Differential cellular localization of CELSR2 and ING4 and correlations with hormone receptor status in breast cancer

Liejun Jiang1, Xiliu Zhang2, Chenglin Xiang3

  • 1Department of Laboratory Medicine, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, China.

Insights

The study found that both CELSR2 and ING4 show increased cytoplasmic expression in breast tumors compared to normal cells. ING4 cytoplasmic expression was linked to HER2 positivity in breast cancer.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Pathology

Background:

  • The roles of CELSR2 (a potential contact-mediated communication receptor) and ING4 (a tumor suppressor) in cancer are not fully understood.
  • Investigating their expression patterns in breast cancer is crucial for understanding their involvement in tumorigenesis.

Purpose of the Study:

  • To analyze and compare the expression and cellular localization of CELSR2 and ING4 in breast tumors versus benign epithelial cells.
  • To correlate their expression status with key breast cancer biomarkers: HER2, ER, and PR.

Main Methods:

  • Immunohistochemistry was employed to detect and quantify CELSR2 and ING4 protein levels.
  • Differential cellular localization (cytoplasmic vs. nuclear) was assessed in both tumor and benign tissues.
  • Expression data were correlated with HER2, ER, and PR status.

Main Results:

  • Both CELSR2 and ING4 exhibited significantly stronger cytoplasmic expression in tumors than in benign cells.
  • Conversely, nuclear expression of both markers was significantly higher in benign cells compared to tumors.
  • Cytoplasmic ING4 expression was associated with HER2 positivity in breast tumors.
  • No correlation was found between CELSR2 expression and HER2, ER, or PR status.

Conclusions:

  • Increased cytoplasmic localization of CELSR2 and ING4 in breast cancer cells suggests a potential role in mammary neoplasia pathogenesis.
  • ING4's association with HER2 positivity warrants further investigation into its specific role in HER2-positive breast cancers.

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