TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells

0301 basic medicine Cancer Research Clinical Biochemistry Pharmaceutical Science Apoptosis Tripartite Motif Proteins Neuroblastoma 2.1 Biological and endogenous factors anzsrc-for: 31 Biological Sciences RNA, Small Interfering Lung Cancer Membrane Potential, Mitochondrial Enzyme Precursors Tumor Lung Cancer anzsrc-for: 3101 Biochemistry and Cell Biology Caspase 2 Mitochondrial Mitochondria 3. Good health DNA-Binding Proteins Gene Expression Regulation, Neoplastic anzsrc-for: 111201 Cancer Cell Biology Cysteine Endopeptidases Organ Specificity anzsrc-for: 0601 Biochemistry and Cell Biology Signal Transduction 570 Ubiquitin-Protein Ligases 610 3101 Biochemistry and Cell Biology Small Interfering Membrane Potential Cell Line anzsrc-for: 1116 Medical Physiology 03 medical and health sciences Rare Diseases Cell Line, Tumor Breast Cancer Humans Pharmacology Biochemistry, medical Neoplastic Original Paper anzsrc-for: 111403 Paediatrics Neurosciences Cell Biology HEK293 Cells Gene Expression Regulation Women's Health RNA 31 Biological Sciences Transcription Factors
DOI: 10.1007/s10495-013-0813-y Publication Date: 2013-02-12T03:59:40Z
ABSTRACT
TRIM16 exhibits tumour suppressor functions by interacting with cytoplasmic vimentin and nuclear E2F1 proteins in neuroblastoma squamous cell carcinoma cells, reducing migration replication. Reduced expression a range of human primary malignant tissues correlates increased potential. also induces apoptosis breast lung cancer unknown mechanisms. Here we show that overexpression (MCF7) (BE(2)-C) but not non-malignant HEK293 cells. procaspase-2 protein levels MCF7 induced caspase-2 activity both BE(2)-C We directly interact cells co-localise Most importantly, the induction is required for to initiate apoptosis. Our data suggest novel mechanism which can promote modulating activity.
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