title: Natural inhibitors of PI3K/AKT signaling in breast cancer: emphasis on newly-discovered molecular mechanisms of action.
abstract: Epidermal growth factor receptor (EGFR) plays a critical role in the initiation and progression of a variety of human cancers, including breast cancer. An important signaling pathway downstream of EGFR is the PI3K/AKt pathway, which regulates cellular processes as diverse as cell growth, survival, proliferation and migration. Deregulated activity of this pathway may lead to uncontrolled cell growth, survival, migration and invasion, contributing to tumor formation. In this review, we evaluate natural compounds that, in vitro (breast cancer cell lines) and/or in vivo (animal model, clinical) studies, suppress breast cancer cells or tumors mainly by suppressing the PI3K/AKT signaling pathway. The effect of these compounds on cell cycle arrest, inhibition of cell migration and invasion, tumor angiogenesis and metastasis in breast cancer are discussed.
authors.affiliation: Biotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Biotechnology, Faculty of Advanced Medical Technologies, Golestan University of Medical Sciences, Gorgan, Iran. Electronic address: Safdari_14@yahoo.com.
authors.forename: Yaghoub
authors.initials: Y
authors.lastname: Safdari
authors.affiliation: Pharmaceutical Sciences Research Center, Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran; Student Research Committee, School of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran. Electronic address: mkhalili_ps@yahoo.com.
authors.forename: Masoumeh
authors.initials: M
authors.lastname: Khalili
authors.affiliation: Pharmaceutical Sciences Research Center, Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran.
authors.forename: Mohammad Ali
authors.initials: MA
authors.lastname: Ebrahimzadeh
authors.affiliation: Infectious Diseases Research Center and Laboratory Science Research Center, Golestan University of Medical Sciences, Gorgan, Iran.
authors.forename: Yaghoub
authors.initials: Y
authors.lastname: Yazdani
authors.affiliation: Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Safar
authors.initials: S
authors.lastname: Farajnia
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D066246:ErbB Receptors / Q000378:metabolism; D005260:Female; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors* / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D000970:Antineoplastic Agents; D066246:ErbB Receptors; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt
keywords: AKT; Ascofuranone (PubChem CID: 6434242); BYL-719 (PubChem CID: 56649450); Breast cancer; CDRI 85-287 (PubChem CID: 159508); Fenretinide: (PubChem CID: 5288209); Isoliquiritigenin (PubChem CID: 638278); Natural inhibitors; PI3K; Platycodin D (PubChem CID: 162859); Quercetin (PubChem CID: 5280343); Thymoquinone (PubChem CID:10281); Wogonin (PubChem CID: 5281703)