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Kisspeptin agonist-KP10 and antagonist-KP234 significantly regulated the migration and invasion of endometrial cancer cells through FAK, Src, and ERK1/2-mediated MMP-2/9 expression. (A) The treatment with KP10 significantly decreased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. Meantime, the challenge with KP234 significantly increased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. (B) To verify the effects of FAK, Src, and ERK1/2 inhibitors in RL95-2 endometrial cancer cells, cells were pretreated with FAK inhibitor <t>(PF573228),</t> Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated expressions of FAK, Src, and ERK1/2 were inhibited by FAK, Src, and ERK1/2 inhibitors individually. (C) RL95-2 endometrial cancer cells were pretreated with FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated MMP-2/9 expression was weakened by FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually. Results are expressed as mean ± SEM of 3 independent experiments (* P < .05 vs control).
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Kisspeptin agonist-KP10 and antagonist-KP234 significantly regulated the migration and invasion of endometrial cancer cells through FAK, Src, and ERK1/2-mediated MMP-2/9 expression. (A) The treatment with KP10 significantly decreased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. Meantime, the challenge with KP234 significantly increased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. (B) To verify the effects of FAK, Src, and ERK1/2 inhibitors in RL95-2 endometrial cancer cells, cells were pretreated with FAK inhibitor <t>(PF573228),</t> Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated expressions of FAK, Src, and ERK1/2 were inhibited by FAK, Src, and ERK1/2 inhibitors individually. (C) RL95-2 endometrial cancer cells were pretreated with FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated MMP-2/9 expression was weakened by FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually. Results are expressed as mean ± SEM of 3 independent experiments (* P < .05 vs control).
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Kisspeptin agonist-KP10 and antagonist-KP234 significantly regulated the migration and invasion of endometrial cancer cells through FAK, Src, and ERK1/2-mediated MMP-2/9 expression. (A) The treatment with KP10 significantly decreased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. Meantime, the challenge with KP234 significantly increased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. (B) To verify the effects of FAK, Src, and ERK1/2 inhibitors in RL95-2 endometrial cancer cells, cells were pretreated with FAK inhibitor <t>(PF573228),</t> Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated expressions of FAK, Src, and ERK1/2 were inhibited by FAK, Src, and ERK1/2 inhibitors individually. (C) RL95-2 endometrial cancer cells were pretreated with FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated MMP-2/9 expression was weakened by FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually. Results are expressed as mean ± SEM of 3 independent experiments (* P < .05 vs control).
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Kisspeptin agonist-KP10 and antagonist-KP234 significantly regulated the migration and invasion of endometrial cancer cells through FAK, Src, and ERK1/2-mediated MMP-2/9 expression. (A) The treatment with KP10 significantly decreased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. Meantime, the challenge with KP234 significantly increased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. (B) To verify the effects of FAK, Src, and ERK1/2 inhibitors in RL95-2 endometrial cancer cells, cells were pretreated with FAK inhibitor <t>(PF573228),</t> Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated expressions of FAK, Src, and ERK1/2 were inhibited by FAK, Src, and ERK1/2 inhibitors individually. (C) RL95-2 endometrial cancer cells were pretreated with FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated MMP-2/9 expression was weakened by FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually. Results are expressed as mean ± SEM of 3 independent experiments (* P < .05 vs control).
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Kisspeptin agonist-KP10 and antagonist-KP234 significantly regulated the migration and invasion of endometrial cancer cells through FAK, Src, and ERK1/2-mediated MMP-2/9 expression. (A) The treatment with KP10 significantly decreased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. Meantime, the challenge with KP234 significantly increased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. (B) To verify the effects of FAK, Src, and ERK1/2 inhibitors in RL95-2 endometrial cancer cells, cells were pretreated with FAK inhibitor <t>(PF573228),</t> Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated expressions of FAK, Src, and ERK1/2 were inhibited by FAK, Src, and ERK1/2 inhibitors individually. (C) RL95-2 endometrial cancer cells were pretreated with FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated MMP-2/9 expression was weakened by FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually. Results are expressed as mean ± SEM of 3 independent experiments (* P < .05 vs control).
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Kisspeptin agonist-KP10 and antagonist-KP234 significantly regulated the migration and invasion of endometrial cancer cells through FAK, Src, and ERK1/2-mediated MMP-2/9 expression. (A) The treatment with KP10 significantly decreased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. Meantime, the challenge with KP234 significantly increased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. (B) To verify the effects of FAK, Src, and ERK1/2 inhibitors in RL95-2 endometrial cancer cells, cells were pretreated with FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated expressions of FAK, Src, and ERK1/2 were inhibited by FAK, Src, and ERK1/2 inhibitors individually. (C) RL95-2 endometrial cancer cells were pretreated with FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated MMP-2/9 expression was weakened by FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually. Results are expressed as mean ± SEM of 3 independent experiments (* P < .05 vs control).

Journal: Journal of the Endocrine Society

Article Title: Kisspeptin Regulates Cell Invasion and Migration in Endometrial Cancer

doi: 10.1210/jendso/bvae001

Figure Lengend Snippet: Kisspeptin agonist-KP10 and antagonist-KP234 significantly regulated the migration and invasion of endometrial cancer cells through FAK, Src, and ERK1/2-mediated MMP-2/9 expression. (A) The treatment with KP10 significantly decreased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. Meantime, the challenge with KP234 significantly increased MMP-2/9 protein expression in RL95-2 endometrial cancer cell line when compared with the normal control. (B) To verify the effects of FAK, Src, and ERK1/2 inhibitors in RL95-2 endometrial cancer cells, cells were pretreated with FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated expressions of FAK, Src, and ERK1/2 were inhibited by FAK, Src, and ERK1/2 inhibitors individually. (C) RL95-2 endometrial cancer cells were pretreated with FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually, and then treated with KP234 for 2 hours. Cell lysates were collected for immunoblot analysis. The KP234-stimulated MMP-2/9 expression was weakened by FAK inhibitor (PF573228), Src inhibitor (SU6656), and ERK1/2 inhibitor (U0126) individually. Results are expressed as mean ± SEM of 3 independent experiments (* P < .05 vs control).

Article Snippet: The FAK inhibitor PF573228 (Tocris Bioscience Cat#3239, RRID:AB_3076559), the Src inhibitor SU6656 (Tocris Bioscience Cat#6475, RRID: AB_3076557), and the ERK1/2 inhibitor U0126 (Sigma-Aldrich, Cat#U120, RRID: AB_3076557) were purchased from Tocris Bioscience (Bristol, UK) and Sigma-Aldrich Chemie GmbH (Steinheim, Germany).

Techniques: Migration, Expressing, Control, Western Blot