Prohibitin as a novel target protein of luteinizing hormone in ovarian epithelial carcinogenesis

L Jia1, X F Yi, Z B Zhang

  • 1Department of Obstetrics and Gynecology, Qilu Shandong University, Jinan 250012, China.

Neoplasma
|February 1, 2011
PubMed

Insights

Luteinizing hormone (LH) up-regulates prohibitin, a protein that decreases with ovarian cancer progression. This suggests LH may inhibit ovarian cancer development and progression.

Area of Science:

  • Endocrinology
  • Oncology
  • Proteomics

Background:

  • The roles of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in ovarian epithelial carcinoma (OEC) remain unclear.
  • Understanding the molecular mechanisms underlying OEC development is crucial for targeted therapies.

Purpose of the Study:

  • To investigate the relationship between gonadotropins and specific proteins in ovarian epithelial tumor (OET) cells.
  • To identify proteins modulated by LH and FSH and their potential role in OEC pathogenesis.

Main Methods:

  • Proteomic analysis of OET cells treated with gonadotropins.
  • Validation of prohibitin as a target protein using Western blot.
  • Immunohistochemical detection of prohibitin expression in human serous ovarian tumors.

Main Results:

  • LH significantly up-regulated prohibitin expression in OET cells (up to 2.5-fold at 200 mIU/mL).
  • Prohibitin expression decreased progressively from benign serous cystadenomas to borderline tumors and serous carcinomas (P < 0.0001).
  • Significant differences in prohibitin expression were observed between all tumor groups (P < 0.001).

Conclusions:

  • Prohibitin is an LH-associated protein potentially involved in ovarian cancer.
  • LH may exert a protective effect against ovarian cancer development and progression.
  • LH might play an inhibitory role in ovarian tumorigenesis.

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...