OBJECTIVE: To explore the role of estrogen receptor-α36 (ER-α36) in epidermal growth factor receptor (EGFR)-related carcinogenesis in endometrial cancer. STUDY DESIGN: The expression of ER-α36, EGFR, and phospho-extracellular signal-regulated kinase was analyzed using immunohistochemistry in endometrial cancer samples. The cellular localization of ER-α36 and EGFR was determined using immunofluorescence in the endometrial cancer Hec1A cells. The level of phospho-extracellular signal-regulated kinase of Hec1A cells was determined using Western blotting after treatment with epidermal growth factor. RESULTS: Positive rate of ER-α36 was increased in high-stage (P = .03) and high-grade (P = .224) endometrial cancer; expression of ER-α36 and EGFR exhibited a significant positive correlation (r = 0.334, P = .025) and they showed substantial colocalization on the plasma membrane of glandular cells; phospho-extracellular signal-regulated kinase positive rate in ER-α36 positive group and EGFR positive group was higher than that of ER-α36 negative group (P = .014) and EGFR negative group (P = .016); finally, ER-α36 mediated epidermal growth factor-stimulated extracellular signal-regulated kinase activation in Hec1A cells. CONCLUSION: ER-α36 mediates EGFR-related extracellular signal-regulated kinase activation in endometrial cancer.
OBJECTIVE: To explore the role of estrogen receptor-α36 (ER-α36) in epidermal growth factor receptor (EGFR)-related carcinogenesis in endometrial cancer. STUDY DESIGN: The expression of ER-α36, EGFR, and phospho-extracellular signal-regulated kinase was analyzed using immunohistochemistry in endometrial cancer samples. The cellular localization of ER-α36 and EGFR was determined using immunofluorescence in the endometrial cancer Hec1A cells. The level of phospho-extracellular signal-regulated kinase of Hec1A cells was determined using Western blotting after treatment with epidermal growth factor. RESULTS: Positive rate of ER-α36 was increased in high-stage (P = .03) and high-grade (P = .224) endometrial cancer; expression of ER-α36 and EGFR exhibited a significant positive correlation (r = 0.334, P = .025) and they showed substantial colocalization on the plasma membrane of glandular cells; phospho-extracellular signal-regulated kinase positive rate in ER-α36 positive group and EGFR positive group was higher than that of ER-α36 negative group (P = .014) and EGFR negative group (P = .016); finally, ER-α36 mediated epidermal growth factor-stimulated extracellular signal-regulated kinase activation in Hec1A cells. CONCLUSION: ER-α36 mediates EGFR-related extracellular signal-regulated kinase activation in endometrial cancer.
Authors: Yu-Jie Dai; Yi-Bo Qiu; Rong Jiang; Man Xu; Ling-Yao Liao; George G Chen; Zhi-Min Liu Journal: Cell Oncol (Dordr) Date: 2018-01-24 Impact factor: 6.730
Authors: Zbynek Heger; Miguel Angel Merlos Rodrigo; Sona Krizkova; Ondrej Zitka; Miroslava Beklova; Rene Kizek; Vojtech Adam Journal: Oncol Lett Date: 2014-02-26 Impact factor: 2.967