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PELP1/MNAR suppression inhibits proliferation and metastasis of endometrial carcinoma cells

Jing Wan1, Xiaomao Li

  • 1Department of Gynecology and Obstetrics, The Third Affiliated Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510630, PR China.

Oncology Reports
|September 21, 2012
PubMed

Insights

Proline-rich protein 1 (PELP1/MNAR) drives endometrial cancer growth and metastasis. Downregulating PELP1/MNAR in cancer cells reduced proliferation and invasion, suggesting it as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Proline-, glutamic acid- and leucine-rich protein-1/modulator of non-genomic activity of estrogen receptor (PELP1/MNAR) is a nuclear receptor co-activator.
  • PELP1/MNAR is implicated as a proto-oncogene with deregulated expression in hormone-responsive cancers.

Purpose of the Study:

  • To investigate the role of PELP1/MNAR in endometrial carcinoma progression and metastasis.
  • To assess PELP1/MNAR as a potential therapeutic target for endometrial cancer.

Main Methods:

  • PELP1/MNAR expression was downregulated using RNA interference in Ishikawa endometrial carcinoma cells.
  • Cell proliferation, migration, and invasion assays (Boyden chamber) were performed.
  • Expression levels of MMP-2 and MMP-9 were analyzed.

Main Results:

  • Downregulation of PELP1/MNAR significantly reduced endometrial carcinoma cell proliferation.
  • Decreased migration and invasion abilities were observed in PELP1/MNAR-knockdown cells.
  • Expression of matrix metalloproteinases MMP-2 and MMP-9 was reduced.

Conclusions:

  • PELP1/MNAR plays a significant role in endometrial cancer progression and metastasis.
  • PELP1/MNAR is a potential therapeutic target for endometrial cancer treatment.

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