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

Patrick Y. Kim, Aldwin Suryo Rahmanto, Owen Tan, Murray D. Norris, Michelle Haber, Glenn M. Marshall, Belamy B. Cheung

Research output: Contribution to journalArticleResearchpeer-review

Abstract

TRIM16 exhibits tumour suppressor functions by interacting with cytoplasmic vimentin and nuclear E2F1 proteins in neuroblastoma and squamous cell carcinoma cells, reducing cell migration and replication. Reduced TRIM16 expression in a range of human primary malignant tissues correlates with increased malignant potential. TRIM16 also induces apoptosis in breast and lung cancer cells, by unknown mechanisms. Here we show that overexpression of TRIM16 induces apoptosis in human breast cancer (MCF7) and neuroblastoma (BE(2)-C) cells, but not in non-malignant HEK293 cells. TRIM16 increased procaspase-2 protein levels in MCF7 and induced caspase-2 activity in both MCF7 and BE(2)-C cells. We show that TRIM16 and caspase-2 proteins directly interact in both MCF7 and BE(2)-C cells and co-localise in MCF7 cells. Most importantly, the induction of caspase-2 activity is required for TRIM16 to initiate apoptosis. Our data suggest a novel mechanism by which TRIM16 can promote apoptosis by directly modulating caspase-2 activity.

LanguageEnglish
Pages639-651
Number of pages13
JournalApoptosis
Volume18
Issue number5
DOIs
Publication statusPublished - 1 May 2013
Externally publishedYes

Fingerprint

Caspase 2
Chemical activation
Cells
Apoptosis
Neoplasms
Neuroblastoma
Breast Neoplasms
HEK293 Cells
MCF-7 Cells
Vimentin
Nuclear Proteins
Cell Movement
Tumors
Squamous Cell Carcinoma
Lung Neoplasms
Proteins
Tissue

Bibliographical note

Copyright The Author(s) 2013. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

Keywords

  • Apoptosis
  • Caspase-2
  • Cytochrome c
  • Mitochondrial depolarisation
  • TRIM16

Cite this

Kim, P. Y., Rahmanto, A. S., Tan, O., Norris, M. D., Haber, M., Marshall, G. M., & Cheung, B. B. (2013). TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells. Apoptosis, 18(5), 639-651. https://doi.org/10.1007/s10495-013-0813-y
Kim, Patrick Y. ; Rahmanto, Aldwin Suryo ; Tan, Owen ; Norris, Murray D. ; Haber, Michelle ; Marshall, Glenn M. ; Cheung, Belamy B. / TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells. In: Apoptosis. 2013 ; Vol. 18, No. 5. pp. 639-651.
@article{4515779a0c4a400889ec92c379ddbada,
title = "TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells",
abstract = "TRIM16 exhibits tumour suppressor functions by interacting with cytoplasmic vimentin and nuclear E2F1 proteins in neuroblastoma and squamous cell carcinoma cells, reducing cell migration and replication. Reduced TRIM16 expression in a range of human primary malignant tissues correlates with increased malignant potential. TRIM16 also induces apoptosis in breast and lung cancer cells, by unknown mechanisms. Here we show that overexpression of TRIM16 induces apoptosis in human breast cancer (MCF7) and neuroblastoma (BE(2)-C) cells, but not in non-malignant HEK293 cells. TRIM16 increased procaspase-2 protein levels in MCF7 and induced caspase-2 activity in both MCF7 and BE(2)-C cells. We show that TRIM16 and caspase-2 proteins directly interact in both MCF7 and BE(2)-C cells and co-localise in MCF7 cells. Most importantly, the induction of caspase-2 activity is required for TRIM16 to initiate apoptosis. Our data suggest a novel mechanism by which TRIM16 can promote apoptosis by directly modulating caspase-2 activity.",
keywords = "Apoptosis, Caspase-2, Cytochrome c, Mitochondrial depolarisation, TRIM16",
author = "Kim, {Patrick Y.} and Rahmanto, {Aldwin Suryo} and Owen Tan and Norris, {Murray D.} and Michelle Haber and Marshall, {Glenn M.} and Cheung, {Belamy B.}",
note = "Copyright The Author(s) 2013. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.",
year = "2013",
month = "5",
day = "1",
doi = "10.1007/s10495-013-0813-y",
language = "English",
volume = "18",
pages = "639--651",
journal = "Apoptosis",
issn = "1360-8185",
publisher = "Springer, Springer Nature",
number = "5",

