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Oestrogen receptor-mediated expression of Olfactomedin 4 regulates the progression of endometrial adenocarcinoma.

Duan C, Liu X, Liang S, Yang Z, Xia M, Wang L, Chen S, Yu L - J. Cell. Mol. Med. (2014)

Bottom Line: The mechanism of OLFM4 in tumuorigenesis is elusive.Down-regulation of OLFM4 was associated with decreased cumulative survival rate of patients with endometrioid adenocarcinoma.Our data suggested that impairment of ERα signal-mediated OLFM4 expression promoted the malignant progression of endometrioid adenocarcinoma, which may have significance for the therapy of this carcinoma.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, The First Affiliated Hospital, Sun Yat-sen (Zhongshan) University, Guangzhou, China.

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Expression of Olfactomedin 4 (OLFM4) is regulated by the oestrogen receptor-α (ERα) signalling in endometrial carcinoma cells. (A and B) Oestrogen antagonist ICI 182 780 attenuated the OLFM4 mRNA increase induced by E2. (C and D) ERα-specific agonist PPT, but not ERβ-specific agonist DPN, induced OLFM4 mRNA expression. (E–H) Knockdown of ERα with siRNA reduced E2-induced expression of OLFM4. *P < 0.05, **P < 0.001. E2, 17β-estradiol; ICI, ICI 182 780; PPT, 4′,4″,4‴-(4- propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol; DPN, 2,3-bis-(4–ydroxyphenyl)–propionitrile; BC: blank control; NC: negative control (non-specific siRNA group).
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fig03: Expression of Olfactomedin 4 (OLFM4) is regulated by the oestrogen receptor-α (ERα) signalling in endometrial carcinoma cells. (A and B) Oestrogen antagonist ICI 182 780 attenuated the OLFM4 mRNA increase induced by E2. (C and D) ERα-specific agonist PPT, but not ERβ-specific agonist DPN, induced OLFM4 mRNA expression. (E–H) Knockdown of ERα with siRNA reduced E2-induced expression of OLFM4. *P < 0.05, **P < 0.001. E2, 17β-estradiol; ICI, ICI 182 780; PPT, 4′,4″,4‴-(4- propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol; DPN, 2,3-bis-(4–ydroxyphenyl)–propionitrile; BC: blank control; NC: negative control (non-specific siRNA group).

Mentions: We also investigated whether the expression of OLFM4 in endometrial adenocarcinoma cell lines is regulated by oestrogen receptor signalling. Both Ishikawa and HEC-1B cells expressed ERα, ERβ, PR-A and PR-B, but the expression levels in Ishikawa cells were higher than that in HEC-1B (Fig. S1A). Similarly, OLFM4 mRNA expression in HEC-1B cells was lower than that in Ishikawa cells (Fig. S1B and C). When the cells were stimulated with oestrogen E2, OLFM4 mRNA expression was increased (Fig. 3A and B). Addition of oestrogen receptor antagonist ICI 182 780 attenuated the OLFM4 mRNA increase induced by E2. In contrast, OLFM4 mRNA expression was enhanced upon the stimulation of ERα-specific agonist PPT, whereas ERβ-specific agonist DPN had no effect (Fig. 3C and D). ICI 182 780 attenuated the OLFM4 mRNA increase induced by PPT. Knockdown of ERα in HEC-1B and Ishikawa cells using siRNA attenuated the E2-induced expression of OLFM4 (Fig. 3F and H). Results suggested that ERα-mediated signalling regulated expression of OLFM4.


Oestrogen receptor-mediated expression of Olfactomedin 4 regulates the progression of endometrial adenocarcinoma.

Duan C, Liu X, Liang S, Yang Z, Xia M, Wang L, Chen S, Yu L - J. Cell. Mol. Med. (2014)

Expression of Olfactomedin 4 (OLFM4) is regulated by the oestrogen receptor-α (ERα) signalling in endometrial carcinoma cells. (A and B) Oestrogen antagonist ICI 182 780 attenuated the OLFM4 mRNA increase induced by E2. (C and D) ERα-specific agonist PPT, but not ERβ-specific agonist DPN, induced OLFM4 mRNA expression. (E–H) Knockdown of ERα with siRNA reduced E2-induced expression of OLFM4. *P < 0.05, **P < 0.001. E2, 17β-estradiol; ICI, ICI 182 780; PPT, 4′,4″,4‴-(4- propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol; DPN, 2,3-bis-(4–ydroxyphenyl)–propionitrile; BC: blank control; NC: negative control (non-specific siRNA group).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4119392&req=5

fig03: Expression of Olfactomedin 4 (OLFM4) is regulated by the oestrogen receptor-α (ERα) signalling in endometrial carcinoma cells. (A and B) Oestrogen antagonist ICI 182 780 attenuated the OLFM4 mRNA increase induced by E2. (C and D) ERα-specific agonist PPT, but not ERβ-specific agonist DPN, induced OLFM4 mRNA expression. (E–H) Knockdown of ERα with siRNA reduced E2-induced expression of OLFM4. *P < 0.05, **P < 0.001. E2, 17β-estradiol; ICI, ICI 182 780; PPT, 4′,4″,4‴-(4- propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol; DPN, 2,3-bis-(4–ydroxyphenyl)–propionitrile; BC: blank control; NC: negative control (non-specific siRNA group).
Mentions: We also investigated whether the expression of OLFM4 in endometrial adenocarcinoma cell lines is regulated by oestrogen receptor signalling. Both Ishikawa and HEC-1B cells expressed ERα, ERβ, PR-A and PR-B, but the expression levels in Ishikawa cells were higher than that in HEC-1B (Fig. S1A). Similarly, OLFM4 mRNA expression in HEC-1B cells was lower than that in Ishikawa cells (Fig. S1B and C). When the cells were stimulated with oestrogen E2, OLFM4 mRNA expression was increased (Fig. 3A and B). Addition of oestrogen receptor antagonist ICI 182 780 attenuated the OLFM4 mRNA increase induced by E2. In contrast, OLFM4 mRNA expression was enhanced upon the stimulation of ERα-specific agonist PPT, whereas ERβ-specific agonist DPN had no effect (Fig. 3C and D). ICI 182 780 attenuated the OLFM4 mRNA increase induced by PPT. Knockdown of ERα in HEC-1B and Ishikawa cells using siRNA attenuated the E2-induced expression of OLFM4 (Fig. 3F and H). Results suggested that ERα-mediated signalling regulated expression of OLFM4.

Bottom Line: The mechanism of OLFM4 in tumuorigenesis is elusive.Down-regulation of OLFM4 was associated with decreased cumulative survival rate of patients with endometrioid adenocarcinoma.Our data suggested that impairment of ERα signal-mediated OLFM4 expression promoted the malignant progression of endometrioid adenocarcinoma, which may have significance for the therapy of this carcinoma.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, The First Affiliated Hospital, Sun Yat-sen (Zhongshan) University, Guangzhou, China.

Show MeSH
Related in: MedlinePlus