Fig. 4: GnRHa reverses the CTX-induced inhibition of AMH secretion. | npj Breast Cancer

Fig. 4: GnRHa reverses the CTX-induced inhibition of AMH secretion.

From: GnRHa protects the ovarian reserve by reducing endoplasmic reticulum stress during cyclophosphamide-based chemotherapy

Fig. 4

KGN cells were treated with CTX or CTX plus GnRHa for 36 h. a AMH concentration in KGN cells verified by western blot. Compared with CTX-treated cells, the accumulation of AMH was remitted by co-treatment with GnRHa. b AMH level in cell-culture medium verified by ELISA. Significant reductions of secreted AMH were prevented by co-treatment with GnRHa. c AMH mRNA levels of cells verified by qPCR. d Typical immunocytochemistry images demonstrate the accumulation of AMH in the cytoplasm of cells treated with 750 µg/mL CTX, which was released by co-treatment with GnRHa. e Colocalization of AMH and GRP78 in KGN cells. Cells were transfected with a plasmid expressing FLAG-tagged AMH, and were treated with the indicated reagents for 36 h. Yellow in the merged images indicates the colocalization of AMH and GRP78. Nuclei were stained with DAPI (4’,6’-diamidino-2-phenylindole). CTX750, 750 µg/mL CTX. CG750, 750 µg/mL CTX+ Goserelin. CTX1000, 1000 µg/mL CTX. CG1000, 1000 µg/mL CTX + Goserelin. Scale bars represent 100 µm. Error bars show the standard error of the mean. One-way ANOVA was used for b–c, *P < 0.05, **P < 0.001, and ***P < 0.0001.

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