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Article: Membrane Metalloendopeptidase (MME) suppresses metastasis of esophageal squamous cell carcinoma (ESCC) by inhibiting FAK-RhoA signaling axis

TitleMembrane Metalloendopeptidase (MME) suppresses metastasis of esophageal squamous cell carcinoma (ESCC) by inhibiting FAK-RhoA signaling axis
Authors
Issue Date2019
PublisherElsevier Inc. The Journal's web site is located at http://ajp.amjpathol.org/
Citation
The American Journal of Pathology, 2019, v. 189 n. 7, p. 1462-1472 How to Cite?
AbstractEsophageal squamous cell carcinoma (ESCC) is a typical neoplastic disease and a frequent cause of death in China. Although great achievements have been made in diagnostic strategies and combination therapies in recent years, the prognosis of ESCC is still poor. Metastasis/recurrence has been the major factor responsible for poor prognosis. However, the underlying mechanism of ESCC dissemination remains elusive. Membrane metalloendopeptidase (MME) is a transmembrane glycoprotein that degrades a number of substrates. This study's results indicated that the down-regulation of MME is significantly associated with advanced clinical stage (P < 0.05) and lymph node metastasis (P < 0.05). The down-regulation of MME in ESCC tumor tissues is correlated to poorer prognosis of the patients. Functional studies demonstrated that MME could significantly inhibit ESCC tumor cell metastasis in vitro and in vivo. MME overexpression could also interrupt ESCC tumor cell adhesion. Mechanistically, MME inhibits the phosphorylation of FAK thus interrupting the FAK-RhoA axis, which is important in cell movement. Taken together, these data show that MME regulates ESCC via FAK-RhoA axis. High expression of MME may indicate a beneficial outcome for patients. © 2019 American Society for Investigative Pathology
Persistent Identifierhttp://hdl.handle.net/10722/276317
ISSN
2019 Impact Factor: 3.491
2015 SCImago Journal Rankings: 2.653
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, M-
dc.contributor.authorWang, L-
dc.contributor.authorZhan, Y-
dc.contributor.authorZeng, T-
dc.contributor.authorZhang, X-
dc.contributor.authorGuan, X-
dc.contributor.authorLi, Y-
dc.date.accessioned2019-09-10T03:00:34Z-
dc.date.available2019-09-10T03:00:34Z-
dc.date.issued2019-
dc.identifier.citationThe American Journal of Pathology, 2019, v. 189 n. 7, p. 1462-1472-
dc.identifier.issn0002-9440-
dc.identifier.urihttp://hdl.handle.net/10722/276317-
dc.description.abstractEsophageal squamous cell carcinoma (ESCC) is a typical neoplastic disease and a frequent cause of death in China. Although great achievements have been made in diagnostic strategies and combination therapies in recent years, the prognosis of ESCC is still poor. Metastasis/recurrence has been the major factor responsible for poor prognosis. However, the underlying mechanism of ESCC dissemination remains elusive. Membrane metalloendopeptidase (MME) is a transmembrane glycoprotein that degrades a number of substrates. This study's results indicated that the down-regulation of MME is significantly associated with advanced clinical stage (P < 0.05) and lymph node metastasis (P < 0.05). The down-regulation of MME in ESCC tumor tissues is correlated to poorer prognosis of the patients. Functional studies demonstrated that MME could significantly inhibit ESCC tumor cell metastasis in vitro and in vivo. MME overexpression could also interrupt ESCC tumor cell adhesion. Mechanistically, MME inhibits the phosphorylation of FAK thus interrupting the FAK-RhoA axis, which is important in cell movement. Taken together, these data show that MME regulates ESCC via FAK-RhoA axis. High expression of MME may indicate a beneficial outcome for patients. © 2019 American Society for Investigative Pathology-
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://ajp.amjpathol.org/-
dc.relation.ispartofThe American Journal of Pathology-
dc.titleMembrane Metalloendopeptidase (MME) suppresses metastasis of esophageal squamous cell carcinoma (ESCC) by inhibiting FAK-RhoA signaling axis-
dc.typeArticle-
dc.identifier.emailGuan, X: xyguan@hku.hk-
dc.identifier.authorityGuan, X=rp00454-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ajpath.2019.04.007-
dc.identifier.pmid31054987-
dc.identifier.scopuseid_2-s2.0-85067551044-
dc.identifier.hkuros302613-
dc.identifier.volume189-
dc.identifier.issue7-
dc.identifier.spage1462-
dc.identifier.epage1472-
dc.identifier.isiWOS:000473836900014-
dc.publisher.placeUnited States-

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