Table 3.
Molecular mechanisms underlying the effects of ERCC1 in cervical cancer.
| Study/Reference | Treatments for cervical cancer | Experimental model | Main findings |
|---|---|---|---|
| Britten et al. (36) | Cisplatin resistance | Cervical carcinoma lines (HT137, HT155, HT172, HT180 and HT212) | There was a significant correlation between ERCC1 mRNA expression and cisplatin resistance in all cervical carcinoma lines (all P< 0.05), but such an association was not significant in ERCC1 protein expression (all P>0.05). It might be possible to identify cervical tumors likely to be resistant to cisplatin by examining pre-treatment ERCC1 mRNA levels. |
| Torii et al. (21) | Cisplatin and 5-FU | Uterine cervical adenocarcinoma cells (HCA-1 and TCO-2) | There was an association between ERCC1 expression and sensitivity to cisplatin in cervical adenocarcinoma cells. A cisplatin-resistant cell line HCA-1R showed a dramatically higher level of ERCC1 mRNA expression than the native cells. Co-administration of cisplatin and 5-FU showed the synergistic or additive effects via inhibiting of ERCC1 expression. |
| Almeida et al. (37) | Radiotherapy | CASKI and C33A cells | Absent or weak modulations of ERCC1 was detected after exposure to 1.8 Gy of radiotherapy in cell lines, which might be associated with the inhibition of the regulatory axis p53-EGFR-ERCC1. Increased expressions of ERCC1 (5/10 patients; P=0.0294) was found in malignant tissues after radiotherapy with the same radiation dose. This study showed that upregulation of ERCC1 may be part of a radioresistance mechanism in cervical cancer. |
ERCC1, excision repair cross-complementation group1; EGFR, epidermal growth factor receptor.