Overexpression of NELFCD promotes colorectal cancer cells proliferation, migration, and invasion
Authors Song S, Li D, Yang C, Yan P, Bai Y, Zhang Y, Hu G, Lin C, Li X
Received 3 September 2018
Accepted for publication 30 October 2018
Published 5 December 2018 Volume 2018:11 Pages 8741—8750
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr XuYu Yang
Shenglei Song, Daojiang Li, Chunxing Yang, Peicheng Yan, Yang Bai, Yi Zhang, Gui Hu, Changwei Lin, Xiaorong Li
Department of Gastrointestinal Surgery, The Third Xiang Ya Hospital of Central South University, Changsha, Hunan 410013, China
Purpose: Negative elongation factor complex member C/D (NELFCD), mapped to chromosome 20q13.32, has been found to be significantly overexpressed in colorectal cancer (CRC) by our previous research. However, whether its overexpression contributes to CRC development is unknown. We aimed to explore the biological and clinical roles of NELFCD in CRC.
Materials and methods: The expression of NELFCD was detected by qRT-PCR and Western blot. The biological function of NELFCD on CRC cell proliferation, migration, invasion, and apoptosis was detected by cell counting kit-8, plate colony formation assay, transwell migration and invasion assays, and flow cytometry in vitro and by murine xenograft tumor growth in vivo. Moreover, we evaluated the correction between its expression level and clinicopathologic parameters.
Results: We found NELFCD was overexpressed in 50 pairs of CRC tissues in comparison to the adjacent nontumor tissues (P<0.05). Knockdown of NELFCD significantly impaired cell proliferation, migration and invasion abilities, facilitated cell apoptosis in vitro, and inhibited tumorigenesis of CRC cells in vivo. NELFCD levels were remarkably connected with tumor location in CRC patients.
Conclusion: NELFCD is overexpressed and plays an oncogenic role in CRC. Targeting NELFCD may provide a potential therapeutic option for NELFCD-amplified tumors.
Keywords: NELFCD, colorectal carcinoma, CRC, oncogene
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