Curcumin enhances ATG3-dependent autophagy and inhibits metastasis in cervical carcinoma

Cervical carcinoma poses a significant health threat, with traditional treatments proving inadequate in advanced stages. Curcumin, a bioactive compound derived from turmeric, exhibits notable anti-inflammatory, antioxidant, and antineoplastic properties, potentially modulating autophagy, and metastasis in cancer cells. This study examines curcumin's impact on autophagy and metastasis in cervical carcinoma, focusing on its interaction with autophagy-related gene 3 (ATG3). SiHa and HeLa cervical carcinoma cell lines were treated with curcumin, ATG3 knockdown (shATG3), and their combination. Cell migration was evaluated via wound healing assays, while cell proliferation was evaluated with CCK-8 assays. LC3 expression was assessed using immunofluorescence and western blotting. Molecular docking simulations identified curcumin's binding interactions with key proteins. Curcumin and shATG3 significantly inhibited both cell migration and proliferation, with a synergistic effect observed when combined. LC3 expression was enhanced, indicating increased autophagy. Docking studies revealed curcumin's potential binding to MMP2, MMP9, TGF-β, ATG3, LC3, and p62, suggesting modulation of these pathways. The combination of curcumin and ATG3 knockdown significantly inhibited cervical carcinoma cell migration and proliferation, while also enhancing autophagy, supporting the potential of curcumin as a therapeutic agent for cervical carcinoma. Further clinical research is needed to validate these findings.

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Publication Details

Journal
Cell Division
Published
2024-11-28
DOI
https://doi.org/10.1186/s13008-024-00138-6
Citations
7
Primary Topic
Autophagy in Disease and Therapy
Type
article
Field-Weighted Citation Impact
2.71
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article

Curcumin enhances ATG3-dependent autophagy and inhibits metastasis in cervical carcinoma

Fei Zheng, Danli Ma, Jingjing Lu, Huimin Yu et al.
7 citations
Cell Division
Autophagy in Disease and Therapy
2.71
article

Curcumin enhances ATG3-dependent autophagy and inhibits metastasis in cervical carcinoma

Fei Zheng, Danli Ma, Jingjing Lu, Huimin Yu, Chuhan Wang, Yanhong Fu
article en
7 citations

Abstract

Cervical carcinoma poses a significant health threat, with traditional treatments proving inadequate in advanced stages. Curcumin, a bioactive compound derived from turmeric, exhibits notable anti-inflammatory, antioxidant, and antineoplastic properties, potentially modulating autophagy, and metastasis in cancer cells. This study examines curcumin's impact on autophagy and metastasis in cervical carcinoma, focusing on its interaction with autophagy-related gene 3 (ATG3). SiHa and HeLa cervical carcinoma cell lines were treated with curcumin, ATG3 knockdown (shATG3), and their combination. Cell migration was evaluated via wound healing assays, while cell proliferation was evaluated with CCK-8 assays. LC3 expression was assessed using immunofluorescence and western blotting. Molecular docking simulations identified curcumin's binding interactions with key proteins. Curcumin and shATG3 significantly inhibited both cell migration and proliferation, with a synergistic effect observed when combined. LC3 expression was enhanced, indicating increased autophagy. Docking studies revealed curcumin's potential binding to MMP2, MMP9, TGF-β, ATG3, LC3, and p62, suggesting modulation of these pathways. The combination of curcumin and ATG3 knockdown significantly inhibited cervical carcinoma cell migration and proliferation, while also enhancing autophagy, supporting the potential of curcumin as a therapeutic agent for cervical carcinoma. Further clinical research is needed to validate these findings.

Cell DivisionVol. 19(1)
Ningbo No. 2 Hospital (CN), Ningbo University Affiliated Hospital (CN), University of Chinese Academy of Sciences (CN)
Zero hunger
Openalex Percentile: Top 9%
Autophagy in Disease and Therapy
2.71
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Curcumin enhances ATG3-dependent autophagy and inhibits metastasis in cervical carcinoma — Fei Zheng, Danli Ma, et al. · Cell Division (2024) | TGRS Research Map | TGRS