Regulation of Cell Signaling Pathways and miRNAs by Resveratrol in Different Cancers.
Ammad Ahmad FarooqiSumbul KhalidAamir AhmadPublished in: International journal of molecular sciences (2018)
Genomic and proteomic studies have helped improve our understanding of the underlying mechanism(s) of cancer development and progression. Mutations, overexpressed oncogenes, inactivated/downregulated tumor suppressors, loss of apoptosis, and dysregulated signal transduction cascades are some of the well-studied areas of research. Resveratrol has gained considerable attention in the last two decades because of its pleiotropic anticancer activities. In this review, we have summarized the regulation of WNT, SHH (sonic hedgehog)/GLI (glioma-associated oncogene homolog), TGFβ1 (transforming growth factor beta 1)/SMAD, NOTCH, TRAIL (tumor necrosis factor-related apoptosis-inducing ligand), STAT (signal transducer and activator of transcription), and microRNAs by resveratrol in different cancers. The importance of these signaling pathways in cancer progression, along with their modulation by resveratrol, is discussed. Further, we also evaluate the mechanisms and implications of the downregulation of oncogenic miRNAs and the upregulation of tumor suppressor miRNAs by resveratrol, both of which also define its ability to inhibit tumor growth and metastasis. It is envisioned that designing effective clinical trials will be helpful for the identification of resveratrol responders and non-responders and the elucidation of how this phytochemical can be combined with current therapeutic options to improve their clinical efficacy and reduce off-target effects.
Keyphrases
- transforming growth factor
- signaling pathway
- cell proliferation
- epithelial mesenchymal transition
- clinical trial
- papillary thyroid
- oxidative stress
- endoplasmic reticulum stress
- squamous cell
- pi k akt
- cell cycle arrest
- cell death
- randomized controlled trial
- single cell
- young adults
- squamous cell carcinoma
- working memory
- mesenchymal stem cells
- induced apoptosis
- cell therapy
- lymph node metastasis
- inflammatory response
- genome wide
- phase ii
- dna methylation