Phosphatidylinositol 4-phosphate adaptor protein 2 accelerates the proliferation and invasion of hepatocellular carcinom
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Phosphatidylinositol 4-phosphate adaptor protein 2 accelerates the proliferation and invasion of hepatocellular carcinoma cells by enhancing Wnt/β-catenin signaling Wanhu Fan 1 & Fenjing Du 1
&
Xiaojing Liu 1
Received: 6 August 2020 / Accepted: 3 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Phosphatidylinositol 4-phosphate adaptor protein 2 (FAPP2) has been recently identified as a tumor-associated regulator that is closely related to tumorigenesis. Yet, the precise role of FAPP2 in hepatocellular carcinoma (HCC) is still largely unknown. This study was designed to determine the function and molecular mechanisms of FAPP2 in HCC. Elevated expression of FAPP2 commonly occurred in the tumor tissue of HCC compared with normal controls. High expression of FAPP2 was also detected in HCC cell lines and its knockdown markedly decreased the proliferation, colony formation and invasion of HCC cells. Upregulation of FAPP2 by using a FAPP2 expression vector markedly promoted the proliferation, colony formation and invasion of HCC cells. FAPP2 was found to promote the activation of Wnt/β-catenin signaling. Importantly, inhibition of Wnt/β-catenin signaling abrogated the FAPP2 overexpression-conferred oncogenic effect in HCC cells. In addition, xenograft tumor experiments revealed that knockdown of FAPP2 significantly decreased the tumorigenicity of HCC cells in vivo. Taken together, the data of our study reported a tumor-promotion function of FAPP2 in HCC and demonstrate that knockdown of FAPP2 was capable of suppressing HCC cell proliferation and invasion through downregulation of Wnt/β-catenin signaling. This study indicated that FAPP2 might be an attractive candidate anticancer target for HCC. Keywords FAPP2 . Hepatocellular carcinoma . Wnt/β-catenin . Oncogene
Introduction Hepatocellular carcinoma (HCC) is the most common malignant neoplasm of the liver, causing high mortality globally (Bray et al. 2018; Ferlay et al. 2019). In spite of advances in HCC therapy, the clinical outcome for HCC patients has worsened, with a five-year survival rate less than 18% (Siegel et al. 2018). There are many pathogenic factors involved in the occurrence and progression of HCC (Islami et al. 2018); however, the exact molecular mechanisms underlying this condition are still poorly understood. Delineation of the signaling mechanisms of HCC will shed light on the pathology, and help identify novel targets and potential strategies to combat this disease.
* Fenjing Du [email protected] 1
Department of Infectious Diseases, First Affiliated Hospital of Xi’an Jiaotong University, No. 277 Yanta West Road, Xi’an 710061, People’s Republic of China
Phosphatidylinositol 4-phosphate adaptor protein 2 (FAPP2), harboring a pleckstrin homology domain, is a newly identified member of the FAPP proteins (Godi et al. 2004). The FAPP2 gene is located at chromosome 7p21 and encodes a protein composed of 519 amino acids (Godi et al. 2004). FAPP2 is localized to the trans-Golgi network and is a cytoplasmic l
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