title: Recent development in targeting PI3K-Akt-mTOR signaling for anticancer therapeutic strategies.
abstract: Cancer is a diverse class of diseases which differ widely in their cause and biology. The aberrant behavior of cancer reflects up regulation of certain oncogenic signaling pathways that promote proliferation, inhibit apoptosis, and enable the cancer to spread and evoke angiogenesis. Phosphoinositide-3-kinase(PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway controls various biological processes that are important for normal functioning of the cell via cell cycle progression, survival, migration, transcription, translation and metabolism. However, PI3K signaling pathway is dysregulated almost in all cancers which is due to the amplification and genetic mutation of PI3K gene, encoding catalytic and regulatory subunit of PI3K isoforms. The current review focuses on the structural features of various PI3K isoforms including Akt and mTOR and their inhibition using specific small molecule inhibitors in an attempt to achieve an attractive target for cancer prevention and chemotherapy.
authors: Asif Khurshid
authors: AK
authors: Qazi
authors: Aashiq
authors: A
authors: Hussain
authors: Abid
authors: A
authors: Hamid
authors: Yasrib
authors: Y
authors: Qurishi
authors: Rabiya
authors: R
authors: Majeed
authors: Mudassier
authors: M
authors: Ahmad
authors: Rauf Ahmad
authors: RA
authors: Najar
authors: Javeed Ahmad
authors: JA
authors: Bhat
authors: Shashank Kumar
authors: SK
authors: Singh
authors: Mohmmad Afzal
authors: MA
authors: Zargar
authors: Shakir
authors: S
authors: Ali
authors: Cancer Pharmacology Division, Indian Institute of Integrative Medicine, Medicine (Council of Scientific and Industrial Research) Canal Road, Jammu-Tawi 180001, India. ahdar@iiim.ac.in.
authors: Ajit Kumar
authors: AK
authors: Saxena
mesh_terms: D000970:Antineoplastic Agents / Q000138:chemical synthesis / Q000627:therapeutic use; D049109:Cell Proliferation / Q000187:drug effects; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D058990:Molecular Targeted Therapy; D009154:Mutation; D009369:Neoplasms / Q000188:drug therapy* / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics* / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D047428:Protein Kinase Inhibitors / Q000138:chemical synthesis / Q000627:therapeutic use; D021122:Protein Subunits / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D036341:Intercellular Signaling Peptides and Proteins; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D047428:Protein Kinase Inhibitors; D021122:Protein Subunits; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; C546842:MTOR protein, human