KIAA1522 promotes the progression of hepatocellular carcinoma via the activation of the Wnt/β-catenin signaling pathway

Abstract

Purpose: KIAA1522 was previously identified to play a crucial role in cancer development and progression. However, its functions and underlying mechanisms in hepatocellular carcinoma (HCC) remain elusive. Materials and Methods: To elucidate the role of KIAA1522 in HCC, its expression was assessed using The Cancer Genome Atlas and GEPIA databases. Next, these results were validated by quantitative reverse transcription-polymerase chain reaction, Western blotting, and immunohistochemistry of HCC tissues and cell lines. Flow cytometry, CCK-8, EDU, colony formation, Transwell invasion, and wound healing assays were performed to explore the function of KIAA1522 in HCC in vivo and in vitro. Finally, gene set enrichment analysis was used to identify the pathways involved. Results: Our results demonstrated that KIAA1522 was highly expressed in HCC tissues and cell lines. Furthermore, KIAA1522 overexpression was associated with unfavorable clinicopathological characteristics. Survival analyses revealed that KIAA1522 overexpression predicted lower recurrence-free and overall survival rates in patients with HCC. Functional studies suggested that KIAA1522 facilitated HCC proliferation, migration, and invasion both in vitro and in vivo. Moreover, KIAA1522 up-regulated the Wnt/β-catenin signaling pathway, as confirmed by TOP-flash/FOP-flash luciferase reporter assays and Western blotting. Conclusion: In conclusion, we highlighted the oncogenic role of KIAA1522 in HCC and determined its potential as a therapeutic target for HCC.