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Four-color Fluorescence Immunohistochemistry of T-cell Subpopulations in Archival Formalin-fixed, Paraffin-embedded Human Oropharyngeal Squamous Cell Carcinoma Samples
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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
PubMed

Insights

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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