Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

NIOSHTIC-2 Publications Search

Search Results

Translation elongation factor 1A2 (TEF1A2) is a tumor marker and an inhibitor of cadmium-induced apoptosis.

Joseph-P; O'Kernick-CM; Othumpangar-S
Proceedings of the American Association for Cancer Research (AACR) 95th Annual Meeting, March 27-31 2004. Philadelphia, PA: American Association for Cancer Research, 2004 Mar; 45:209
Translation factors are essential for cells to synthesize proteins, and their aberrant expression may result in pathological conditions including cancer. Certain translation factors, for example translation elongation factor-1A2 (TEF1A2), have been found overexpressed in cancer samples compared to normal control samples. It is also known that TEF1A2 is oncogenic and its overexpression can result in cell transformation and tumorigenesis. Presently, we have investigated the expression profile of TEF1A2 using a panel of human cancer cell lines and tumor tissues. Up to a 2000-fold overexpression of TEF1A2 was detected in 90% (nine out of 10) of the cancer cell lines derived from various human tissues compared to their corresponding controls. Similarly, at least a two-fold overexpression of TEF1A2 was noticed in approximately 30% of the human cancer tissue samples (colon, lungs, ovary, kidney and rectum) that were represented on a cancer profiling array (BD Biosciences, Palo Alto, CA) consisting of 241 paired cDNA samples generated from cancer/non-cancer tissues. Since TEF1A2 overexpression has previously been shown to be oncogenic, we have further investigated its role in apoptosis as a potential mechanism responsible for its oncogenic function. Transgenic CHO cells permanently overexpressing TEF1A2 were developed and used to investigate the role of TEF1A2 in apoptosis induced by cadmium - a well-known human chemical carcinogen. Exposure of CHO cells to 2.5 and 10 um cadmium chloride for 24-hours resulted in significant apoptosis in all cell lines at 24- and 48-hours following the exposure. However, the cadmium-induced apoptosis was significantly lower in the transgenic CHO cells permanently overexpressing TEF1A2 compared with the vector-alone transfected control cells. Collectively, these results indicated that: 1) TEFA12 is significantly overexpressed in human tumor cell lines and tumor tissue samples, 2) the cellular expression level of TEF1A2 may be used as a tumor marker, and 3) the anti-apoptotic role of TEF1A2 may potentially be responsible for its oncogenic function.
Cadmium-compounds; Cancer; Sampling-methods; Sampling; Cell-transformation; Tumorigenesis; Carcinogens; Exposure-levels; Oncogenesis
Publication Date
Document Type
Conference/Symposia Proceedings
Fiscal Year
NTIS Accession No.
NTIS Price
NIOSH Division
Priority Area
Research Tools and Approaches: Cancer Research Methods
Source Name
Proceedings of the American Association for Cancer Research (AACR) 95th Annual Meeting, March 27-31 2004