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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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Effects of Olfactomedin 4 (OLFM4) on the biological features of endometrial carcinoma cells. (A) Effects of OLFM4 on proliferation of Ishikawa measured by MTT (*P < 0.05, **P < 0.001). (B) OLFM4 did not affect apoptosis in Ishikawa cells analysed by flow cytometry. (C) Effects of OLFM4 on migration and invasion of Ishikawa cells measured by transwell assay (200×). (D) In vitro scratch assay detected effects of OLFM4 on Ishikawa cell migration (100×).
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fig04: Effects of Olfactomedin 4 (OLFM4) on the biological features of endometrial carcinoma cells. (A) Effects of OLFM4 on proliferation of Ishikawa measured by MTT (*P < 0.05, **P < 0.001). (B) OLFM4 did not affect apoptosis in Ishikawa cells analysed by flow cytometry. (C) Effects of OLFM4 on migration and invasion of Ishikawa cells measured by transwell assay (200×). (D) In vitro scratch assay detected effects of OLFM4 on Ishikawa cell migration (100×).

Mentions: We further studied the effects of OLFM4 on biological features of endometrial adenocarcinoma cells. E2-treatment slightly enhanced the proliferation of Ishikawa cells (Fig. 4A). Knockdown of OLFM4 increased tumour cell proliferation with and without E2 stimulation, suggesting that OLFM4 partially suppresses tumour cell proliferation. However, reducing OLFM4 expression did not affect cell apoptosis (Fig. 4B). The in vitro scratch assay demonstrated that suppression of OLFM4 expression with siRNA increased Ishikawa cell migration (Fig. 4D). The transwell migration and invasion assay indicated that knockdown of OLFM4 enhanced the tumour cell capacity for migration and invasion (Fig. 4C). In contrast, OLFM4 over-expression suppressed proliferation and invasion of endometrial adenocarcinoma cells (data not shown). It appeared that OLFM4 was involved in suppression of migration and invasion of endometrial carcinoma cells.


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)

Effects of Olfactomedin 4 (OLFM4) on the biological features of endometrial carcinoma cells. (A) Effects of OLFM4 on proliferation of Ishikawa measured by MTT (*P < 0.05, **P < 0.001). (B) OLFM4 did not affect apoptosis in Ishikawa cells analysed by flow cytometry. (C) Effects of OLFM4 on migration and invasion of Ishikawa cells measured by transwell assay (200×). (D) In vitro scratch assay detected effects of OLFM4 on Ishikawa cell migration (100×).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig04: Effects of Olfactomedin 4 (OLFM4) on the biological features of endometrial carcinoma cells. (A) Effects of OLFM4 on proliferation of Ishikawa measured by MTT (*P < 0.05, **P < 0.001). (B) OLFM4 did not affect apoptosis in Ishikawa cells analysed by flow cytometry. (C) Effects of OLFM4 on migration and invasion of Ishikawa cells measured by transwell assay (200×). (D) In vitro scratch assay detected effects of OLFM4 on Ishikawa cell migration (100×).
Mentions: We further studied the effects of OLFM4 on biological features of endometrial adenocarcinoma cells. E2-treatment slightly enhanced the proliferation of Ishikawa cells (Fig. 4A). Knockdown of OLFM4 increased tumour cell proliferation with and without E2 stimulation, suggesting that OLFM4 partially suppresses tumour cell proliferation. However, reducing OLFM4 expression did not affect cell apoptosis (Fig. 4B). The in vitro scratch assay demonstrated that suppression of OLFM4 expression with siRNA increased Ishikawa cell migration (Fig. 4D). The transwell migration and invasion assay indicated that knockdown of OLFM4 enhanced the tumour cell capacity for migration and invasion (Fig. 4C). In contrast, OLFM4 over-expression suppressed proliferation and invasion of endometrial adenocarcinoma cells (data not shown). It appeared that OLFM4 was involved in suppression of migration and invasion of endometrial carcinoma cells.

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