Effects Of RNA Helicase DHX32on Cell Proliferation,Migration And Invasion In Human Colorectal Cancer Cell Lines

RNA helicases are important enzymes involved in RNA metabolism, which could utilize the energy derived from NTP to participate in RNA processing, including pre-mRNA splicing, translation initiation, RNA transport, ribosome generation, RNA degradation and post-transcriptional processing in mitochondria and cell nucleus. Based on the different sequence at the motifs of the helicase domain, RNA helicases are divided into two families, DHX and DDX. Previous studies have shown that some RNA helicases are dysregulated in various of cancer. And some RNA helicases are involved in cell differentiation, cell cycle, apoptosis, oncogene expression and drug resistance gene expression. DHX32is a novel putative RNA helicase, which belongs to the DHX family of RNA helicases. The expression of DHX32is down-regulated in acute lymphoblastic leukemia. Our previous study firstly reported that the expression level of DHX32in colorectal cancer tissues was significantly overexpressed compared to its adjacent normal tissues by real time RT-PCR and was associated with cancer location, differentiation grade, cancer nodal status, lymph gland metastasis and Dukes’stage. However, the exact biological function and molecular mechanism of DHX32are unknown.In this study, we also detected the expression of DHX32was up-regulated in the human colorectal cancer cell lines. In order to explored the role of DHX32in the development of colorectal cancer, DHX32-knockdown and DHX32-overexpressing stable cell lines were established. Our results showed that knockdown of DHX32inhibited cell proliferation by CCK-8, BrdU and Colony formation assays in SW480and HCT-8cell lines. Transwell assays were performed to study the role of DHX32in SW480and HCT-8cell migration and invasion. Our results showed that the migration and invasion capabilities of SW480and HCT-8cells were reduced after DHX32knockdown compared with their control cells. We also carried out wound healing assays in SW480cell line to study cell migration. As expected, the rate of migration was gradually reduced after DHX32knockdown. In order to further verify the above function of DHX32, we successfully established stable DHX32-overexpressing SW480cell line. Correspondingly, our results show that overexpression of DHX32promoted SW480cell proliferation, migration and invasion. Moreover, our data showed that the activation of Akt was reduced in the DHX32knockdown cells. Previous studies have shown that the Akt signaling pathway is involved in cell proliferation, migration, invasion and apoptosis in the colorectal cancer. Thus, our results suggest that DHX32may play an important role in the development of colorectal cancer by the Akt signaling pathway. However, the identification of the exact molecular mechanism involved requires further investigation. Taken together, the results of our study suggest DHX32may be a new oncogene.