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Article

Novel role of semaphorin 3A in the growth and progression of hepatocellular carcinoma

  • Authors:
    • Xuedong Li
    • Qing Chen
    • Dan Yin
    • Shiming Shi
    • Lei Yu
    • Shaolai Zhou
    • Erbao Chen
    • Zhengjun Zhou
    • Yinghong Shi
    • Jia Fan
    • Jian Zhou
    • Zhi Dai
  • View Affiliations / Copyright

    Affiliations: Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China
  • Pages: 3313-3320
    |
    Published online on: May 2, 2017
       https://doi.org/10.3892/or.2017.5616
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Abstract

Semaphorin 3A (SEMA3A), a secretory protein, is a founding member of the semaphorin family and functions in both the biological behavior of tumor cells and the modulation of tumor-associated macrophages. However, the role of SEMA3A in hepatocellular carcinoma (HCC) is still not well established. In the present study, we investigated the expression levels of SEMA3A in 80 HCC tissues and cell lines, using RT-qPCR, western blotting and immunohistochemistry. Expression profile analysis revealed that SEMA3A was significantly overexpressed in human HCC patients and positively correlated with the metastatic potential of HCC cells. Lentiviral transfection into PLC/PRF/5 and HCCLM3 cells was performed to stably upregulate and downregulate the expression of SEMA3A in HCC cells. Cell Counting Kit-8 (CCK-8), wound-healing and invasion assays revealed that SEMA3A promoted the proliferation and migration of HCC cells in vitro. Proteome profiler antibody microarray analysis revealed that overexpression of SEMA3A in HCC cells induced a significant increase in the expression levels of gelsolin-like capping protein (CapG), galectin-3, enolase 2 and epithelial cell adhesion molecule (EpCAM). Furthermore, the upregulation of SEMA3A in HCC cells promoted tumor growth and progression in an HCC mouse model. These results indicate that SEMA3A enhances CapG, galectin-3, enolase 2 and EpCAM expression to promote HCC progression and is a potential therapeutic target for HCC.
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Copy and paste a formatted citation
Spandidos Publications style
Li X, Chen Q, Yin D, Shi S, Yu L, Zhou S, Chen E, Zhou Z, Shi Y, Fan J, Fan J, et al: Novel role of semaphorin 3A in the growth and progression of hepatocellular carcinoma. Oncol Rep 37: 3313-3320, 2017.
APA
Li, X., Chen, Q., Yin, D., Shi, S., Yu, L., Zhou, S. ... Dai, Z. (2017). Novel role of semaphorin 3A in the growth and progression of hepatocellular carcinoma. Oncology Reports, 37, 3313-3320. https://doi.org/10.3892/or.2017.5616
MLA
Li, X., Chen, Q., Yin, D., Shi, S., Yu, L., Zhou, S., Chen, E., Zhou, Z., Shi, Y., Fan, J., Zhou, J., Dai, Z."Novel role of semaphorin 3A in the growth and progression of hepatocellular carcinoma". Oncology Reports 37.6 (2017): 3313-3320.
Chicago
Li, X., Chen, Q., Yin, D., Shi, S., Yu, L., Zhou, S., Chen, E., Zhou, Z., Shi, Y., Fan, J., Zhou, J., Dai, Z."Novel role of semaphorin 3A in the growth and progression of hepatocellular carcinoma". Oncology Reports 37, no. 6 (2017): 3313-3320. https://doi.org/10.3892/or.2017.5616
Copy and paste a formatted citation
x
Spandidos Publications style
Li X, Chen Q, Yin D, Shi S, Yu L, Zhou S, Chen E, Zhou Z, Shi Y, Fan J, Fan J, et al: Novel role of semaphorin 3A in the growth and progression of hepatocellular carcinoma. Oncol Rep 37: 3313-3320, 2017.
APA
Li, X., Chen, Q., Yin, D., Shi, S., Yu, L., Zhou, S. ... Dai, Z. (2017). Novel role of semaphorin 3A in the growth and progression of hepatocellular carcinoma. Oncology Reports, 37, 3313-3320. https://doi.org/10.3892/or.2017.5616
MLA
Li, X., Chen, Q., Yin, D., Shi, S., Yu, L., Zhou, S., Chen, E., Zhou, Z., Shi, Y., Fan, J., Zhou, J., Dai, Z."Novel role of semaphorin 3A in the growth and progression of hepatocellular carcinoma". Oncology Reports 37.6 (2017): 3313-3320.
Chicago
Li, X., Chen, Q., Yin, D., Shi, S., Yu, L., Zhou, S., Chen, E., Zhou, Z., Shi, Y., Fan, J., Zhou, J., Dai, Z."Novel role of semaphorin 3A in the growth and progression of hepatocellular carcinoma". Oncology Reports 37, no. 6 (2017): 3313-3320. https://doi.org/10.3892/or.2017.5616
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