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Radiotherapy modulates expression of EGFR, ERCC1 and p53 in cervical cancer
V H de Almeida1,2, A C de Melo1, D D Meira3
1Divisão de Pesquisa Clínica e Desenvolvimento Tecnológico, Instituto Nacional de Câncer, Rio de Janeiro, RJ, Brasil.
Abstract:
Cervical cancer is a public health problem and the molecular mechanisms underlying radioresistance are still poorly understood. Here, we evaluated the modulation of key molecules involved in cell proliferation, cell cycle and DNA repair in cervical cancer cell lines (CASKI and C33A) and in malignant tissues biopsied from 10 patients before and after radiotherapy. The expression patterns of epidermal growth factor receptor (EGFR), excision repair cross-complementation group 1 (ERCC1) and p53 were evaluated in cancer cell lines by quantitative PCR and western blotting, and in human malignant tissues by immunohistochemistry. The mutation status of TP53 gene was evaluated by direct sequencing. Among cell lines, absent or weak modulations of EGFR, ERCC1 and p53 were observed after exposure to 1.8 Gy. Conversely, increased expressions of p53 (5/10 patients; P=0.0239), ERCC1 (5/10 patients; P=0.0294) and EGFR (4/10 patients; P=0.1773) were observed in malignant tissues after radiotherapy with the same radiation dose. TP53 mutations were found only in one patient. Here we show that a single dose of radiotherapy induced EGFR, ERCC1 and p53 expression in malignant tissues from cervical cancer patients but not in cancer cell lines, highlighting the gap between in vitro and in vivo experimental models. Studies on larger patient cohorts are needed to allow an interpretation that an upregulation of p53, EGFR and ERCC1 may be part of a radioresistance mechanism.
Insights
Radiotherapy can increase expression of p53, ERCC1, and EGFR in cervical cancer tissues, but not cell lines. This suggests a potential radioresistance mechanism in patients, differing from in vitro models.
Area of Science:
- Oncology
- Molecular Biology
- Radiotherapy Research
Background:
- Cervical cancer remains a significant public health concern.
- The molecular basis of radioresistance in cervical cancer is not fully understood.
Purpose of the Study:
- To investigate the modulation of key molecules (EGFR, ERCC1, p53) in response to radiotherapy in cervical cancer.
- To compare the in vitro response of cancer cell lines with the in vivo response of patient tissues.
Main Methods:
- Quantitative PCR and Western blotting for EGFR, ERCC1, and p53 expression in CASKI and C33A cell lines.
- Immunohistochemistry for EGFR, ERCC1, and p53 in patient tissues before and after radiotherapy.
- TP53 gene mutation analysis by direct sequencing.
Main Results:
- Cell lines showed minimal modulation of EGFR, ERCC1, and p53 after 1.8 Gy irradiation.
- Malignant tissues from patients exhibited increased expression of p53 (P=0.0239) and ERCC1 (P=0.0294) post-radiotherapy.
- EGFR expression also increased in patient tissues (P=0.1773), though less significantly. TP53 mutations were rare.
Conclusions:
- A single radiotherapy dose induces EGFR, ERCC1, and p53 expression in patient tissues, unlike cancer cell lines.
- This highlights a discrepancy between in vitro and in vivo models for cervical cancer radioresistance.
- Further studies with larger patient cohorts are needed to confirm if this upregulation contributes to radioresistance.
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