Correlation study between long non-coding RNA MALAT1 and radiotherapy efficiency on cervical carcinoma and generation of radiotherapy resistant model of cancer.

This study aims to construct a radiotherapy model on cervical carcinoma cells and to illustrate the correlation between long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcription 1 (MALAT1) and radiotherapy efficiency.A total of 60 cervical carcinoma patients were recruited, and quantitative PCR (qPCR) was employed to detect MALAT1 expression. A dosage-time curve helped to construct radiotherapy resistant model on cervical carcinoma cell CaSki. Lentivirus transfection was used to silence MALAT1 expression, followed by quantification of clonal formation, apoptosis, and cycle after combined radiotherapy. Bioinformatics tool (miRcode.org), reporter gene and qPCR were used to predict microRNA (miR) interaction with MALAT1. By combining MALAT1 silencing, miR over-expression and radiotherapy, effects on the cervical cancer cell clonal formation, apoptosis, and cycle were observed.Comparing to radiotherapy sensitive tissues, the MALAT1 level was significantly elevated in radiotherapy resistant tissues (0.52 ± 0.18 vs. 1.29 ± 0.34, p<0.05). MALAT1 expression in cervical carcinoma cell CaSki was further elevated with elongated radiation time and dosage (p<0.05). Comparing to controlled cells, MALAT1 silencing decreased viable cell percentage, enhanced apoptosis, increased G1 phase cells, and decreased G2/M ratio. Bioinformatics, reporter gene, and qPCR showed that MALAT1 exerted its roles in cervical carcinoma cells via interacting with miR-143, both of which had a significant correlation (r=0.77, p<0.01). MALAT1 silencing combined with miR-143 plus radiotherapy decreased viable cell percentage, enhanced apoptosis, increased G1 phase ratio, and decreased S or G2/M cells.In cervical carcinoma, MALAT1 can interact with miR-143 to modulate tumor cell survival, apoptosis and cell cycle, thus affecting radiotherapy efficiency.