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

Background: Receptor Expressed in Lymphoid Tissues (RELT) is a TNFRSF member that has two paralogs, RELL1 and RELL2; the three proteins are collectively referred to as RELT family members (RELTfms).

Methods: We sought to evaluate RELT expression in cancerous cells by using real-time PCR, western blotting, flow cytometry, and immunohistochemistry (IHC). The mechanism of RELT-induced cell death was assessed by western blotting, flow cytometry, luciferase assays, and morphology staining.

Depicting Biomarkers for HER2-Inhibitor Resistance: Implication for Therapy in HER2-Positive Breast Cancer.

HER2 (human epidermal growth factor receptor 2) is highly expressed in a variety of cancers, including breast, lung, gastric, and pancreatic cancers. Its amplification is linked to poor clinical outcomes. At the genetic level, HER2 is encoded by the ERBB2 gene (v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 2), which is frequently mutated or amplified in cancers, thus spurring extensive research into HER2 modulation and inhibition as viable anti-cancer strategies.

Myocardial Infarction Suppresses Protein Synthesis and Causes Decoupling of Transcription and Translation.

Gene expression involves transcription, translation, and mRNA and protein degradation. Advanced RNA sequencing measures mRNA levels for cell state assessment, but mRNA level does not fully reflect protein level. Identifying heart cell proteomes and their stress response is crucial.

The RELT Family of Proteins: An Increasing Awareness of Their Importance for Cancer, the Immune System, and Development.

This review highlights Receptor Expressed in Lymphoid Tissues (RELT), a Tumor Necrosis Factor Superfamily member, and its two paralogs, RELL1 and RELL2. Collectively, these three proteins are referred to as RELTfms and have gained much interest in recent years due to their association with cancer and other human diseases. A thorough knowledge of their physiological functions, including the ligand for RELT, is lacking, yet emerging evidence implicates RELTfms in a variety of processes including cytokine signaling and pathways that either promote cell death or survival.