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
AUTHORS (7)
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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CITATIONS (23)
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