Fig 1: Progesterone receptors expression in adenomyosis and normal myometrium. Characterization of PGR expression at gene (a) and protein (b) level, PAQR7 gene (c) and protein (d) level, PAQR8 gene (e) and protein (f) level, PAQR5, gene (g) and protein (h) level, PGRMC1 gene (i) and protein (j) level and PGRMC2 gene (k) and protein (l) level. The columns represent the ratio of the expression of the gene tested and ACTB ± SEM. Asterisk indicates significant differences (* p ≤ 0.05). Original magnification, 40×; scale bar, 50 μm. A, adenomyosis; M, myometrium.
Fig 2: PR gene profiling in MF- and P4-treated transgenic Inhα/Tag mice and cell proliferation and invasion in vitro.qPCR analysis of Pgr (a), Pgrmc1, Pgrmc2, Serbp1 (b), Paqr7 (mPRα), Paqr8 (mPRβ), and Paqr5 (mPRγ) (c) expression in the non-, MF- and P4-treated tumors of Inhα/Tag TG mice. Each bar represents the mean ± SEM relative to Ppia. Immunohistochemical staining of PGR in the control (d), MF-treated (f) and P4-treated (h) tumors and of PGRMC1 in control (e), MF-treated (g) and P4-treated (i) tumors of Inhα/Tag TG mice. The boxes on the right show higher magnifications of the boxes outlined on the left, revealing different PR cell localizations. Original magnification, 10×; scale bar, 200 μm. Box magnification, 40×; scale bar, 50 μm. Effects of MF and P4 with or without the AG-205 inhibitor on KK-1 cell proliferation (j). Cell proliferation of the treated groups is presented as the percentage of the control (considered as 100%). Effects of MF and P4 with or without the AG-205 inhibitor on KK-1 cell invasion (k). Cell invasion of the treated groups is presented as the percentage of the control group (considered as 100%). Asterisks indicate significant differences between the control and treated groups (*, P < .05; **, P < .01; ***, P < .001; ****, P < .0001) (One-way ANOVA with the post-hoc Bonferroni's test). C, control; AG-205, PGRMC1 inhibitor; Inhα/Tag mice; transgenic mice expressing the SV40 Taq oncogene under the inhibin α promoter; MF, mifepristone; P4, progesterone.
Fig 3: Schematic overview of the potential non-genomic P4 action in colorectal cancer. P4 may initiate rapid non-classical signaling through the complex of PGRMC1 and NENF, leading to increased proliferation and invasion of colorectal cancer cells. However, P4 cannot activate the classical genomic signaling pathway due to weak PGR expression in colorectal cancer cells (arrow: ↓PGR—weak PGR expression). P4 or NENF may significantly increase the release of IL-8 by colorectal cancer cells (arrow: ↑IL-8—increased release of IL-8). P4 significantly up-regulates mPRα and mPRγ expression in colorectal cancer cells (arrow: ↑mPR-α, ↑mPR-γ—increased expression of mPR-α and mPR-γ). NENF, neuron-derived neurotrophic factor; P4, progesterone; PGR, nuclear progesterone receptor; and PGRMC1, progesterone receptor membrane component 1.
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