Chong Geng1,2, Qiang Wang2, Peng-Fei Xing3, Min Wang2, Shao-Dong Tong2, Ju-Ying Zhou4. 1. Department of Radiation Oncology, The First Affiliated Hospital of Soochow University, Jiangsu Province, No.188 Shizi street, Suzhou, 215006, China. 2. Department of Radiation Oncology, Xuzhou Cancer Hospital, Xuzhou, 221005, China. 3. Department of Radiotherapy Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China. 4. Department of Radiation Oncology, The First Affiliated Hospital of Soochow University, Jiangsu Province, No.188 Shizi street, Suzhou, 215006, China. zhoujuyingsy@163.com.
Abstract
BACKGROUND: Esophageal cancer was recognized as one of the malignant tumors with poor prognosis. Germ cell associated 2 (GSG2) has been reported to be of great significance in cell growth and tumor formation. This study aimed to investigate the biological function and molecular mechanism of GSG2 in esophageal cancer. METHODS: First, relationship between GSG2 expression and tumor characteristics in esophageal cancer patients was analyzed through immunohistochemical (IHC) staining. MTT assay, flow cytometry, cloning formation assay, wound-healing assay and Transwell assay were used to determine proliferation, apoptosis and migration of esophageal cancer cell with GSG2 knockdown in vitro. Expression of apoptosis related proteins and downstream pathway proteins after GSG2 knockdown were detected through Human Apoptosis Antibody Array and western blot analysis. The GSG2 knockdown function in vivo was explored through a xenograft tumor model. RESULTS: GSG2 was highly expressed in tumor tissues, which has clinical significance in predicting the malignant degree of patients with esophageal cancer. In addition, GSG2 knockdown significantly inhibited a variety of malignant biological behaviors of esophageal cancer cells, such as inhibiting proliferation, reducing colony formation, promoting apoptosis, hindering migration. The decrease of GSG2 expression in esophageal cancer cells can inhibit the xenograft tumor growth. CONCLUSIONS: In conclusion, GSG2 was involved in esophageal cancer progression and development, which may provide an effective molecular target for the treatment of esophageal cancer in the future.
BACKGROUND: Esophageal cancer was recognized as one of the malignant tumors with poor prognosis. Germ cell associated 2 (GSG2) has been reported to be of great significance in cell growth and tumor formation. This study aimed to investigate the biological function and molecular mechanism of GSG2 in esophageal cancer. METHODS: First, relationship between GSG2 expression and tumor characteristics in esophageal cancer patients was analyzed through immunohistochemical (IHC) staining. MTT assay, flow cytometry, cloning formation assay, wound-healing assay and Transwell assay were used to determine proliferation, apoptosis and migration of esophageal cancer cell with GSG2 knockdown in vitro. Expression of apoptosis related proteins and downstream pathway proteins after GSG2 knockdown were detected through Human Apoptosis Antibody Array and western blot analysis. The GSG2 knockdown function in vivo was explored through a xenograft tumor model. RESULTS: GSG2 was highly expressed in tumor tissues, which has clinical significance in predicting the malignant degree of patients with esophageal cancer. In addition, GSG2 knockdown significantly inhibited a variety of malignant biological behaviors of esophageal cancer cells, such as inhibiting proliferation, reducing colony formation, promoting apoptosis, hindering migration. The decrease of GSG2 expression in esophageal cancer cells can inhibit the xenograft tumor growth. CONCLUSIONS: In conclusion, GSG2 was involved in esophageal cancer progression and development, which may provide an effective molecular target for the treatment of esophageal cancer in the future.
Authors: Levent Dizdar; Lisa M Jünemann; Thomas A Werner; Pablo E Verde; Stephan E Baldus; Nikolas H Stoecklein; Wolfram T Knoefel; Andreas Krieg Journal: Oncol Lett Date: 2018-01-09 Impact factor: 2.967