RELT Is Upregulated in Breast Cancer and Induces Death in Breast Cancer Cells

Area of Science:

• Oncology
• Molecular Biology
• Immunology

Background:

• Receptor Expressed in Lymphoid Tissues (RELT) is a member of the TNFRSF superfamily, with paralogs RELL1 and RELL2, collectively known as RELT family members (RELTfms).

Purpose of the Study:

• To investigate the expression and function of RELT in cancer cells.
• To elucidate the mechanism of RELT-mediated cell death.
• To determine the subcellular localization of RELT.

Main Methods:

• Real-time PCR, western blotting, flow cytometry, and immunohistochemistry (IHC) were used to assess RELT expression.
• Apoptosis was evaluated using assays for phosphatidylserine externalization and Caspase-3/7 activation.
• Immunofluorescence and co-immunoprecipitation were employed to study RELT localization and interactions.

Main Results:

• RELT and RELL1 protein expression were significantly elevated in breast and lung cancer cell lines and malignant breast cancer biopsies.
• RELT overexpression induced apoptosis in breast cancer cells, characterized by phosphatidylserine externalization and Caspase-3/7 activation.
• RELT was found to translocate to the nucleus, and its apoptotic function did not require OXSR1 phosphorylation.

Conclusions:

• RELT induces apoptosis in breast cancer cells through a pathway independent of OXSR1 phosphorylation.
• The nuclear localization of RELT is a novel finding requiring further investigation.
• RELT family members show differential expression patterns in cancer, suggesting potential roles in tumorigenesis.