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Role of Xeroderma Pigmentosum Group D in Cell Cycle and Apoptosis in Cutaneous Squamous Cell Carcinoma A431 Cells
Ou-Gen Liu1, Xiao-Yan Xiong2, Chun-Ming Li1
1Department of Dermatology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China (mainland).
Abstract:
BACKGROUND Cutaneous squamous cell carcinoma (cSCC) is the second most widespread cancer in humans and its incidence is rising. Novel therapy with better efficacy is needed for clinical treatment of cSCC. Many studies have shown the importance of DNA repair pathways during the development of cancer. A key nucleotide excision repair (NER) protein, xeroderma pigmentosum group D (XPD), is responsible for the excision of a large variety of bulky DNA lesions. MATERIAL AND METHODS To explore the role of XPD in A431 cells, we overexpressed XPD in A431 cells and performed MTT assay, flow cytometry, and Western blot analysis to examine cell proliferation, cell apoptosis, and genes expression. RESULTS We found that the overexpression of XPD suppressed cell viability, induced cell cycle arrest at G1 phase, and promoted cell apoptosis. Additionally, XPD blocked the expression of c-myc, cdc25A, and cdk2, and improved the levels of HIPK2 and p53. CONCLUSIONS These results provide new evidence to reveal the role of XPD in cSCC A431 cells and suggest that XPD may serve as an anti-oncogene during cSCC development.
Insights
Xeroderma pigmentosum group D (XPD) protein overexpression suppressed cutaneous squamous cell carcinoma (cSCC) cell viability and promoted apoptosis. XPD acts as an anti-oncogene in cSCC development.
Area of Science:
- Molecular Biology
- Oncology
- DNA Repair Mechanisms
Background:
- Cutaneous squamous cell carcinoma (cSCC) is a prevalent and increasing cancer requiring novel therapies.
- DNA repair pathways, particularly nucleotide excision repair (NER), are crucial in cancer development.
- The xeroderma pigmentosum group D (XPD) protein is a key NER factor involved in repairing bulky DNA lesions.
Purpose of the Study:
- To investigate the functional role of the XPD protein in A431 cells, a model for cSCC.
- To determine the impact of XPD overexpression on cSCC cell proliferation, apoptosis, and gene expression.
Main Methods:
- Overexpression of XPD in A431 cells.
- MTT assay to assess cell viability.
- Flow cytometry for cell cycle analysis and apoptosis detection.
- Western blot analysis to evaluate gene and protein expression levels.
Main Results:
- XPD overexpression significantly suppressed cell viability in A431 cells.
- Overexpression of XPD induced G1 phase cell cycle arrest and promoted apoptosis.
- XPD modulated the expression of key cell cycle regulators, downregulating c-myc, cdc25A, and cdk2, while upregulating HIPK2 and p53.
Conclusions:
- XPD plays a significant role in regulating cSCC cell behavior.
- The findings suggest XPD functions as an anti-oncogene in the context of cSCC.
- XPD modulation presents a potential therapeutic avenue for cSCC treatment.
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