Expressions of Orphan Nuclear Receptor TR3/Nur77 in Chronic Hepatopathy and Its Clinical Significance

Yingling Zeng1, Xiaoguang Ye2, Degui Liao3

  • 1Departments of Preventative Medicine, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, P. R. China.

Journal of Clinical & Experimental Oncology
|September 1, 2017
PubMed
Abstract

Insights

Orphan nuclear receptor TR3 (human)/Nur77 (mouse) is highly expressed in hepatocellular carcinoma (HCC), especially with hepatitis B virus (HBV) infection. This suggests TR3 is a key target in HCC progression and development.

Area of Science:

  • Hepatology
  • Oncology
  • Molecular Biology

Background:

  • Current cancer therapies face challenges like resistance and side effects.
  • Orphan nuclear receptor TR3 (human)/Nur77 (mouse) is a potential therapeutic target.
  • TR3/Nur77 expression correlates with hepatic cancer progression.

Purpose of the Study:

  • To investigate the correlation of TR3/Nur77 expression in hepatocellular carcinoma (HCC) with chronic hepatitis.
  • To analyze TR3/Nur77 expression in HCC, cirrhosis, and chronic hepatitis tissues.
  • To assess the impact of hepatitis B virus (HBV) infection on TR3/Nur77 expression in HCC.

Main Methods:

  • Immunohistochemical staining of TR3/Nur77 in human primary hepatic cancer and para-tumor tissues.
  • Statistical analysis to compare TR3/Nur77 expression rates in HCC, cirrhosis, and chronic hepatitis.
  • Stratification of HCC samples based on HBV infection status (HBV+ and HBV-).

Main Results:

  • TR3/Nur77 positive expression rates were 66.67% in HCC, 30% in cirrhosis, and 20% in chronic hepatitis (p<0.05).
  • TR3/Nur77 expression was significantly higher in HBV-infected HCC (81.25%) compared to non-infected HCC (20%) (p<0.05).

Conclusions:

  • TR3/Nur77 expression is significantly elevated in HCC compared to chronic hepatitis and cirrhosis.
  • HBV infection is associated with higher TR3/Nur77 expression in HCC.
  • TR3/Nur77 plays a crucial role in the progression of chronic hepatitis and the development of HCC.

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