Apigenin: Molecular Mechanisms and Therapeutic Potential against Cancer Spreading.
Valeria NaponelliMaria Teresa RocchettiDomenica MangieriPublished in: International journal of molecular sciences (2024)
Due to its propensity to metastasize, cancer remains one of the leading causes of death worldwide. Thanks in part to their intrinsic low cytotoxicity, the effects of the flavonoid family in the prevention and treatment of various human cancers, both in vitro and in vivo, have received increasing attention in recent years. It is well documented that Apigenin (4',5,7-trihydroxyflavone), among other flavonoids, is able to modulate key signaling molecules involved in the initiation of cancer cell proliferation, invasion, and metastasis, including JAK/STAT, PI3K/Akt/mTOR, MAPK/ERK, NF-κB, and Wnt/β-catenin pathways, as well as the oncogenic non-coding RNA network. Based on these premises, the aim of this review is to emphasize some of the key events through which Apigenin suppresses cancer proliferation, focusing specifically on its ability to target key molecular pathways involved in angiogenesis, epithelial-to-mesenchymal transition (EMT), maintenance of cancer stem cells (CSCs), cell cycle arrest, and cancer cell death.
Keyphrases
- papillary thyroid
- cell proliferation
- signaling pathway
- cell death
- squamous cell
- pi k akt
- cell cycle arrest
- epithelial mesenchymal transition
- squamous cell carcinoma
- oxidative stress
- inflammatory response
- vascular endothelial growth factor
- young adults
- smoking cessation
- toll like receptor
- induced pluripotent stem cells
- cell migration
- wound healing