NDC1 promotes hepatocellular carcinoma tumorigenesis by targeting BCAP31 to activate PI3K/AKT signaling

Author:

Liu Ya‐ping123,Guo Gang3,Ren Mudan12,Li Ya‐rui12,Guo Dan12,She Jun‐jun34,He Shui‐xiang12ORCID

Affiliation:

1. Department of Gastroenterology The First Affiliated Hospital of Xi'an Jiaotong University Xi'an China

2. Clinical Medical Research Center for Digestive Diseases of Shaanxi Province (Oncology) Xi'an China

3. Department of Talent Highland The First Affiliated Hospital of Xi'an Jiaotong University Xi'an China

4. Department of General Surgery The First Affiliated Hospital of Xi'an Jiaotong University Xi'an China

Abstract

AbstractHepatocellular carcinoma (HCC) is among the world's worst malignancies. Nuclear division cycle 1 (NDC1) is an essential membrane‐integral nucleoporin, found in this study to be significantly increased in primary HCC. A multivariate analysis revealed that higher NDC1 expression was linked to worse outcome in HCC patients. Mouse xenograft tumors overexpressing NDC1 grew rapidly, and HCC cells overexpressing NDC1 showed enhanced proliferation, invasion, and migration in vitro. In contrast, knocking down NDC1 had the opposite effects in vitro. Furthermore, co‐immunoprecipitation and liquid chromatograph mass spectrometer analyses revealed that NDC1 activated PI3K/AKT signaling by interacting with BCAP31. In summary, NDC1 and BCAP31 cooperate to promote the PI3K/AKT pathway, which is essential for HCC carcinogenesis. This suggests that NDC1 is predictive of prognosis in HCC.

Publisher

Wiley

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