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Relative down-regulation of apoptosis and autophagy genes in colorectal cancer


Fen-Pi Chou, Institute of Biochemistry and Biotechnology, Chung Shan Medical University, No. 110, Sec. 1, Jianguo N. Rd., Taichung 402, Taiwan. Tel.: (886) 4 24730022, ext.11676; fax: (886) 4 23248195; e-mail:


Eur J Clin Invest 2010; 41 (1): 84–92


Background  Cancer is often caused by disturbance in the regulation and/or execution of programmed cell death (PCD, including apoptosis and autophagy). Our aim was to investigate these two pathways simultaneously in the same samples to understand further the pathological roles of PCDs in colorectal cancer.

Materials and methods  Real time quantitative PCR (RT-qPCR) array was used to analyse the mRNA levels of 22 apoptosis and autophagy-related genes involved in pro- and anti-action of the pathways in 15 paired (tumour and non-cancerous part) colorectal samples using Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as the reference gene.

Results  GAPDH mRNA content was significantly higher (approximately 4·01 fold) in tumour tissue than that of paired non-cancerous part. The absolute mRNA levels for most of the 22 genes were higher in the tumour tissue also. However, after normalization with GAPDH Ct, the expressions of all the analysed genes were decreased in the tumour tissues, except for damage-regulated autophagy modulator (DRAM). The expression of most of the genes involved in the same pathway was closely correlated to each other in both tumour and non-cancerous tissues, and the correlation of tumour necrosis factor receptor (TNFR) and Akt to other genes in the same pathway was increased in tumour tissues.

Conclusions  The high level expression of GAPDH might reflect the metabolic state of cancer cells, and PCDs were down-regulated in the tumour tissues when metabolic state was taken into consideration. This relative suppression of PCDs in tumour tissue is supposed to be in favour of cancer cell survival.