PTPRJ is downregulated in cervical squamous cell carcinoma.
Anirban Roychowdhury1, Mukta Basu, Debolina Pal
1Department of Oncogene Regulation, Chittaranjan National Cancer Institute, Kolkata 700 026, India. ckpanda.cnci@gmail.com.
Journal of Genetics
|July 6, 2022
Summary
Protein tyrosine phosphatase receptor J (PTPRJ) is downregulated in cervical cancer due to gene deletion and promoter methylation. Enhanced PTPRJ expression improved cisplatin chemotherapy response in cell lines.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cervical squamous cell carcinoma (CSCC) is a significant cause of mortality in Indian women.
- The tumor suppressor gene Protein tyrosine phosphatase receptor J (PTPRJ/DEP1) has not been molecularly characterized in CSCC.
- Understanding PTPRJ's role could reveal new therapeutic targets for cervical cancer.
Purpose of the Study:
- To investigate the molecular status and expression of PTPRJ in Indian CSCC patients.
- To determine the association between PTPRJ alterations and clinical prognosis.
- To explore the functional role of PTPRJ in response to cisplatin chemotherapy.
Main Methods:
- Transcriptional analysis and immunohistochemistry were performed on CSCC samples (n=31).
- Copy number variation and promoter methylation analysis of PTPRJ were conducted in a larger cohort (n=155).
- Statistical analysis assessed the correlation between PTPRJ status and patient prognosis (n=76).
- Functional assays were performed in the SiHa cell line to evaluate PTPRJ's effect on cisplatin sensitivity.
Main Results:
- Frequent downregulation of PTPRJ mRNA and protein expression was observed in CSCC samples.
- Genetic alterations including deletion (14.8%) and promoter methylation (33.5%) were identified as mechanisms for PTPRJ downregulation.
- No statistically significant association was found between PTPRJ molecular status and patient prognosis.
- Increased PTPRJ expression enhanced the efficacy of cisplatin chemotherapy in the SiHa cell line.
Conclusions:
- PTPRJ is frequently downregulated in cervical cancer through genetic and epigenetic mechanisms.
- While not directly linked to prognosis in this cohort, PTPRJ modulation may influence chemotherapy response.
- Further research is warranted to elucidate the precise role of PTPRJ in cervical cancer pathogenesis and its therapeutic potential.
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