作者: Ulku Ozbey , Rukset Attar , Mirna Azalea Romero , Saleh S Alhewairini , Behnaz Afshar
DOI: 10.1002/JCB.27575
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摘要: Wealth of information gleaned from decades high-impact research work; scientists have disentangled the complicated web versatile regulators that underlie cancer development and progression. Use structural biology approaches functional genomics helped us to gain new insights into complex nature cancer, it is now clear genetic/epigenetic mutations, overexpression oncogenes, inactivation tumor suppressors, loss apoptosis, versatility protein binding partners contributory roles in carcinogenesis metastatic spread. It becoming progressively more understandable reprogramming gene expression during nontranscriptional changes progression are initiated controlled by deregulated signal transduction cascades, all which collectively create an incalculable complexity. Data obtained through preclinical clinical trials revealed alterations targeted oncogenes other downstream, parallel pathways played a central role resistance against different therapeutics. Phytochemicals regained limelight, natural products currently being tested for efficacy studies. Apigenin, plant-derived flavonoid has considerable pharmacological value reportedly involved regulation signaling cascades. In this review, we attempted summarize rapidly evolving understanding molecular biologists pharmacologists about potential apigenin cancers. We emphasized on WNT/β-catenin janus kinase/signal transducers activators transcription (JAK-STAT) pathways. also comprehensively discuss how restored apoptosis necrosis factor-related apoptosis-inducing ligand (TRAIL)-resistant The review gives snapshot microRNAs (miRNAs) regulate wide-ranging biological processes, each miRNA can control hundreds targets. Apigenin was noted upregulate miR-520b miR-101 cancers inhibit growth. Moreover, apigenin-induced apoptotic rate significantly higher when used combination with miR-423-5p inhibitors or miR-138 mimics. Better comprehension linear integrated will be helpful effective therapeutic targeting inhibit/prevent cancer.