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NME1 suppression promotes growth, adhesion and implantation of endometrial stromal cells via Akt and MAPK/Erk1/2 signal pathways in the endometriotic milieu.
Hum Reprod. 2013 Oct; 28(10):2822-31.HR

Abstract

STUDY QUESTION

Is Nometastatic gene 23-H1 (NME1, also known as nm23-H1) involved in regulating the biological behavior of endometrial stromal cells (ESCs), and does it participate in the pathogenesis of endometriosis?

SUMMARY ANSWER

NME1 suppression induces ESC dysfunction in the endometriotic milieu.

WHAT IS KNOWN ALREADY

NME1 is a wide-spectrum tumor metastasis suppressor gene that plays an important role in suppressing the invasion and metastasis of tumor cells.

STUDY DESIGN, SIZE, DURATION

An in vitro investigation of the effect of NME1 on the proliferation, adhesion and invasion of eutopic ESCs from patients with endometriosis.

PARTICIPANTS/MATERIALS, SETTING, METHODS

Primary ESCs were prepared from 12 samples of ectopic endometrial tissue (6 peritoneal and 6 ovarian lesions), 18 samples of eutopic endometrial tissues (16 from women with ovarian and 2 from women with pelvic endometriomas) and 12 samples of normal endometrial tissue from women without endometriosis, after the tissues had been analyzed histologically. The growth, invasiveness and adhesion of ESCs were studied by the 5-bromo-2'-deoxyuridine cell proliferation assay and by the Matrigel invasion and adhesion assay. Additionally, the effects of NME1 on the activation or expression of related regulatory proteins were investigated by in-cell Western and flow cytometry assays.

MAIN RESULTS AND THE ROLE OF CHANCE

Expression of NME1 in ESCs derived from eutopic or ectopic endometrium from women with endometriosis is lower than in ESCs from women without endometriosis. Estrogen could down-regulate NME1 expression in ESCs. Silencing NME1 in ESCs promoted the expression of proliferating cell nuclear antigen (PCNA), the anti-apoptotic molecule, survivin, and the adhesion-related molecules, integrin β1 and integrin ανβ3. Silencing NME1 also stimulated ESC proliferation, adhesion and invasion but these effects were inhibited by MAPK/Erk and/or Akt blockers.

LIMITATIONS, REASONS FOR CAUTION

Further studies are needed to examine the regulatory mechanism of estrogen on NME1 expression of ESCs.

WIDER IMPLICATIONS OF THE FINDINGS

Abnormally low expression of NME1 in ESCs may be involved in the pathogenesis of endometriosis by up-regulating growth, adhesion and invasion of ESCs via activating the Akt and MAPK/Erk1/2 signal pathways.

STUDY FUNDING/COMPETING INTEREST(S)

This work was supported by National Natural Science Foundation of China (NSFC) (31270969, 31101064 and 81270677) and Program for ZhouXue of Fudan University. None of the authors has any conflict of interest to declare.

Authors+Show Affiliations

Laboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, No. 413, Zhaozhou Road, Shanghai 200011, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23856325

