerut Bypass Road, Meerut - 250005, India.
Anurag
A
Chaudhary
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D001343:Autophagy / Q000187:drug effects*; D055808:Drug Discovery / Q000379:methods; D019008:Drug Resistance, Neoplasm / Q000187:drug effects*; D006801:Humans; D058990:Molecular Targeted Therapy; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
D000970:Antineoplastic Agents; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases