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  • br Declaration of Competing Interest br The authors declare


    Declaration of Competing Interest
    The authors declare no conflict of interest.
    The authors thank the patients and their families for their involve-ment in this study.  Gene Reports 16 (2019) 100463
    Availability of data and materials
    The data that support the findings of this study are available from the corresponding author on reasonable request.
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    Contents lists available at ScienceDirect
    Research paper
    APPBP2 enhances non-small cell lung cancer proliferation and invasiveness through regulating PPM1D and SPOP
    Huiyuan Gong a,b,1, Fei Liu c,e,1, Xiaoyu Liu d, Shengping Min c, Nan Wu c, Xincheng Liu c, Yueguang Liu e, Sue Han e, Yijie Zhang e, Yuefang Zhang e, Yudong Hu f, Xuegang Liu a,b, , Xiaojing Wang c,
    a School of Medicine, Shandong University, No. 44 Wenhua West-Road, Ji Nan, Shandong Province 250012, China
    b Department of Thoracic Surgery, First Affiliated Hospital, Bengbu Medical College, No. 287 Changhuai Road, Bengbu, Anhui Province 233000, China
    c Anhui Clinical and Preclinical Key Laboratory of Respiratory Disease, Department of Respiration, First Affiliated Hospital, Bengbu Medical College, No. 287 Changhuai Road, Bengbu, Anhui Province 233000, China d Department of Radiology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine. No. 1665 Kongjiang Road, Shanghai 200031, China
    e Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue Yang Road, Shanghai 200031, China
    f School of Biotechnology, Jiangnan University, 1800 Lihu Road, Wuxi 214122, Jiangsu, China
    Article history:
    Lung cancer
    Non-small cell lung cancer
    Background: The influence of amyloid protein-binding protein 2 (APPBP2) on lung cancer is unknown. Methods: The function and mechanisms of APPBP2 were investigated in the NSCLC cell lines A549 and H1299. The ectopic expression of APPBP2, PPM1D and SPOP in NSCLS were examined in samples collected from ten pairs of human lung adenocarcinoma cancer tissues and adjacent normal lung tissues. shRNA vector was used for APPBP2 knockdown. Quantitative PCR and western blot assays quantified the mRNA and protein level of APPBP2, PPM1D, and SPOP. Cell proliferation was measured with BrdU, MTT, colony formation assays, and xenograft tumour growth experiments. Cell migration and invasion were analysed with transwell and wound healing assays. Co-Immunoprecipitation assay detected protein–protein interactions.
    Findings: APPBP2 was upregulated in NSCLC tissues. Silencing APPBP2 in A549 and H1299 cells resulted in the in-hibition of cell proliferation, migration, and invasion, enhancement of apoptosis, and a significant decrease in the expression of PPM1D and SPOP. Overexpression of PPM1D and SPOP attenuated the APPBP2-knockdown inhibi-tion of NSCLC cells. Co-IP assay showed that PPM1D interacted with APPBP2.
    Interpretation: The expression level of APPBP2 positively correlates with NSCLC cell proliferation, migration, and invasiveness. APPBP2 contributes to NSCLC progression through regulating the PPM1D and SPOP signalling path-way. This novel molecular mechanism, underlying NSCLC oncogenesis, suggests APPBP2 is a potential target for diagnosis and therapeutic intervention in NSCLC.
    Fund: Key Program of Natural Science Research of Higher Education of Anhui Province (No. KJ2017A241), the National Natural Science Foundation of China (No. 81772493).