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Triptolide inhibits esophageal squamous cell carcinoma progression by regulating the circNOX4/miR-153-3p/SATB1
Hanping Liang1, Weibi Che1, Fengyuan Peng1
1Department of thoracic surgery, Gaozhou people's Hospital, Gaozhou, China.
Background:
To explore the role and mechanism of triptolide in regulating esophageal squamous cell carcinoma (ESCC) progression by mediating the circular RNA (circRNA)-related pathway.
Methods:
The expression levels of circNOX4, miR-153-3p and special AT-rich sequence binding protein-1 (SATB1) were measured by qRT-PCR. Cell proliferation was confirmed by cell counting kit-8 assay and colony formation assay. Flow cytometry was employed to measure cell apoptosis and cell cycle process. Moreover, cell migration and invasion were detected using transwell assay. The protein levels of epithelial-mesenchymal transformation markers and SATB1 were determined by western blot analysis. Furthermore, dual-luciferase reporter assay and RIP assay were performed to confirm the interaction between miR-153-3p and circNOX4 or SATB1. Xenograft tumor models were built to verify the effects of triptolide and circNOX4 on ESCC tumor growth.
Results:
CircNOX4 was highly expressed in ESCC tissues and cells, and its expression could be reduced by triptolide. Triptolide could inhibit ESCC proliferation, cell cycle process, migration, invasion, EMT process, and promote apoptosis, while these effects were reversed by circNOX4 overexpression. MiR-153-3p could be sponged by circNOX4, and the promotion effect of circNOX4 on the progression of triptolide-treated ESCC cells was abolished by miR-153-3p overexpression. SATB1 was a target of miR-153-3p. Also, SATB1 knockdown reversed the enhancing effect of miR-153-3p inhibitor on the progression of triptolide-treated ESCC cells. Triptolide reduced ESCC tumor growth by regulating the circNOX4/miR-153-3p/SATB1 axis.
Conclusion:
Triptolide could hinder ESCC progression, which was mainly achieved by regulating the circNOX4/miR-153-3p/SATB1 axis.
Insights
Triptolide inhibits esophageal squamous cell carcinoma (ESCC) progression by regulating the circNOX4/miR-153-3p/SATB1 pathway. This study reveals a novel mechanism for triptolide
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Esophageal squamous cell carcinoma (ESCC) is a prevalent cancer with complex progression mechanisms.
- Circular RNAs (circRNAs) are increasingly recognized as key regulators in various cancers, including ESCC.
- Triptolide, a natural compound, shows potential in cancer therapy, but its precise role in ESCC requires elucidation.
Purpose of the Study:
- To investigate the role of triptolide in ESCC progression.
- To elucidate the underlying molecular mechanism involving circular RNA pathways.
- To identify key molecular players in triptolide-mediated regulation of ESCC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) for gene expression analysis.
- Cell proliferation, apoptosis, cell cycle, migration, and invasion assays.
- Western blot for protein level determination.
- Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays for interaction confirmation.
- Xenograft tumor models for in vivo validation.
Main Results:
- CircNOX4 expression is elevated in ESCC and reduced by triptolide.
- Triptolide inhibits ESCC proliferation, migration, invasion, and EMT, while promoting apoptosis.
- CircNOX4 overexpression reverses triptolide's inhibitory effects.
- Triptolide acts via the circNOX4/miR-153-3p/SATB1 axis to regulate ESCC progression.
Conclusions:
- Triptolide effectively hinders ESCC progression.
- The circNOX4/miR-153-3p/SATB1 axis is a critical pathway mediating triptolide's anti-cancer effects in ESCC.
- This study provides a molecular basis for triptolide as a potential therapeutic agent for ESCC.
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