Rationalizing the therapeutic potential of apigenin against cancer

Ahmed, Semim Akhtar; Dey, Parama; Daimari, Enush; Girisa, Sosmitha; Banik, Kishore; Harsha, Choudhary; Dutta, Uma; Kunnumakkara, Ajaikumar B.

doi:10.1016/j.lfs.2020.118814

Cited by 72 publications

(55 citation statements)

References 531 publications

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“…Apigenin sensitizes doxorubicin-resistant hepatocellular carcinoma cells to doxorubicin through the inhibition of the PI3K/Akt/Nrf2 pathway [180] and sensitizes pancreatic cancer cells, to chemotherapy [181]. However, in addition to Nrf2 inhibition, apigenin affects molecular pathways such as those associated with the hypoxia-inducible factor (HIF), vascular endothelial growth factor (VEGF), and glucose transporter-1 (GLUT-1) [182,183]. Apigenin reached a clinical trial in 2008 (NCT00609310) in combination with epigallocatechin gallate in the treatment of disease relapse in patients with colorectal cancer, investigating the prevention of neoplasia recurrence.…”

Section: Nrf2 Inhibitors In the Treatment Of Chemoresistant Tumorsmentioning

confidence: 99%

Control of Oxidative Stress in Cancer Chemoresistance: Spotlight on Nrf2 Role

et al. 2021

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Chemoresistance represents the main obstacle to cancer treatment with both conventional and targeted therapy. Beyond specific molecular alterations, which can lead to targeted therapy, metabolic remodeling, including the control of redox status, plays an important role in cancer cell survival following therapy. Although cancer cells generally have a high basal reactive oxygen species (ROS) level, which makes them more susceptible than normal cells to a further increase of ROS, chemoresistant cancer cells become highly adapted to intrinsic or drug-induced oxidative stress by upregulating their antioxidant systems. The antioxidant response is principally mediated by the transcription factor Nrf2, which has been considered the master regulator of antioxidant and cytoprotective genes. Nrf2 expression is often increased in several types of chemoresistant cancer cells, and its expression is mediated by diverse mechanisms. In addition to Nrf2, other transcription factors and transcriptional coactivators can participate to maintain the high antioxidant levels in chemo and radio-resistant cancer cells. The control of expression and function of these molecules has been recently deepened to identify which of these could be used as a new therapeutic target in the treatment of tumors resistant to conventional therapy. In this review, we report the more recent advances in the study of Nrf2 regulation in chemoresistant cancers and the role played by other transcription factors and transcriptional coactivators in the control of antioxidant responses in chemoresistant cancer cells.

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Section: Nrf2 Inhibitors In the Treatment Of Chemoresistant Tumorsmentioning

confidence: 99%

Control of Oxidative Stress in Cancer Chemoresistance: Spotlight on Nrf2 Role

et al. 2021

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“…Apigenin, a flavone present in select fruits, vegetables, and herbs, can induce apoptosis and inhibit proliferation and angiogenesis in several cancer cell lines [66]. The anti-cancer activities of apigenin result from its ability to interact with the PI3K/protein kinase B (ERK)/mTOR, JAK/STAT, NF-κB, MAPK, and Wnt/β-catenin pathways [67]. Interference with mTOR signaling is a dominant mechanism by which apigenin inhibits skin cancer development and progression [68].…”

Section: Apigeninmentioning

confidence: 99%

Flavonoids in Skin Senescence Prevention and Treatment

Domaszewska-Szostek

Puzianowska-Kuźnicka

Kuryłowicz

2021

IJMS

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Skin aging is associated with the accumulation of senescent cells and is related to many pathological changes, including decreased protection against pathogens, increased susceptibility to irritation, delayed wound healing, and increased cancer susceptibility. Senescent cells secrete a specific set of pro-inflammatory mediators, referred to as a senescence-associated secretory phenotype (SASP), which can cause profound changes in tissue structure and function. Thus, drugs that selectively eliminate senescent cells (senolytics) or neutralize SASP (senostatics) represent an attractive therapeutic strategy for age-associated skin deterioration. There is growing evidence that plant-derived compounds (flavonoids) can slow down or even prevent aging-associated deterioration of skin appearance and function by targeting cellular pathways crucial for regulating cellular senescence and SASP. This review summarizes the senostatic and senolytic potential of flavonoids in the context of preventing skin aging.

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“…Similarly, apigenin is related to the naringenin flavone compound, known historically as a coloring agent. However, now apigenin is known for its wide pharmacological activities on several signalling pathways (NF-κB, JAK/STAT, PI3K/AKT/mTOR, MAPK/ERK, and others); thus, it is an effective suppressor of chronic inflammation-mediated diseases [ 225 ] and several types of cancer [ 226 ]. Similarly to naringenin, apigenin prevents NLRP3 inflammasome activation and reduces the release of IL-1β and IL-18 cytokines, but also has a direct effect on the mitochondria (discussed earlier ammonia detoxification pathway) manifested via reduced urea acid production [ 219 ].…”

Section: Therapymentioning

confidence: 99%

Mitochondrial Mutations and Genetic Factors Determining NAFLD Risk

Dabravolski

Bezsonov

Baig

et al. 2021

IJMS

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NAFLD (non-alcoholic fatty liver disease) is a widespread liver disease that is often linked with other life-threatening ailments (metabolic syndrome, insulin resistance, diabetes, cardiovascular disease, atherosclerosis, obesity, and others) and canprogress to more severe forms, such as NASH (non-alcoholic steatohepatitis), cirrhosis, and HCC (hepatocellular carcinoma). In this review, we summarized and analyzed data about single nucleotide polymorphism sites, identified in genes related to NAFLD development and progression. Additionally, the causative role of mitochondrial mutations and mitophagy malfunctions in NAFLD is discussed. The role of mitochondria-related metabolites of the urea cycle as a new non-invasive NAFLD biomarker is discussed. While mitochondria DNA mutations and SNPs (single nucleotide polymorphisms) canbe used as effective diagnostic markers and target for treatments, age and ethnic specificity should be taken into account.

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Rationalizing the therapeutic potential of apigenin against cancer

Cited by 72 publications

References 531 publications

Control of Oxidative Stress in Cancer Chemoresistance: Spotlight on Nrf2 Role

Control of Oxidative Stress in Cancer Chemoresistance: Spotlight on Nrf2 Role

Flavonoids in Skin Senescence Prevention and Treatment

Mitochondrial Mutations and Genetic Factors Determining NAFLD Risk

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