Figure 6: Silencing of DHCR24 enhances the sensitivity of endometrial cancer cells to medroxyprogesterone acetate treatment. | Scientific Reports

Figure 6: Silencing of DHCR24 enhances the sensitivity of endometrial cancer cells to medroxyprogesterone acetate treatment.

From: Cholesterol Synthetase DHCR24 Induced by Insulin Aggravates Cancer Invasion and Progesterone Resistance in Endometrial Carcinoma

Figure 6

(A) The cell viability of HEC-1B cells was determined in the DHCR24-silenced group and the control group treated with different concentration of MPA ranging from 0 to 30 μM. (B) The cell viability of DHCR24-silenced and control KLE cells was measured after treatment with MPA (10 μM). (C) The cell viability of DHCR24-silenced and control HEC1B cells was measured after treatment with MPA (10 μM). (D) The cell viability was determined in HEC-1B cells treated with MPA, insulin, GSK1904529A or Stattic or with silenced DHCR24. (E) Schematic summary of the findings presented in this study on the role of DHCR24 in endometrial cancer. Insulin up-regulated DHCR24 expression via STAT3, directly binding to the DHCR24 promoter region, which modulated cell metastasis and the response to progestin therapy. (**p < 0.01).

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