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. 2020 May 7;11(5):335. doi: 10.1038/s41419-020-2549-2

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a, b MHCC97H and PLC/RLF/5 cell lines were overexpressed with GFP (CON) or GFP-tagged NT5DC2 (OE). Verification of NT5DC2 overexpression (OE) in MHCC97H and PLC/RLF/5 cell lines at both the mRNA (a) and protein levels (b). c, d Verification of NT5DC2 knockdown (shRNA) in MHCC97H and PLC/RLF/5 cell lines at both the mRNA (c) and protein levels (d). e CCK8 assays for cell proliferation of MHCC97H-NT5DC2-overexpression and PLC/RLF/5-NT5DC2-overexpression cells compared with their vector controls (CON). NT5DC2 promoted liver cancer cell proliferation in vitro. f CCK8 assays for cell proliferation of MHCC97H-NT5DC2-knockdown and PLC/RLF/5-NT5DC2-knockdown cells compared with their vector controls. NT5DC2 knockdown inhibited liver cancer cell proliferation in vitro. g Clone formation of MHCC97H-NT5DC2-overexpression and PLC/RLF/5-NT5DC2-overexpression cells compared with their vector controls. NT5DC2 promoted cell clone formation in vitro. h Clone formation of MHCC97H-NT5DC2-knockdown and PLC/RLF/5-NT5DC2-knockdown cells compared with their vector controls. NT5DC2 knockdown inhibited cell clone formation in vitro. i MHCC97H cells with NT5DC2 overexpression (OE) or its vector control (CON) were subcutaneously implanted into nude mice, and the tumors were harvested 3 weeks later (left). Compared with the controls, NT5DC2 overexpression significantly promoted tumor growth (right). j MHCC97H cells with NT5DC2 knockdown (shRNA) or its vector control (scramble) were subcutaneously implanted into nude mice, and the tumors were harvested 5 weeks later (left). Compared with the controls, NT5DC2 knockdown significantly inhibited tumor growth (right). k Tumor slides were analyzed via immunohistochemistry for PCNA expression (left). Compared with the controls, NT5DC2 overexpression significantly increased the proportions of PCNA-positive cells, while NT5DC2 knockdown significantly decreased the proportions of PCNA-positive cells (right). *p < 0.05; **p < 0.01; ***p < 0.001.