MicroRNA-221 controls CDKN1C/P57 expression in human colorectal carcinoma / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the expression of microRNA-221 (miR-221) and CDKN1C/P57 in colorectal carcinoma (CRC) and adjacent non-cancerous tissues. The effect of miR-221-specific inhibitor on cell proliferation and apoptosis in CRC cells was also assessed.</p><p><b>METHODS</b>The expression of miR-221 was detected by real-time RT-PCR. CDKN1C/P57 mRNA and corresponding protein expression pattern were detected by semi-quantitative RT-PCR and Western-blot. The specific 2'-methoxy-modified RNA oligonucleotide of miR-221(miRNA inhibitor,anti-miR-221) was designed, synthesized and transfected into Caco2 cell by liposome. Finally, the status of CRC cell proliferation and apoptosis were detected by MTT assay and flow cytometry.</p><p><b>RESULTS</b>The expression of miR-221 was significantly up-regulated in CRC tissues as compared to the adjacent non-cancerous tissues(2.041±1.401 vs. 0.806±0.341, P<0.01). There was no significant difference in CDKN1C/P57 mRNA expression between CRC and non-cancerous tissues, whereas CDKN1C/P57 protein markedly decreased in CRC (3.019±1.708 vs. 0.972±0.316, P<0.01). miR-221-specific inhibitor significantly enhanced CDKN1C/P57 protein expression, inhibited proliferation of CRC cells and induced apoptosis of CRC cells(P<0.01).</p><p><b>CONCLUSIONS</b>miR-221 inhibits CDKN1C/P57 expression by post-transcriptional gene silencing to promote CRC development and progression. miR-221-specific inhibitor potentially inhibits the growth of CRC cells. Therefore, it may be a new target for the biologic therapy for CRC.</p>

Effect of miR-221-specific inhibitor on the proliferation and apoptosis of human colorectal carcinoma cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate miRNA-221 expression in human colorectal carcinoma (CRC) cells and the effects of miR-221-specific inhibitor on the proliferation and apoptosis of CRC cells.</p><p><b>METHODS</b>Four human CRC cell lines (HT-29, Lovo, SW-480, and CaCO2) were examined for miRNA-221 expression using real-time Q-PCR. The specific 2,-methoxy-modified RNA oligonucleotides of miR-221 (anti-miR-221) were synthesized and transfected into Caco2 cells via liposome, and the changes in the expression of miR-221 in the cells were detected by real-time Q-PCR. The proliferation and apoptosis of the transfected CRC cells were detected using MTT assay and flow cytometry.</p><p><b>RESULTS</b>The 4 human CRC cells showed significantly upregulated expression of miR-221 compare with HUVECs (P<0.01). The miR-221-specific inhibitor, anti-miR-221, significantly inhibited the expression of miR-221 in Caco2 cells and suppressed the cell proliferation, causing also obvious cell apoptosis (P<0.01).</p><p><b>CONCLUSION</b>The miR-221-specific inhibitor shows potent inhibitory effect on the growth of CRC cells, suggesting its value as a potential anti-tumor candidate for treatment of CRC.</p>

Relationship between survivin expression and paclitaxel drug-resistance and research of reversed drug-resistance by matrine in non-small cell lung cancer / 肿瘤研究与临床

Objective To study the correlation between drug-resistance of paclitaxel and the expres- sion levels of anti-apoptotic protein survivin and the role of matrine reversal resistance of PTX in non-small cell lung cancer.Methods The expressions of survivin in 120 samples of human lung cancer with paclitaxel chemotherapy were detected by immunohistochemical staining.Results The positive expression rate of sur- vivin was 57.5%.In the positive expression of survivin group,chemotherapy combined matrine could improve response rate and survival time(P0.05).Conclusion The survivin expression was related to the response rate of paclitaxel in lung cancer.It might be a valuable new marker to predict the drug-resistance of paclitaxel.In this prospective research,survivin protein,which promoted the apoptosis caused by paclitaxel,may be the target of martine.It could partly reverse the drug re- sistance to paclitaxel.