Colorectal cancer (CRC) brings more than 600 000 deaths every year around the globe, making itself the third most frequently occurred carcinoma. The great progress human achieved in diagnosis and treatment of various cancers has failed to reverse this trend. Fortunately, growing evidence has implied the relationship between lncRNAs and cancer progression. Long noncoding RNA (lncRNA) PRKCQ‐AS1 was heightened in CRC cells and tissues and related with dismal prognosis of CRC patients. Knockdown of PRKCQ‐AS1 would induce a decrease in proliferative and migrating ability of CRC cells. Also, PRKCQ‐AS1 enriched in cytoplasm of CRC cells and negatively regulated miR‐1287‐5p level. More important, PRKCQ‐AS1 could bind to argonaute 2 and function in the RNA‐induced silencing complex with miR‐1287‐5p. Therefore, PRKCQ‐AS1 was a competing endogenous RNA for miR‐1287‐5p. Subsequently, it was validated that miR‐1287‐5p could suppress the proliferative and migratory functions in CRC. Furthermore, PRKCQ‐AS1 could upregulate the mRNA and protein level of YBX1 targeted by miR‐1287‐5p. And YBX1 expression was elevated in CRC cells and tissues. Rescue assays in vitro and in vivo showed that overexpression of YBX1 could partly offset the effect of CRC progression induced by knocking down PRKCQ‐AS1, demonstrating PRKCQ‐AS1 mediating CRC progression via miR‐1287‐5p/YBX1 pathway.

中文翻译：

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长非编码RNA PRKCQ-AS1通过调节miR-1287-5p / YBX1轴促进CRC细胞增殖和迁移。

结直肠癌（CRC）每年在全球范围内造成60万多人死亡，成为第三大最常见的癌症。人类在各种癌症的诊断和治疗中取得的巨大进步未能扭转这一趋势。幸运的是，越来越多的证据暗示了lncRNA与癌症进展之间的关系。CRC细胞和组织中的长非编码RNA（lncRNA）PRKCQ-AS1升高，并且与CRC患者的预后不良有关。抑制PRKCQ-AS1会导致CRC细胞的增殖和迁移能力降低。而且，PRKCQ-AS1富含CRC细胞的细胞质，并且对miR-1287-5p的水平产生负调控。更重要的是，PRKCQ-AS1可以与argonaute 2结合，并在miR-1287-5p的RNA诱导的沉默复合物中起作用。因此，PRKCQ-AS1是miR-1287-5p的竞争性内源RNA。随后，证实了miR-1287-5p可以抑制CRC中的增殖和迁移功能。此外，PRKCQ-AS1可能上调miR-1287-5p靶向的YBX1的mRNA和蛋白水平。YBX1表达在CRC细胞和组织中升高。体内和体外的拯救试验表明，YBX1的过表达可以部分抵消通过敲低PRKCQ-AS1诱导的CRC进展的作用，这表明PRKCQ-AS1通过miR-1287-5p / YBX1途径介导CRC的进展。