Differentiated embryonic chondrocyte-expressed gene 1 is associated with hypoxia-inducible factor 1α and Ki67 in human gastric cancer
1 Central Laboratory, Jinan Central Hospital Affiliated to Shandong University, Jinan, 250013,, Shandong Province, China
2 Shandong Province Key Lab of Tumor Target Molecule, Jinan Central Hospital Affiliated to Shandong University, Jinan, 250013,, Shandong Province, China
3 Shandong University School of Medicine, Jinan, 250012,, Shandong Province, China
4 Gynecology and obstetrics, Jinan Central Hospital Affiliated to Shandong University, Jinan, 250013,, Shandong Province, China
Diagnostic Pathology 2013, 8:37 doi:10.1186/1746-1596-8-37Published: 27 February 2013
Gastric cancer is a leading causes of cancer-related deaths ,but the underlying molecular mechanisms of its progression are largely unknown. Differentiated embryonic chondrocyte-expressed gene 1 (DEC1), is an important transcription factor involved in the progression of tumors and has recently been identified to be strongly inducible by hypoxia. Little is known about the contribution of DEC1 to the intracellular hypoxia and proliferation signaling events in gastric cancer.
Immunohistochemistry was used to detect the expression of DEC1, hypoxia-inducible factor 1(HIF-1α) and Ki67 in 173 human gastric cancer samples and adjacent non-tumor tissues samples. The relationship between DEC1, HIF-1α and Ki67 was evaluated.
DEC1 protein was persistently expressed in the nucleus and cytoplasm of gastric cancer tissue. The protein expression of DEC1 and HIF-1α in tumour tissues was 83.8% and 54.3%, respectively, and was significantly higher than that in adjacent normal tissues (83.8% vs 23.7%, P <0.001; 54.3% vs 12.7%, P< 0.001). The expression of DEC1 and HIF-1α was associated with poor histological differentiation. (P < 0. 01). Furthermore, DEC1 level was positively correlated with HIF-1α (P < 0. 01, r=0.290) and Ki67 expression (P < 0. 01, r=0.249).
The upregulation of DEC1 may play an important role in hypoxia regulation and cell proliferation in gastric cancer. The relevant molecular mechanism requires further investigation.
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