Positive associations between upregulated levels of stress-induced phosphoprotein 1 and matrix metalloproteinase-9 in endometriosis/adenomyosis

PLoS One. 2018 Jan 5;13(1):e0190573. doi: 10.1371/journal.pone.0190573. eCollection 2018.

Abstract

Stress-induced phosphoprotein-1 (STIP1), an adaptor protein that coordinates the functions of HSP70 and HSP90 in protein folding, has been implicated in the development of human gynecologic malignancies. This case-control study investigates STIP1 serum levels and tissue expression in relation to endometriosis/adenomyosis in Taiwanese population. Female patients with surgically confirmed endometriosis/adenomyosis were compared with women free of endometriosis/adenomyosis. Serum STIP1 levels were measured using an enzyme-linked immunosorbent assay and surgical tissues were analyzed by immunohistochemistry. Both epithelial and stromal cells in surgical tissues of endometriosis and adenomyosis expressed STIP1 and MMP-9. Notably, MMP-9 expression was significantly decreased when STIP1 expression was knocked-down. In vitro experiments revealed that STIP1 was capable of binding to the MMP-9 promoter and enhanced its transcriptional expression. The preoperative serum STIP1 levels of patients with endometriosis/adenomyosis were significantly higher than those of the controls. In brief, our data suggest an association between STIP1 levels and endometriosis/adenomyosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Case-Control Studies
  • Cell Line, Tumor
  • Endometriosis / enzymology*
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Heat-Shock Proteins / blood
  • Heat-Shock Proteins / genetics
  • Heat-Shock Proteins / metabolism*
  • Humans
  • Immunohistochemistry
  • Matrix Metalloproteinase 9 / genetics
  • Matrix Metalloproteinase 9 / metabolism*
  • Promoter Regions, Genetic
  • Taiwan
  • Up-Regulation*

Substances

  • Heat-Shock Proteins
  • STIP1 protein, human
  • Matrix Metalloproteinase 9

Grants and funding

This research was financially supported by grants from the Chang Gung Medical Research Foundation (CRRPG3D0021/2/3 to AC, CRRPG3D0031/2/3 to THW, and CMRPG3G0371 and CMRPG3F1621 to CLT) and the Ministry of Science and Technology (MOST105-2314-B-182-056 to AC).