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Noninvasive Monitoring of Lesion Size in a Heterologous Mouse Model of Endometriosis
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Enolase-1 is a therapeutic target in endometrial carcinoma

Mengyang Zhao1,2, Weiyi Fang1,2, Yan Wang2,3

  • 1Cancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, Guangdong, China.

Oncotarget
|May 8, 2015
PubMed

Insights

Enolase 1 (ENO1) drives endometrial carcinoma (EC) progression by promoting glycolysis and metastasis. Suppressing ENO1 inhibits tumor growth and enhances cisplatin sensitivity, highlighting ENO1 as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Enolase 1 (ENO1) has a complex role in tumor development, but its specific function and clinical significance in endometrial carcinoma (EC) are not well understood.
  • The mechanisms by which ENO1 influences EC pathogenesis and its potential as a therapeutic target require investigation.

Purpose of the Study:

  • To investigate the role of ENO1 in endometrial carcinoma (EC) pathogenesis, including its effects on cellular functions and response to therapy.
  • To explore the clinical significance of ENO1 expression in EC patients and its association with patient survival.

Main Methods:

  • ENO1 was silenced in EC cells and normal human endometrial epithelial cells (HEEC) to assess effects on glycolysis, proliferation, migration, and invasion in vitro.
  • Tumorigenesis and metastasis were evaluated in vivo following ENO1 silencing.
  • PI3K/AKT signaling pathway and downstream targets, including epithelial-mesenchymal transition (EMT)-associated genes, were analyzed.
  • The sensitivity of EC cells to cisplatin (DDP) after ENO1 knockdown was determined.
  • ENO1 expression levels (mRNA and protein) were compared between EC tissues and normal endometrium tissues.
  • The correlation between ENO1 expression and patient overall survival was analyzed.

Main Results:

  • ENO1 silencing significantly reduced glycolysis, proliferation, migration, and invasion in EC cells, but not in HEEC.
  • In vivo, ENO1 suppression inhibited tumor growth and metastasis by modulating p85, leading to PI3K/AKT pathway inactivation.
  • ENO1 knockdown enhanced EC cell sensitivity to cisplatin (DDP) and reduced xenograft tumor growth.
  • Higher ENO1 mRNA and protein levels were observed in EC tissues compared to normal endometrium.
  • Elevated ENO1 expression correlated with significantly shorter overall survival in EC patients.

Conclusions:

  • ENO1 promotes endometrial carcinoma (EC) carcinogenesis, proliferation, glycolysis, and metastasis through PI3K/AKT pathway modulation.
  • ENO1 is a potential prognostic biomarker and a promising target for gene-based therapy in endometrial carcinoma.
  • Targeting ENO1 can enhance the efficacy of chemotherapy, such as cisplatin, in EC treatment.
Keywords:
EMTENO1cell growthendometrial carcinomaglycolysis

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