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Article

ER‑α36‑mediated gastric cancer cell proliferation via the c‑Src pathway

  • Authors:
    • Xuming Wang
    • Hao Deng
    • Feng Zou
    • Zhenqi Fu
    • Ying  Chen
    • Zhaoyi Wang
    • Lijiang Liu
  • View Affiliations / Copyright

    Affiliations: Department of Pathology and Pathophysiology, School of Basic Medical Science of Wuhan University, Wuhan, Hubei, P.R. China, Department of Pathology and Pathophysiology, School of Medicine, Jianghan University, Wuhan, Hubei, P.R. China, Department of Medical Microbiology and Immunology, Creighton University Medical School, Omaha, NE, USA
  • Pages: 329-335
    |
    Published online on: June 20, 2013
       https://doi.org/10.3892/ol.2013.1416
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Abstract

Previously, a novel variant of estrogen receptor (ER)‑α, ER‑α36, was identified and cloned and reported to mainly mediate non‑genomic estrogen signaling. More recently, we identified that ER‑α36 is important for the invasion and lymph node metastasis of human gastric cancer. In the present study, the c‑Src signaling pathway was demonstrated to be involved in the non‑genomic estrogen signaling mediated by ER‑α36 in SGC7901 gastric cancer cells. SGC7901 cells were subjected to the siRNA‑mediated knockdown of ER‑α36 (PLKO.1‑PURO‑SP6‑ER‑α36‑L) or transfected with an ER‑α36 upregulated expression plasmid (PLJM1‑ER‑α36‑H) and treated with 17β‑estradiol (E2β) and PP2, a c‑Src protein inhibitor. The expression of ER‑α36 and c‑src/p‑c‑Src and cyclin D1 was examined by western blot analysis, and tumor cell growth was analyzed by cell proliferation and nude mouse xenograft assays. The ER variant, ER‑α36, was shown to enhance gastric cancer cell proliferation through activation of the membrane‑initiated c‑Src signaling pathways, indicating that ER‑α36 is important for the regulation of proliferation in gastric cancer. In addition, ER‑α36 was shown to directly interact with c‑Src by immunoprecipitation. The results of the present study indicate that the use of ER‑α36 may be a targeted therapeutic approach in gastric cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Wang X, Deng H, Zou F, Fu Z, Chen Y, Wang Z and Liu L: ER‑α36‑mediated gastric cancer cell proliferation via the c‑Src pathway. Oncol Lett 6: 329-335, 2013.
APA
Wang, X., Deng, H., Zou, F., Fu, Z., Chen, Y., Wang, Z., & Liu, L. (2013). ER‑α36‑mediated gastric cancer cell proliferation via the c‑Src pathway. Oncology Letters, 6, 329-335. https://doi.org/10.3892/ol.2013.1416
MLA
Wang, X., Deng, H., Zou, F., Fu, Z., Chen, Y., Wang, Z., Liu, L."ER‑α36‑mediated gastric cancer cell proliferation via the c‑Src pathway". Oncology Letters 6.2 (2013): 329-335.
Chicago
Wang, X., Deng, H., Zou, F., Fu, Z., Chen, Y., Wang, Z., Liu, L."ER‑α36‑mediated gastric cancer cell proliferation via the c‑Src pathway". Oncology Letters 6, no. 2 (2013): 329-335. https://doi.org/10.3892/ol.2013.1416
Copy and paste a formatted citation
x
Spandidos Publications style
Wang X, Deng H, Zou F, Fu Z, Chen Y, Wang Z and Liu L: ER‑α36‑mediated gastric cancer cell proliferation via the c‑Src pathway. Oncol Lett 6: 329-335, 2013.
APA
Wang, X., Deng, H., Zou, F., Fu, Z., Chen, Y., Wang, Z., & Liu, L. (2013). ER‑α36‑mediated gastric cancer cell proliferation via the c‑Src pathway. Oncology Letters, 6, 329-335. https://doi.org/10.3892/ol.2013.1416
MLA
Wang, X., Deng, H., Zou, F., Fu, Z., Chen, Y., Wang, Z., Liu, L."ER‑α36‑mediated gastric cancer cell proliferation via the c‑Src pathway". Oncology Letters 6.2 (2013): 329-335.
Chicago
Wang, X., Deng, H., Zou, F., Fu, Z., Chen, Y., Wang, Z., Liu, L."ER‑α36‑mediated gastric cancer cell proliferation via the c‑Src pathway". Oncology Letters 6, no. 2 (2013): 329-335. https://doi.org/10.3892/ol.2013.1416
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