ARC (apoptosis repressor with caspase recruitment domain) is a novel marker of human colon cancer

Isabelle Mercier, Magalis Vuolo, Jean Francois Jasmin, Christina M. Medina, Mark Williams, John M. Mariadason, Hong Qian, Xiaonan (Nan) Xue, Richard G. Pestell, Michael P. Lisanti, Richard N. Kitsis

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

The ability of cells to escape apoptosis is critical for carcinogenesis as well as resistance to radiation and chemotherapy. ARC (Apoptosis Repressor with CARD (caspase recruitment domain)) is an unusual inhibitor of apoptosis in that it antagonizes both the extrinsic (death receptor) and intrinsic (mitochondrial/ER) apoptosis pathways. ARC is expressed predominantly in terminally differentiated cells such as cardiac and skeletal myocytes and neurons. Recently, however, the abundance of ARC was noted to be markedly increased in the epithelium of primary human breast cancers compared with benign breast tissue and to confer chemo- and radiation-resistance. Whether the induction of ARC is specific to breast cancer or a more general feature of neoplasia remains unknown. In this study, we assessed the abundance and subcellular localization of ARC in 21 human colon cancer cell lines and in 44 primary human colon adenocarcinomas and adjacent benign colonic tissue. ARC was present at high levels in most colon cancer cell lines and in almost all primary colon cancers compared with corresponding controls. Levels of ARC in the cytoplasm were increased in well, moderately, and poorly differentiated cancers compared with benign tissue, while levels of nuclear ARC were increased only in moderately differentiated tumors. Moreover, epithelial cancers of the ovary and cervix exhibited increased ARC abundance compared with controls. These results demonstrate that ARC is a novel marker of human colon cancer and suggest that it may be a general feature of epithelial cancers.

Original languageEnglish (US)
Pages (from-to)1640-1647
Number of pages8
JournalCell Cycle
Volume7
Issue number11
StatePublished - Jun 1 2008

Fingerprint

AIDS-Related Complex
Caspases
Colonic Neoplasms
Apoptosis
Tissue
Cells
Radiation
Death Domain Receptors
Chemotherapy
Neurons
Tumors
Neoplasms
Caspase Activation and Recruitment Domain
Breast Neoplasms
Cell Line
Skeletal Muscle Fibers
Cardiac Myocytes
Uterine Cervical Neoplasms
Ovarian Neoplasms
Colon

Keywords

  • Apoptosis
  • ARC
  • Cervical cancer
  • Colon cancer
  • Epithelial
  • Ovarian cancer

ASJC Scopus subject areas

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Cite this

Mercier, I., Vuolo, M., Jasmin, J. F., Medina, C. M., Williams, M., Mariadason, J. M., ... Kitsis, R. N. (2008). ARC (apoptosis repressor with caspase recruitment domain) is a novel marker of human colon cancer. Cell Cycle, 7(11), 1640-1647.

ARC (apoptosis repressor with caspase recruitment domain) is a novel marker of human colon cancer. / Mercier, Isabelle; Vuolo, Magalis; Jasmin, Jean Francois; Medina, Christina M.; Williams, Mark; Mariadason, John M.; Qian, Hong; Xue, Xiaonan (Nan); Pestell, Richard G.; Lisanti, Michael P.; Kitsis, Richard N.

In: Cell Cycle, Vol. 7, No. 11, 01.06.2008, p. 1640-1647.

Research output: Contribution to journalArticle

Mercier, I, Vuolo, M, Jasmin, JF, Medina, CM, Williams, M, Mariadason, JM, Qian, H, Xue, XN, Pestell, RG, Lisanti, MP & Kitsis, RN 2008, 'ARC (apoptosis repressor with caspase recruitment domain) is a novel marker of human colon cancer', Cell Cycle, vol. 7, no. 11, pp. 1640-1647.
Mercier I, Vuolo M, Jasmin JF, Medina CM, Williams M, Mariadason JM et al. ARC (apoptosis repressor with caspase recruitment domain) is a novel marker of human colon cancer. Cell Cycle. 2008 Jun 1;7(11):1640-1647.
Mercier, Isabelle ; Vuolo, Magalis ; Jasmin, Jean Francois ; Medina, Christina M. ; Williams, Mark ; Mariadason, John M. ; Qian, Hong ; Xue, Xiaonan (Nan) ; Pestell, Richard G. ; Lisanti, Michael P. ; Kitsis, Richard N. / ARC (apoptosis repressor with caspase recruitment domain) is a novel marker of human colon cancer. In: Cell Cycle. 2008 ; Vol. 7, No. 11. pp. 1640-1647.
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