Linc-ROR promotes endometrial cell proliferation by activating the PI3K-Akt pathway.

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Linc-ROR expression is elevated in ectopic adenomyosis endometrium and promotes cell proliferation by activating the PI3K-Akt pathway.

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This study examined linc-ROR expression and PI3K-Akt pathway proteins in ectopic endometrium compared with eutopic endometrium and normal endometrium from patients with adenomyosis, using qRT-PCR and Western blot, with CCK-8 assays to assess endometrial cell proliferation. The authors found higher linc-ROR expression in ectopic adenomyosis endometrium, along with decreased PTEN and increased Akt, p-Akt, and p-PTEN, and they reported associations between linc-ROR levels and the type and severity of dysmenorrhea, while noting no relationship with age, cesarean section, uterine surgery, or menstrual cycle. In adenomyosis cells, linc-ROR knockdown reduced proliferation and increased PTEN with decreased p-Akt, p-PTEN, and p-PDK1, whereas linc-ROR overexpression produced opposite protein changes. This paper is centrally about adenomyosis — it investigates linc-ROR’s role in ectopic adenomyosis endometrial cell proliferation via activation of the PI3K-Akt pathway.

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Abstract

OBJECTIVE: To observe the expressions of Linc-ROR and proteins in the PI3K-Akt pathway in an ectopic lesion of adenomyosis. PATIENTS AND METHODS: The expression of Linc-ROR in the ectopic endometrium, eutopic endometrium, and normal endometrium of adenomyosis was detected by qRT-PCR. Western blot was used to detect the protein expressions of PI3K-Akt in endometriosis and lesion endometriosis. Cell counting kit-8 (CCK-8) assay was utilized to detect cell proliferative activity. After interfering or overexpressing Linc-ROR, protein expressions of the PI3K-Akt pathway were detected by Western blot. RESULTS: Linc-ROR expression in the ectopic endometrium of adenomyosis was higher than that in the eutopic endometrium and normal endometrium, and the expression level of PTEN in adenomyosis tissues was decreased, whilst expression levels of Akt, p-Akt, p-PTEN were increased. Clinical data of enrolled patients indicated that there was a relationship between Linc-ROR expression and the type and severity of dysmenorrhea of adenomyosis. However, no relationship was observed between Linc-ROR expression and age, cesarean section, uterine surgery, and menstrual cycle. Cell counting kit-8 (CCK-8) assay showed that the proliferative activity of cells was significantly decreased after knockdown of Linc-ROR in the adenomyosis cells. Western blot revealed that the expression level of PTEN increased but the expression levels of p-Akt, p-PTEN and p-PDK1 decreased. Overexpression of Linc-ROR obtained the opposite results. CONCLUSIONS: Linc-ROR is highly expressed in the ectopic endometrium of adenomyosis, and it can promote the proliferative activity of endometrial cells by activating the PI3K-Akt pathway.
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Objective

To observe the expressions of Linc-ROR and proteins in the PI3K-Akt pathway in an ectopic lesion of adenomyosis. PATIENTS AND METHODS: The expression of Linc-ROR in the ectopic endometrium, eutopic endometrium, and normal endometrium of adenomyosis was detected by qRT-PCR. Western blot was used to detect the protein expressions of PI3K-Akt in endometriosis and lesion endometriosis. Cell counting kit-8 (CCK-8) assay was utilized to detect cell proliferative activity. After interfering or overexpressing Linc-ROR, protein expressions of the PI3K-Akt pathway were detected by Western blot.

Results

Linc-ROR expression in the ectopic endometrium of adenomyosis was higher than that in the eutopic endometrium and normal endometrium, and the expression level of PTEN in adenomyosis tissues was decreased, whilst expression levels of Akt, p-Akt, p-PTEN were increased. Clinical data of enrolled patients indicated that there was a relationship between Linc-ROR expression and the type and severity of dysmenorrhea of adenomyosis. However, no relationship was observed between Linc-ROR expression and age, cesarean section, uterine surgery, and menstrual cycle. Cell counting kit-8 (CCK-8) assay showed that the proliferative activity of cells was significantly decreased after knockdown of Linc-ROR in the adenomyosis cells. Western blot revealed that the expression level of PTEN increased but the expression levels of p-Akt, p-PTEN and p-PDK1 decreased. Overexpression of Linc-ROR obtained the opposite results.

Conclusions

Linc-ROR is highly expressed in the ectopic endometrium of adenomyosis, and it can promote the proliferative activity of endometrial cells by activating the PI3K-Akt pathway. Free PDF DownloadThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License To cite this article X.-Y. Xu, J. Zhang, Y.-H. Qi, M. Kong, S.-A. Liu, J.-J. Hu Linc-ROR promotes endometrial cell proliferation by activating the PI3K-Akt pathway Eur Rev Med Pharmacol Sci Year: 2018 Vol. 22 - N. 8 Pages: 2218-2225 DOI: 10.26355/eurrev_201804_14807 Publication History Published online: 28 Apr 2018

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Condition tags

endometriosisadenomyosisdysmenorrhea

MeSH descriptors

Endometrium Phosphatidylinositol 3-Kinases Proto-Oncogene Proteins c-akt RNA, Long Noncoding Signal Transduction Adenomyosis Adenomyosis Adult Cell Proliferation Endometriosis Endometriosis Endometrium Endometrium Female Humans Phosphatidylinositol 3-Kinases Pregnancy Proto-Oncogene Proteins c-akt PTEN Phosphohydrolase PTEN Phosphohydrolase

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