miR‐144 suppresses cell proliferation and migration in colorectal cancer by targeting NRAS

The survival rate of patients with metastatic colorectal cancer (mCRC) has significantly improved with applications of molecularly targeted drugs, such as bevacizumab, and led to a substantial improvement in the overall survival rate. These drugs are capable of specifically targeting the inherent abnormal pathways in cancer cells, which are potentially less toxic than traditional nonselective chemotherapeutics. In this review, the recent clinical information about molecularly targeted therapy for mCRC is summarized, with specific focus on several of the US Food and Drug Administration-approved molecularly targeted drugs for the treatment of mCRC in the clinic. Progression-free and overall survival in patients with mCRC was improved greatly by the addition of bevacizumab and/or cetuximab to standard chemotherapy, in either first- or second-line treatment. Aflibercept has been used in combination with folinic acid (leucovorin)–fluorouracil–irinotecan (FOLFIRI) chemotherapy in mCRC patients and among patients with mCRC with wild-type KRAS, the outcomes were significantly improved by panitumumab in combination with folinic acid (leucovorin)–fluorouracil–oxaliplatin (FOLFOX) or FOLFIRI. Because of the new preliminary studies, it has been recommended that regorafenib be used with FOLFOX or FOLFIRI as first- or second-line treatment of mCRC chemotherapy. In summary, an era of new opportunities has been opened for treatment of mCRC and/or other malignancies, resulting from the discovery of new selective targeting drugs.

Previous research indicated that miR-144-3p was associated with the regulation of the carcinogenic processes, but the role of miR-144-3p in glioblastoma (GBM) remains unclear. In this study, we aimed to analyze the role of miR-144-3p in GBM.

Previous research reported that miR-144-3p functions as tumor suppressor in several tumors, including glioblastoma and hepatocelluar carcinoma, but the role of miR-144-3p in prostate cancer (PCa) remains unclear. In this study, we aimed to analyze the role of miR-144-3p in PCa. By RT-qPCR, we found that expression of miR-144-3p was markedly down-regulated in PCa tissues and cell lines compared with that in paired adjacent normal tissues and normal cell lines. Moreover, miR-144-3p overexpression in PC-3 and DU145 cells by transfection with miR-144-3p mimics significantly inhibited cell proliferation and in vitro by MTT, colony formation assays and suppressed tumor growth in vivo by nude mice model. Flow cytometry analysis further demonstrated that forced expression of miR-144-3p induced cell cycle G1/S phase arrest and apoptosis. Moreover, centrosomal protein of 55 (CEP55) was confirmed as a direct target of miR-144-3p by bioinformatics analysis and luciferase reporter assays. Overexpression of miR-144-3p decreased the CEP5 mRNA and protein levels in PC-3 and DU145 cells. Using Oncomine database analysis, we further found the expression of CEP55 was significantly upregulated in PCa tissues. In addition, knockdown of CEP55 elicited similar effects with miR-144-3p overexpression in PCa cells. Taken together, our results demonstrate that miR-144-3p functions as a tumor suppressor in PCa by downregulating CEP55, supporting the targeting miR-144-3p might be a potentially effective therapeutic approach for PCa.