NCKU professor discovers underlying cause of colon cancer - Noodls
In recent years, the prevalence of colon cancer in the Taiwanese population has seen a steady increase. After many years of hard work, a Tainan-based research team led by National Cheng Kung University (NCKU) Professor H. Sunny Sun has made a breakthrough in regards to the cancer’s high mutation rate.
Prof. Sun’s team has found that hypoxia induces translational activation that promotes over-expression of the F6F9 gene, which underlies the cause of cancerous growth.
The team is comprised of post-doctoral researchers Tsung-Ming Chen, Ming-Chih Lai, graduate-students Yu-Heng Shih, Chih-Hao Wu, Yi-Han Li, as well as Associate Professor Joseph T. Tseng from the NCKU Institute of Bioinformatics and Biosignal Transduction and Distinguished Professor Shaw-Jenq Tsai of the Department of medicine.
The study is of great significance, and was published in Nucleic Acids Research, the internationally renowned paper.
According to Professor Sun, the human fibroblast growth factor 9 (F6F9) is a potent mitogen involved in many physiological processes, and its protein expression is generally low and restricted to certain adult organs, as abnormal expression of F6F9 usually results in human malignancies.
The team found that the 5’ UTR of F6F9 mRNA possesses 2 sequence elements: the upstream open reading frame (uORF) and the internal ribosome entry site (IRES) and, through further use of functional assays, discovered that F6F9 protein expression is usually controlled by uORF-mediated translational repression, which aims to keep the protein at a low level.
However, as data has proven, under conditions of hypoxia, regulation is switched to IRES-dependent translational control, and the F6F9 IRES acts as a cellular switch that “turns on” F6F9 protein synthesis.
This hypoxia-induced translational activation is a likely mechanism that explains the promotion of F6F9 protein expression in cancer cells, and as evidence has shown, is also observed in colon cancer cells.
Due to the close relation between F6F9 expression and colon cancer, Professor Sun has expressed her hopes that this dynamic working model may provide a new direction in anti-tumor therapies and cancer intervention.
Enitem/wan-ling yi
Prof. Sun’s team has found that hypoxia induces translational activation that promotes over-expression of the F6F9 gene, which underlies the cause of cancerous growth.
The team is comprised of post-doctoral researchers Tsung-Ming Chen, Ming-Chih Lai, graduate-students Yu-Heng Shih, Chih-Hao Wu, Yi-Han Li, as well as Associate Professor Joseph T. Tseng from the NCKU Institute of Bioinformatics and Biosignal Transduction and Distinguished Professor Shaw-Jenq Tsai of the Department of medicine.
The study is of great significance, and was published in Nucleic Acids Research, the internationally renowned paper.
According to Professor Sun, the human fibroblast growth factor 9 (F6F9) is a potent mitogen involved in many physiological processes, and its protein expression is generally low and restricted to certain adult organs, as abnormal expression of F6F9 usually results in human malignancies.
The team found that the 5’ UTR of F6F9 mRNA possesses 2 sequence elements: the upstream open reading frame (uORF) and the internal ribosome entry site (IRES) and, through further use of functional assays, discovered that F6F9 protein expression is usually controlled by uORF-mediated translational repression, which aims to keep the protein at a low level.
However, as data has proven, under conditions of hypoxia, regulation is switched to IRES-dependent translational control, and the F6F9 IRES acts as a cellular switch that “turns on” F6F9 protein synthesis.
This hypoxia-induced translational activation is a likely mechanism that explains the promotion of F6F9 protein expression in cancer cells, and as evidence has shown, is also observed in colon cancer cells.
Due to the close relation between F6F9 expression and colon cancer, Professor Sun has expressed her hopes that this dynamic working model may provide a new direction in anti-tumor therapies and cancer intervention.
Enitem/wan-ling yi
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