Te-Sheng Chang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Te-Sheng Chang has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Cheng-Shyong Wu
Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Chiayi 61303, Taiwan
2 shared publications - Chung-Kuang Lu
Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Chiayi 61303, Taiwan
2 shared publications - Kuo-Liang Wei
Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Chiayi 61303, Taiwan
2 shared publications - Ming-Ko Chiang
Department of Life Science, National Chung Cheng University, Chiayi 62102, Taiwan
2 shared publications - Shui-Yi Tung
Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Chiayi 61303, Taiwan
2 shared publications - Yi-Hsing Chen
Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Chiayi 61303, Taiwan
2 shared publications
Latest Publications
- Open Access
- 25 May 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (11) , 4737
Correction: Chang et al. Inhibition of CCAR1, a Coactivator of β-Catenin, Suppresses the Proliferation and Migration of Gastric Cancer Cells. Int. J. Mol. Sci. 2017, 18, 460
- 25 May 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (11) , 4737
Open AccessCorrection: Chang et al. Inhibition of CCAR1, a Coactivator of β-Catenin, Suppresses the Proliferation and Migration of Gastric Cancer Cells. Int. J. Mol. Sci. 2017, 18, 460
- Open Access
- 21 February 2017
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 18 (2) , 460
Inhibition of CCAR1, a Coactivator of β-Catenin, Suppresses the Proliferation and Migration of Gastric Cancer Cells
The aberrant activation of Wnt signaling has been implicated in a variety of human cancers, including gastric cancer. Given the current hypothesis that cancer arises from cancer stem cells (CSCs), targeting the critical signaling pathways that support CSC self-renewal appears to be a useful approach for cancer therapy. Cell cycle and apoptosis regulator 1 (CCAR1) is a transcriptional coactivator which has been shown to be a component of Wnt/β-catenin signaling, and which plays an important role in transcriptional regulation by β-catenin. However, the function and clinical significance of CCAR1 in gastric cancer have not been elucidated. Here, we show that elevated CCAR1 nuclear expression correlates with the occurrence of gastric cancer. In addition, RNAi-mediated CCAR1 reduction not only suppressed the cell growth and increased apoptosis in AGS and MKN28 cells, but also reduced the migration and invasion ability of these cells. Furthermore, an in vivo xenograft assay revealed that the expression level of CCAR1 was critical for tumorigenesis. Our data demonstrates that CCAR1 contributes to carcinogenesis in gastric cancer and is required for the survival of gastric cancer cells. Moreover, CCAR1 may serve as a diagnostic marker and a potential therapeutic target.
- 21 February 2017
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 18 (2) , 460
Open AccessInhibition of CCAR1, a Coactivator of β-Catenin, Suppresses the Proliferation and Migration of Gastric Cancer Cells
The aberrant activation of Wnt signaling has been implicated in a variety of human cancers, including gastric cancer. Given the current hypothesis that cancer arises from cancer stem cells (CSCs), targeting the critical signaling pathways that support CSC self-renewal appears to be a useful approach for cancer therapy. Cell cycle and apoptosis regulator 1 (CCAR1) is a transcriptional coactivator which has been shown to be a component of Wnt/β-catenin signaling, and which plays an important role in transcriptional regulation by β-catenin. However, the function and clinical significance of CCAR1 in gastric cancer have not been elucidated. Here, we show that elevated CCAR1 nuclear expression correlates with the occurrence of gastric cancer. In addition, RNAi-mediated CCAR1 reduction not only suppressed the cell growth and increased apoptosis in AGS and MKN28 cells, but also reduced the migration and invasion ability of these cells. Furthermore, an in vivo xenograft assay revealed that the expression level of CCAR1 was critical for tumorigenesis. Our data demonstrates that CCAR1 contributes to carcinogenesis in gastric cancer and is required for the survival of gastric cancer cells. Moreover, CCAR1 may serve as a diagnostic marker and a potential therapeutic target.