Citation

Li, Ming-Qing, et al. "NME1 Suppression Promotes Growth, Adhesion and Implantation of Endometrial Stromal Cells Via Akt and MAPK/Erk1/2 Signal Pathways in the Endometriotic Milieu." Human Reproduction (Oxford, England), vol. 28, no. 10, 2013, pp. 2822-31.
Li MQ, Shao J, Meng YH, et al. NME1 suppression promotes growth, adhesion and implantation of endometrial stromal cells via Akt and MAPK/Erk1/2 signal pathways in the endometriotic milieu. Hum Reprod. 2013;28(10):2822-31.
Li, M. Q., Shao, J., Meng, Y. H., Mei, J., Wang, Y., Li, H., Zhang, L., Chang, K. K., Wang, X. Q., Zhu, X. Y., & Li, D. J. (2013). NME1 suppression promotes growth, adhesion and implantation of endometrial stromal cells via Akt and MAPK/Erk1/2 signal pathways in the endometriotic milieu. Human Reproduction (Oxford, England), 28(10), 2822-31. https://doi.org/10.1093/humrep/det248
Li MQ, et al. NME1 Suppression Promotes Growth, Adhesion and Implantation of Endometrial Stromal Cells Via Akt and MAPK/Erk1/2 Signal Pathways in the Endometriotic Milieu. Hum Reprod. 2013;28(10):2822-31. PubMed PMID: 23856325.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - NME1 suppression promotes growth, adhesion and implantation of endometrial stromal cells via Akt and MAPK/Erk1/2 signal pathways in the endometriotic milieu. AU - Li,Ming-Qing, AU - Shao,Jun, AU - Meng,Yu-Han, AU - Mei,Jie, AU - Wang,Ying, AU - Li,Hui, AU - Zhang,Li, AU - Chang,Kai-Kai, AU - Wang,Xiao-Qiu, AU - Zhu,Xiao-Yong, AU - Li,Da-Jin, Y1 - 2013/07/14/ PY - 2013/7/17/entrez PY - 2013/7/17/pubmed PY - 2014/6/10/medline KW - NME1 KW - adhesion KW - endometriosis KW - invasion KW - proliferation SP - 2822 EP - 31 JF - Human reproduction (Oxford, England) JO - Hum. Reprod. VL - 28 IS - 10 N2 - STUDY QUESTION: Is Nometastatic gene 23-H1 (NME1, also known as nm23-H1) involved in regulating the biological behavior of endometrial stromal cells (ESCs), and does it participate in the pathogenesis of endometriosis? SUMMARY ANSWER: NME1 suppression induces ESC dysfunction in the endometriotic milieu. WHAT IS KNOWN ALREADY: NME1 is a wide-spectrum tumor metastasis suppressor gene that plays an important role in suppressing the invasion and metastasis of tumor cells. STUDY DESIGN, SIZE, DURATION: An in vitro investigation of the effect of NME1 on the proliferation, adhesion and invasion of eutopic ESCs from patients with endometriosis. PARTICIPANTS/MATERIALS, SETTING, METHODS: Primary ESCs were prepared from 12 samples of ectopic endometrial tissue (6 peritoneal and 6 ovarian lesions), 18 samples of eutopic endometrial tissues (16 from women with ovarian and 2 from women with pelvic endometriomas) and 12 samples of normal endometrial tissue from women without endometriosis, after the tissues had been analyzed histologically. The growth, invasiveness and adhesion of ESCs were studied by the 5-bromo-2'-deoxyuridine cell proliferation assay and by the Matrigel invasion and adhesion assay. Additionally, the effects of NME1 on the activation or expression of related regulatory proteins were investigated by in-cell Western and flow cytometry assays. MAIN RESULTS AND THE ROLE OF CHANCE: Expression of NME1 in ESCs derived from eutopic or ectopic endometrium from women with endometriosis is lower than in ESCs from women without endometriosis. Estrogen could down-regulate NME1 expression in ESCs. Silencing NME1 in ESCs promoted the expression of proliferating cell nuclear antigen (PCNA), the anti-apoptotic molecule, survivin, and the adhesion-related molecules, integrin β1 and integrin ανβ3. Silencing NME1 also stimulated ESC proliferation, adhesion and invasion but these effects were inhibited by MAPK/Erk and/or Akt blockers. LIMITATIONS, REASONS FOR CAUTION: Further studies are needed to examine the regulatory mechanism of estrogen on NME1 expression of ESCs. WIDER IMPLICATIONS OF THE FINDINGS: Abnormally low expression of NME1 in ESCs may be involved in the pathogenesis of endometriosis by up-regulating growth, adhesion and invasion of ESCs via activating the Akt and MAPK/Erk1/2 signal pathways. STUDY FUNDING/COMPETING INTEREST(S): This work was supported by National Natural Science Foundation of China (NSFC) (31270969, 31101064 and 81270677) and Program for ZhouXue of Fudan University. None of the authors has any conflict of interest to declare. SN - 1460-2350 UR - https://www.unboundmedicine.com/medline/citation/23856325/NME1_suppression_promotes_growth_adhesion_and_implantation_of_endometrial_stromal_cells_via_Akt_and_MAPK/Erk1/2_signal_pathways_in_the_endometriotic_milieu_ L2 - https://academic.oup.com/humrep/article-lookup/doi/10.1093/humrep/det248 DB - PRIME DP - Unbound Medicine ER -