Maternal embryo leucine zipper kinase (MELK) has a higher expression level in a variety of cancers and involved in progression of colorectal cancer. The MELK expression levels in colorectal cancer tissues and cells were detected by RT-qPCR. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and transwell assays were used to examine the effect of the MELK konckdown on the proliferation, migration and invasion of colorectal cancer cells. Western blot analysis was used to detect the protein level of MELK and the downstream signaling pathways related proteins. Our findings indicated that MELK expression in colorectal cancer tissues was significantly higher than that in para-carcinoma tissues. Knockdown of MELK with shRNA had strong inhibition effects on the proliferation, migration and invasion of colorectal cancer cells. MELK knockdown could also decrease the phosphorylation level of AKT through FAK/Src pathway. Our results indicated downregulation of MELK retarded the progression of CRC by inhibition of the phosphorylation level of AKT through inactivating FAK/Src pathways. Therefore, MELK has the potential to be explored as a new therapeutic target and knockdown can be used as a potential treatment strategy for colorectal cancer.

母体胚胎亮氨酸拉链激酶（MELK）在多种癌症中具有较高的表达水平，并参与大肠癌的进展。通过RT-qPCR检测大肠癌组织和细胞中的MELK表达水平。使用MTT（3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑溴化物）和transwell分析法检测MELK konckdown对结直肠癌细胞增殖，迁移和侵袭的影响。Western blot分析用于检测MELK的蛋白水平和下游信号通路相关蛋白。我们的发现表明，MELK在大肠癌组织中的表达明显高于癌旁组织。用shRNA敲低MELK对结直肠癌细胞的增殖，迁移和侵袭具有强烈的抑制作用。MELK组合还可通过FAK / Src途径降低AKT的磷酸化水平。我们的结果表明，MELK的下调通过抑制FAK / Src途径抑制AKT的磷酸化水平，从而阻止了CRC的发展。因此，MELK有潜力被探索为新的治疗靶标，而基因敲低可作为结直肠癌的潜在治疗策略。