Non-nuclear activation of Signal transducer and activator of transcription 3 by 17 beta- estradiol in endometrial cancer cells

作者：Guo R X^*; Zhang R F; Wang X Y; Li L X; Shi H R; Qiao Y H

来源：Neoplasma, 2011, 58(6): 532-537.

DOI：10.4149/neo_2011_06_532

• endometrial cancer
• signal transducer and activator of transcription 3
• estrogen
• non-nuclear action
• carcinogenesis
• estrogen receptor

Why estrogen hyperstimulation can lead to endometrial carcinogenesis has not been fully clear yet. Non-nuclear action of estrogen has arised much attention of many experts. Signal transducer and activator of transcription 3 is a very important signal molecule, which plays vital role in endometrial canver. The present study is oriented to the problem whether estrogen can activate STAT3 by non-nuclear action in endometrial cancer cells. So, the levels of phosphorylated STAT3 (P-STAT3) and total STAT3 were examined by western blot in endometrial cancer cells including Ishikawa with rich-expressed estrogen receptor (ER) and HEC-1A with poor-expressed ER after stimulation with 1 mu M estradiol (E2) at different time points and at varied doses of E2 for optimal time. Inhibitory role of AG490 on activation of STAT3 induced by E2 was also tested. P-STAT3/STAT3 was used as a measure of activation of STAT3. We found that maximum P-STAT3/STAT3 took place at 15min in both Ishikawa cells and HEC-1A cells. The activation of STAT3 elicited gradually with increasing doses of E2. AG490 stopped the activating STAT3 in the same dose-dependent manner in both endometrial cancer cells. The results demonstrate that E2 is able to activate STAT3 in both Ishikawa with rich-expressed ER and HEC-1A with poor-expressed ER endometrial cancer cells by non-nuclear action, which provides the preliminary laboratory basis for the probability of endometrial adenocarcinoma treatment with blockage of STAT3 signaling, especially for ER-poor endometrial adenocarcinoma.

• 出版日期2011
• 单位郑州大学