}

Kim, PY, Rahmanto, AS, Tan, O, Norris, MD, Haber, M, Marshall, GM & Cheung, BB 2013, 'TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells', Apoptosis, vol. 18, no. 5, pp. 639-651. https://doi.org/10.1007/s10495-013-0813-y

TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells. / Kim, Patrick Y.; Rahmanto, Aldwin Suryo; Tan, Owen; Norris, Murray D.; Haber, Michelle; Marshall, Glenn M.; Cheung, Belamy B.

In: Apoptosis, Vol. 18, No. 5, 01.05.2013, p. 639-651.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells

AU - Kim, Patrick Y.

AU - Rahmanto, Aldwin Suryo

AU - Tan, Owen

AU - Norris, Murray D.

AU - Haber, Michelle

AU - Marshall, Glenn M.

AU - Cheung, Belamy B.

N1 - Copyright The Author(s) 2013. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

PY - 2013/5/1

Y1 - 2013/5/1

N2 - TRIM16 exhibits tumour suppressor functions by interacting with cytoplasmic vimentin and nuclear E2F1 proteins in neuroblastoma and squamous cell carcinoma cells, reducing cell migration and replication. Reduced TRIM16 expression in a range of human primary malignant tissues correlates with increased malignant potential. TRIM16 also induces apoptosis in breast and lung cancer cells, by unknown mechanisms. Here we show that overexpression of TRIM16 induces apoptosis in human breast cancer (MCF7) and neuroblastoma (BE(2)-C) cells, but not in non-malignant HEK293 cells. TRIM16 increased procaspase-2 protein levels in MCF7 and induced caspase-2 activity in both MCF7 and BE(2)-C cells. We show that TRIM16 and caspase-2 proteins directly interact in both MCF7 and BE(2)-C cells and co-localise in MCF7 cells. Most importantly, the induction of caspase-2 activity is required for TRIM16 to initiate apoptosis. Our data suggest a novel mechanism by which TRIM16 can promote apoptosis by directly modulating caspase-2 activity.

AB - TRIM16 exhibits tumour suppressor functions by interacting with cytoplasmic vimentin and nuclear E2F1 proteins in neuroblastoma and squamous cell carcinoma cells, reducing cell migration and replication. Reduced TRIM16 expression in a range of human primary malignant tissues correlates with increased malignant potential. TRIM16 also induces apoptosis in breast and lung cancer cells, by unknown mechanisms. Here we show that overexpression of TRIM16 induces apoptosis in human breast cancer (MCF7) and neuroblastoma (BE(2)-C) cells, but not in non-malignant HEK293 cells. TRIM16 increased procaspase-2 protein levels in MCF7 and induced caspase-2 activity in both MCF7 and BE(2)-C cells. We show that TRIM16 and caspase-2 proteins directly interact in both MCF7 and BE(2)-C cells and co-localise in MCF7 cells. Most importantly, the induction of caspase-2 activity is required for TRIM16 to initiate apoptosis. Our data suggest a novel mechanism by which TRIM16 can promote apoptosis by directly modulating caspase-2 activity.

KW - Apoptosis

KW - Caspase-2

KW - Cytochrome c

KW - Mitochondrial depolarisation

KW - TRIM16

UR - http://www.scopus.com/inward/record.url?scp=84876067041&partnerID=8YFLogxK

U2 - 10.1007/s10495-013-0813-y

DO - 10.1007/s10495-013-0813-y

M3 - Article

VL - 18

SP - 639

EP - 651

JO - Apoptosis

T2 - Apoptosis

JF - Apoptosis

SN - 1360-8185

IS - 5

ER -