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Ethyl β-carboline-3-carboxylate targets PRDX5/c-Jun axis for novel therapeutic strategy against cervical cancer
Wan-Qiu Xiao1,2, Dong-Hun Lee3, Hakjin Kim4,5
1Stem Cell and Regenerative Biology Laboratory, College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University, Daqing, 163319, Heilongjiang, China.
Objective:
Cervical cancer remains a significant global health challenge, with conventional therapies often proving inadequate due to treatment resistance and adverse effects. This study investigates the therapeutic potential of ethyl β-carboline-3-carboxylate (β-CCE) in cervical cancer and elucidates its molecular mechanism through peroxiredoxin 5 (PRDX5) modulation.
Methods:
Western blot assay were performed to asses the expression of protein levels; The cellular and mitochondrial ROS and mithochondrial membrane potential were observed with fluorescence microscopy; Bioinformatics analysis were used to check the expression levels of PRDX5 and JUN family proteins and prognosis analysis in cervical cancer; Transcriptome analysis was performed to analyse the gene expression levels between mock and shPRDX 5 cells; Serum TNF-α and INF-γ levels were detected by ELISA kits; HE staining analysis were performed to check the organ histopathological changes in mice.
Results:
This effect is mediated through activation of the MAPK signaling cascade, particularly involving P38, ERK, and JNK pathways. Notably, β-CCE treatment promotes apoptosis through c-Jun up-regulation, with PRDX5 knockdown enhancing this effect while its overexpression provides protection. In xenograft mouse models, β-CCE treatment significantly suppressed tumor growth and enhanced anti-tumor immune responses, particularly in PRDX5-depleted conditions, without apparent systemic toxicity. The therapeutic efficacy was evidenced by reduced tumor volume (65.3%) and elevated levels of immunological markers (IFN-γ and TNF-α).
Conclusion:
These findings establish PRDX5 as a critical therapeutic target in cervical cancer and demonstrate β-CCE potential as a novel treatment strategy through its dual mechanism of direct tumor cell apoptosis and immune response modulation. Our study provides compelling evidence for the development of PRDX5-targeted therapies using β-CCE as a promising therapeutic agent for cervical cancer treatment.
Insights
Ethyl β-carboline-3-carboxylate (β-CCE) shows promise for cervical cancer by inducing apoptosis and boosting immunity. Targeting peroxiredoxin 5 (PRDX5) enhances β-CCE
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Cervical cancer poses a global health challenge with limited effective treatments.
- Conventional therapies face issues with resistance and side effects.
- Peroxiredoxin 5 (PRDX5) is implicated in cancer progression.
Purpose of the Study:
- To investigate the therapeutic potential of ethyl β-carboline-3-carboxylate (β-CCE) in cervical cancer.
- To elucidate the molecular mechanism of β-CCE involving PRDX5 modulation.
- To assess the combined effects on tumor cells and anti-tumor immunity.
Main Methods:
- Western blot for protein expression.
- Fluorescence microscopy for ROS and mitochondrial membrane potential.
- Bioinformatics for PRDX5 and JUN family gene analysis.
- Transcriptome analysis.
- ELISA for serum cytokines.
- HE staining for histopathology.
Main Results:
- β-CCE activates MAPK signaling (P38, ERK, JNK) and up-regulates c-Jun, promoting apoptosis.
- PRDX5 knockdown enhances β-CCE-induced apoptosis, while overexpression confers protection.
- β-CCE suppressed tumor growth by 65.3% in xenografts, enhancing anti-tumor immunity (IFN-γ, TNF-α).
- No significant systemic toxicity was observed.
Conclusions:
- PRDX5 is a critical therapeutic target in cervical cancer.
- β-CCE demonstrates dual therapeutic potential via direct apoptosis and immune modulation.
- β-CCE represents a promising novel therapeutic agent for cervical cancer, particularly when targeting PRDX5.
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