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3.2. GPR30 signaling induced by hydroxytamoxifen stimulated proliferation of endometrial cancer cell line ISHIKAWA and KLE
Fig. 2.
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3.3. GPR30 signaling induced by hydroxytamoxifen increased MMP production of endometrial cancer cell line ISHKAWA and KLE
OHT promoted ISHIKAWA and KLE cell proliferation via GPR30 signaling, and its effect on MMP production via GPR30 signaling was evaluated. The MMP-2 (Fig. 3A) and MMP-9 (Fig. 3B) production increased when ISHIKAWA and KLE LY 294002 were treated with E2, OHT or G1 (Fig. 3). Moreover, the increase in secretion of MMP-9 and MMP-2 was blocked by the presence of U0126 or down-regulation of GPR30 protein [removed](Fig. 3A and B).
Fig. 3.
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3.4. GPR30 signaling induced by hydroxytamoxifen promoted invasion of endometrial cancer cell line ISHKAWA and KLE
The effect of E2, OHT and G1 on ISHKAWA and KLE invasion was determined by a Transwell? assay. ISHIKAWA and KLE cells without transfection or transfected with ShGPR30-pGFP-V-RS or shiv-pGFP-V-RS were treated with E2 (10–7 M), OHT (10–7 M) or G1 (10–8 M). The results revealed that incubation with U0126 markedly decreased cell invasion compared to the control (Fig. 3C). Furthermore, reduction of GPR30 inhibited ISHKAWA and KLE cell invasion, induced by E2, OHT or G1 (Fig. 3D). These data suggested that GPR30 signaling mediated invasive effects induced by OHT in endometrial cancer cell lines via the MAPK pathway.