Colorectal cancer (CRC) is the third leading cause of cancer-related death around the world. In this study, we investigated the roles of LncRNA RP11-462C24.1 in CRC. The expressions of RP11-462C24.1 in CRC tissues and cells were measured. Then, the effects of RP11-462C24.1 on CRC proliferation, cell cycle, apoptosis, and invasion were evaluated both in vivo and in vitro; Last, the underlying mechanisms of concerning the signaling pathway regulated by RP11-462C24.1 was determined. From the results, we found that RP11-462C24.1 was significantly decreased in CRC tumor tissues and the CRC cell lines, which were most significant in SW480 and HT-29 cell lines; moreover, transient overexpression of RP11-462C24.1 suppressed the growth and migration while promoted apoptosis of SW480 and HT-29 cells, while knockdown of RP11-462C24.1 has shown the opposite effects; RP11-462C24.1 may also inhibit the growth of CRC tumors in xenograft mice models; additionally, 70 kD heat shock proteins (HSP70) has been identified as one of the most significantly deferentially expressed genes by RNA-seq, and we further confirmed that RP11-462C24.1 may affect the growth and metathesis of CRC cells via regulating HSP70 and PI3K/AKT signaling pathway. In summary, these results indicated that RP11-462C24 may function as a tumor suppressor in the development of CRC.

大肠癌（CRC）是世界范围内与癌症相关的死亡的第三大主要原因。在这项研究中，我们调查了LncRNA RP11-462C24.1在CRC中的作用。检测RP11-462C24.1在CRC组织和细胞中的表达。然后，在体内和体外评估了RP11-462C24.1对CRC增殖，细胞周期，细胞凋亡和侵袭的影响；最后，确定了与RP11-462C24.1调控的信号通路有关的潜在机制。从结果中我们发现，RP11-462C24.1在CRC肿瘤组织和CRC细胞系中显着降低，而在SW480和HT-29细胞系中最为显着。此外，瞬时过表达RP11-462C24.1抑制了生长和迁移，同时促进了SW480和HT-29细胞的凋亡，同时敲低了RP11-462C24。1显示了相反的效果；RP11-462C24.1还可能抑制异种移植小鼠模型中CRC肿瘤的生长。此外，RNA序列已将70 kD热激蛋白（HSP70）鉴定为最显着差异表达的基因之一，我们进一步证实RP11-462C24.1可能通过调节HSP70和HSP70而影响CRC细胞的生长和复分解。 PI3K / AKT信号通路。总之，这些结果表明，RP11-462C24可能在CRC的发生中起着抑癌作用。1可能通过调节HSP70和PI3K / AKT信号通路影响CRC细胞的生长和复分解。总之，这些结果表明，RP11-462C24可能在CRC的发生中起着抑癌作用。1可能通过调节HSP70和PI3K / AKT信号通路影响CRC细胞的生长和复分解。总之，这些结果表明，RP11-462C24可能在CRC的发生中起着抑癌作用。