Correlation of epigenetic aberrance with STAT3 signaling pathway in gastric carcinogenesis

Fuli Gao1, Ying Lv, Yinxin Zhu

  • 1Department of Gastroenterology, The Drum Tower Hospital Affiliated to Medical School of Nanjing University, No. 321 Zhongshan Road, Nanjing 210008, People's Republic of China.

Abstract

Insights

STAT3 signaling pathway activation correlates with epigenetic changes in gastric cancer development. This study investigated the relationship between pSTAT3 and key epigenetic enzymes (DNMT1, HDAC1, EZH2) in gastrocarcinogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • STAT3 signaling is implicated in tumorigenesis and epigenetic regulation.
  • Key epigenetic enzymes like DNMTs, HDACs, and HMTs are potentially regulated by STAT3.
  • The specific role of STAT3 in gastrocarcinogenesis-related epigenetic aberrance remains unexplored.

Purpose of the Study:

  • To investigate the interrelationship between the STAT3 signaling pathway and epigenetic aberrance in gastric cancer.
  • To analyze the expression patterns of pSTAT3 and specific epigenetic enzymes during gastric carcinogenesis.

Main Methods:

  • Immunohistochemistry was used to assess protein expression of pSTAT3, DNMT1, HDAC1, and EZH2.
  • 153 gastric tissue specimens were analyzed, spanning normal epithelium to advanced gastric cancer.
  • Correlations between protein expressions and clinicopathological factors were examined.

Main Results:

  • Expressions of pSTAT3, DNMT1, HDAC1, and EZH2 increased with gastric cancer progression.
  • pSTAT3 expression strongly correlated with DNMT1, but not HDAC1 or EZH2, across all groups.
  • Specific correlations were observed between pSTAT3 and DNMT1/EZH2 in different stages of gastric lesions.
  • STAT3 and epigenetic enzyme expressions showed associations with clinicopathological factors like T staging, gender, and Lauren classification.

Conclusions:

  • STAT3 signaling pathway activation is potentially linked to epigenetic aberrance in gastric cancer.
  • These findings suggest a role for STAT3 in modulating epigenetic modifications during gastrocarcinogenesis.

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