Faculty Collaboration Database

The helix-loop-helix protein Id2 is expressed differentially and induced by myc in T-cell lymphomas. Cancer 2008 Feb 01;112(3):552-61

Date

12/19/2007

Pubmed ID

18085637

DOI

10.1002/cncr.23196

Scopus ID

2-s2.0-38749093745 (requires institutional sign-in at Scopus site)   19 Citations

Abstract

BACKGROUND: Inhibitor of DNA binding 2 (Id2), a helix-loop-helix protein of the inhibitor of differentiation (ID) family, is involved in hematopoiesis, mainly through interaction with the E-family of transcription factors. Recent studies have shown that Id2 is overexpressed in some types of B-cell lymphoma, including classical Hodgkin lymphoma. The authors of the current study hypothesized that Id2 also is overexpressed in T-cell lymphomas.

METHODS: By using reverse-transcriptase polymerase chain reaction (RT-PCR) and Western blot analyses, high Id2 messenger RNA (mRNA) and protein levels, respectively, were detected in all 4 T-cell anaplastic large cell lymphoma (ALCL) cell lines that were tested.

RESULTS: Immunohistochemistry results indicated that Id2 was expressed strongly in 21 of 27 (78%) ALCL tumors (79% anaplastic lymphoma kinase [ALK]-negative and 75% ALK-positive), in 5 of 10 (50%) extranodal natural killer/T (NK/T)-cell lymphomas of the nasal type, in 2 of 8 (25%) cutaneous ALCLs, in 2 of 9 (22%) enteropathy type T-cell lymphomas, in 1 of 5 (20%) peripheral T-cell lymphomas not otherwise specified, and in 1 of 8 (13%) T-cell prolymphocytic leukemias. Other types of T-cell lymphoma were negative for Id2. Because it is known that myc is expressed in ALCL, myc was inhibited selectively in 2 ALCL cell lines, resulting in a concentration-dependent decrease in Id2 mRNA and protein levels. Conversely, forced expression of myc in HEK 293T cells using an myc/green fluorescent protein adenoviral vector resulted in Id2 up-regulation.

CONCLUSIONS: Taken together, the current data suggest that Id2 commonly is overexpressed in highly proliferative T-cell lymphomas, and its expression may result from transcriptional activation of myc in these tumors.

Author List

Cotta CV, Leventaki V, Atsaves V, Vidaki A, Schlette E, Jones D, Medeiros LJ, Rassidakis GZ

MESH terms used to index this publication - Major topics in bold

Cell Line, Tumor
Cell Proliferation
Gene Expression Regulation, Neoplastic
Hodgkin Disease
Humans
Inhibitor of Differentiation Protein 2
Lymphoma, Large-Cell, Anaplastic
Lymphoma, Non-Hodgkin
Lymphoma, T-Cell
Lymphomatoid Papulosis
Proto-Oncogene Proteins c-myc
RNA, Messenger
Skin Neoplasms
Up-Regulation