Abstract | BACKGROUND: METHODS AND RESULT: HCC was induced by N- diethylnitrosamine (DEN) and carbon tetrachloride (CCL4) in Swiss albino mice. Isorhamnetin (100 mg/kg body weight) was given to examine its anti- tumor properties in HCC mice model. Histological analysis and liver function assays were performed to assess changes in liver anatomy. Probable molecular pathways were explored using immunoblot, qPCR, ELISA, and immunohistochemistry techniques. Isorhamnetin inhibited various pro-inflammatory cytokines to suppress cancer-inducing inflammation. Additionally, it regulated Akt and MAPKs to suppress Nrf2 signaling. Isorhamnetin activated PPAR-γ and autophagy while suppressing cell cycle progression in DEN + CCl4-administered mice. Additionally, isorhamnetin regulated various signaling pathways to suppress cell proliferation, metabolism, and epithelial-mesenchymal transition in HCC. CONCLUSION: Regulating diverse cellular signaling pathways makes isorhamnetin a better anti- cancer chemotherapeutic candidate in HCC. Importantly, the anti-TNF-α properties of isorhamnetin could prove it a valuable therapeutic agent in sorafenib-resistant HCC patients. Additionally, anti-TGF-β properties of isorhamnetin could be utilized to reduce the EMT-inducing side effects of doxorubicin.
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Authors | Sayanta Sarkar, Abhishek Kumar Das, Semantee Bhattacharya, Ratan Gachhui, Parames C Sil |
Journal | Medical oncology (Northwood, London, England)
(Med Oncol)
Vol. 40
Issue 7
Pg. 188
(May 24 2023)
ISSN: 1559-131X [Electronic] United States |
PMID | 37226027
(Publication Type: Journal Article)
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Copyright | © 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. |
Chemical References |
- 3-methylquercetin
- Tumor Necrosis Factor Inhibitors
- Quercetin
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Topics |
- Animals
- Mice
- Carcinoma, Hepatocellular
(chemically induced, drug therapy)
- Tumor Necrosis Factor Inhibitors
- Liver Neoplasms
(chemically induced, drug therapy)
- Quercetin
(pharmacology, therapeutic use)
- Drug-Related Side Effects and Adverse Reactions
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