Abstract
Background Hepatocellular carcinoma (HCC) is a common malignant cancer worldwide. CXCL5 has a role in inhibiting cell viability and metastasis in many tumors. In the present study, we investigated the role of CXCL5 in HCC and explored the underlying mechanism. Material and Methods. RT-qPCR and western blot were performed to evaluate the mRNA and protein levels of CXCL5. CCK-8 and transwell assay were applied to measure the proliferative and invasive abilities. Meanwhile, the Kaplan–Meier method was used to assess the survival of HCC patients. Results CXCL5 was upregulated in HCC tissues, which predicted a shorter overall survival in HCC. CXCL5 was a target gene of miR-577, and its expression was mediated by miR-577 in HCC. Knockdown of CXCL5 suppressed HuH-7 cell proliferation, invasion, and EMT and inhibited the NF-κB signaling pathway in cells. Moreover, knockdown of CXCL5 inhibited the xenograft growth of HuH-7 cells. Conclusion Overexpression of CXCL5 predicts poor prognosis in HCC patients. Knockdown of CXCL5 inhibits cell proliferation and invasion through the NF-κB signaling pathway in HCC. The newly identified role of the CXCL5/miR-577/NF-κB axis provides novel insights into the targeted therapy of HCC.
Highlights
Hepatocellular carcinoma (HCC) is a major cause of cancer death, especially in Africa and Asia [1, 2]
TargetScan was used to perform the prediction of target genes of miR-577, and we discovered that CXCL5 was one of the potential target genes. e binding sequence of UUUAUCU and AAAUAGA was mutated to confirm that miR-577 could not bind to the 3-UTR of CXCL5 mRNA in HCC cells. e wild type and the mutational 3’-UTR of CXCL5 were inserted into the dual-luciferase reporter vectors, which were named WT or MUT. e Lipofectamine 2000 Reagent (Invitrogen, USA) was used to cotransfect miR-577 mimic and WT or MUT vector into HuH-7 cells
Upregulation of CXCL5 Predicts Poor Prognosis of HCC Patients. e expression of CXCL5 in HCC tissues and normal tissues was detected in the GEPIA database; the expression of CXCL5 has no significance in HCC tissues than in normal tissues (Figure 1(a)), we observed that the overexpression of CXCL5 in HCC patients predicted poor prognosis (P < 0.05) (Figure 1(b))
Summary
Hepatocellular carcinoma (HCC) is a major cause of cancer death, especially in Africa and Asia [1, 2]. CXCL5 was thought to play roles in cell proliferation, migration, and invasion of cancer [6, 7]. CXCL5 was involved in the interaction between cholangiocarcinoma cells and cancer-associated fibroblasts and inhibition of tumor-stromal interactions [7]. Few studies have elucidated the roles of CXCL5 in HCC. CXCL5 has a role in inhibiting cell viability and metastasis in many tumors. We investigated the role of CXCL5 in HCC and explored the underlying mechanism. Knockdown of CXCL5 suppressed HuH-7 cell proliferation, invasion, and EMT and inhibited the NF-κB signaling pathway in cells. Knockdown of CXCL5 inhibited the xenograft growth of HuH-7 cells. Knockdown of CXCL5 inhibits cell proliferation and invasion through the NF-κB signaling pathway in HCC. Knockdown of CXCL5 inhibits cell proliferation and invasion through the NF-κB signaling pathway in HCC. e newly identified role of the CXCL5/miR-577/NF-κB axis provides novel insights into the targeted therapy of HCC
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