Apigenin inhibits growth and migration of fibroblasts by suppressing FAK signaling

Wang, Hongyi; Guo, Bingyu; Lin, Shu; Chang, Peng; Tao, Kai

doi:10.18632/aging.102006

Cited by 14 publications

(12 citation statements)

References 32 publications

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“…A study reported that apigenin can increase the levels of ERK1/2 and inhibit the activation of p38 kinase in lung and prostate cancer cell lines. Results showed that apigenin can induce apoptosis by inhibiting the MAPK/ERK signaling pathway [138,139].…”

Section: Erk/mapk Pathwaymentioning

confidence: 99%

Pharmacological Properties of 4′, 5, 7-Trihydroxyflavone (Apigenin) and Its Impact on Cell Signaling Pathways

Abid¹,

Ghazanfar²,

Farid

et al. 2022

Molecules

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Plant bioactive compounds, particularly apigenin, have therapeutic potential and functional activities that aid in the prevention of infectious diseases in many mammalian bodies and promote tumor growth inhibition. Apigenin is a flavonoid with low toxicities and numerous bioactive properties due to which it has been considered as a traditional medicine for decades. Apigenin shows synergistic effects in combined treatment with sorafenib in the HepG2 human cell line (HCC) in less time and statistically reduces the viability of tumor cells, migration, gene expression and apoptosis. The combination of anti-cancerous drugs with apigenin has shown health promoting potential against various cancers. It can prevent cell mobility, maintain the cell cycle and stimulate the immune system. Apigenin also suppresses mTOR activity and raises the UVB-induced phagocytosis and reduces the cancerous cell proliferation and growth. It also has a high safety threshold, and active (anti-cancer) doses can be gained by consuming a vegetable and apigenin rich diet. Apigenin also boosted autophagosome formation, decreased cell proliferation and activated autophagy by preventing the activity of the PI3K pathway, specifically in HepG2 cells. This paper provides an updated overview of apigenin’s beneficial anti-inflammatory, antibacterial, antiviral, and anticancer effects, making it a step in the right direction for therapeutics. This study also critically analyzed the effect of apigenin on cancer cell signaling pathways including the PI3K/AKT/MTOR, JAK/STAT, NF-κB and ERK/MAPK pathways.

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Section: Erk/mapk Pathwaymentioning

confidence: 99%

Pharmacological Properties of 4′, 5, 7-Trihydroxyflavone (Apigenin) and Its Impact on Cell Signaling Pathways

Abid¹,

Ghazanfar²,

Farid

et al. 2022

Molecules

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show abstract

“…Apigenin is a kind of dietary flavonoid extracted mainly from celery, parsley, thyme, chamomile, and onions [ 23 ]. It had been reported that apigenin is of great effect in antifibrosis [ 33 – 36 ] and liver protection [ 26 , 40 – 42 ]. Mirzoeva et al demonstrated that apigenin could reduce TGF- β -induced VEGF production and suppress prostate carcinogenesis by regulating the Smad2/3 and Src/Fak/Akt pathways.…”

Section: Discussionmentioning

confidence: 99%

“…Apigenin is a kind of dietary flavonoid extracted mainly from celery, parsley, thyme, chamomile, and onions [ 23 ]. Recently, apigenin has reported many pharmacological effects including anticancer [ 24 – 28 ], anti-inflammation [ 29 – 32 ], antifibrosis [ 33 – 36 ], and so on. Zhang et al confirmed apigenin could downregulate the miR34a expression to suppress mouse peritoneal fibrosis [ 35 ].…”

Section: Introductionmentioning

confidence: 99%

Apigenin Alleviates Liver Fibrosis by Inhibiting Hepatic Stellate Cell Activation and Autophagy via TGF-β1/Smad3 and p38/PPARα Pathways

Dai

et al. 2021

PPAR Research

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Objective. The aim of this study is to confirm the hepatocellular protective functions of apigenin and the molecular mechanism on liver fibrosis in mice. Methods. Carbon tetrachloride (CCl4) and bile duct ligature (BDL) mouse fibrosis models were used to investigate the effects of apigenin on liver fibrosis. Sixty-six male C57 mice were randomly divided into eight groups, including the vehicle group, CCl4 group, CCl4+L-apigenin (20 mg/kg) group, CCl4+H-apigenin (40 mg/kg) group, sham group, BDL group, BDL+L-apigenin(20 mg/kg) group, and BDL+H-apigenin(40 mg/kg) group. Serum liver enzymes (ALT and AST), proteins associated with autophagy, and indicators linked with the TGF-β1/Smad3 and p38/PPARα pathways were detected using qRT-PCR, immunohistochemical staining, and western blotting. Results. Our findings confirmed that apigenin could decrease the levels of ALT and AST, suppress the generation of ECM, inhibit the activation of HSCs, regulate the balance of MMP2 and TIMP1, reduce the expression of autophagy-linked protein, and restrain the TGF-β1/Smad3 and p38/PPARα pathways. Conclusion. Apigenin could alleviate liver fibrosis by inhibiting hepatic stellate cell activation and autophagy via TGF-β1/Smad3 and p38/PPARα pathways.

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“…Quercetin and other antioxidants have been demonstrated to increase integrin αV expression while lowering integrin β1 in dermal cells by phosphorylating two sites, 397 and 861, of the FAK complex ( 118 ). Apigenin inhibited FAK activity and phosphorylation in human fibroblasts by regulating integrin protein levels, which then affected phosphorylation of extracellular regulatory protein kinase1/2 (Erk1/2), which has important implications for fibroblast proliferation and survival ( 119 ). Furthermore, the sarcoma gene (Src) is a complex kinase that frequently works in a functional protein complex with FAK.…”

Section: Flavonoids’ Mechanism For Scar-free Regenerationmentioning

confidence: 99%

The potential of functionalized dressing releasing flavonoids facilitates scar-free healing

et al. 2022

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Scars are pathological marks left after an injury heals that inflict physical and psychological harm, especially the great threat to development and aesthetics posed by oral and maxillofacial scars. The differential expression of genes such as transforming growth factor-β, local adherent plaque kinase, and yes-related transcriptional regulators at infancy or the oral mucosa is thought to be the reason of scarless regenerative capacity after tissue defects. Currently, tissue engineering products for defect repair frequently overlook the management of postoperative scars, and inhibitors of important genes alone have negative consequences for the organism. Natural flavonoids have hemostatic, anti-inflammatory, antioxidant, and antibacterial properties, which promote wound healing and have anti-scar properties by interfering with the transmission of key signaling pathways involved in scar formation. The combination of flavonoid-rich drug dressings provides a platform for clinical translation of compounds that aid in drug disintegration, prolonged release, and targeted delivery. Therefore, we present a review of the mechanisms and effects of flavonoids in promoting scar-free regeneration and the application of flavonoid-laden dressings.

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Apigenin inhibits growth and migration of fibroblasts by suppressing FAK signaling

Cited by 14 publications

References 32 publications

Pharmacological Properties of 4′, 5, 7-Trihydroxyflavone (Apigenin) and Its Impact on Cell Signaling Pathways

Pharmacological Properties of 4′, 5, 7-Trihydroxyflavone (Apigenin) and Its Impact on Cell Signaling Pathways

Apigenin Alleviates Liver Fibrosis by Inhibiting Hepatic Stellate Cell Activation and Autophagy via TGF-β1/Smad3 and p38/PPARα Pathways

The potential of functionalized dressing releasing flavonoids facilitates scar-free healing

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