Shujun Li1, Xuebo Qin2, Airong Cui3, Wenxin Wu3, Libing Ren4, Xiaolu Wang1. 1. Cancer Center, The Second Hospital of Hebei Medical University Shijiazhuang, China. 2. Department of Thoracic Surgery, Hebei Chest Hospital Shijiazhuang, China. 3. Department of Pathology, Hebei Chest Hospital Shijiazhuang, China. 4. Department of Thoracic Surgery, Handan Central Hospital Handan, China.
Abstract
PURPOSE: KLF17 belongs to the Sp/KLF zinc-finger protein family as a regulator in tumor development. However, its expression and biologic function has remained unclear in EC. METHODS: The esophageal carcinoma tissue samples and adjacent normal tissues were obtained from the Second Hospital of Hebei Medical University. Immunohistochemistry, Western blot, and transfection were applied to evaluate the expression and clinical significance of KLF17 in esophageal cancer. RESULTS: In this study, we showed that KLF17 was overexpressed in esophageal normal samples compared to the cancer. Moreover, KLF17 was upregulated at lymph node non-metastatic cancer tissues when compared to metastatic cancer tissues. KLF17 overexpression decreased EC cell proliferation, migration and invasion ability. In contrast, the knockdown of KLF17 increased EC cell proliferation, migration and invasion ability. CONCLUSION: These results suggest that KLF17 inhibits tumor development and may serve as a potential therapeutic target.
PURPOSE:KLF17 belongs to the Sp/KLF zinc-finger protein family as a regulator in tumor development. However, its expression and biologic function has remained unclear in EC. METHODS: The esophageal carcinoma tissue samples and adjacent normal tissues were obtained from the Second Hospital of Hebei Medical University. Immunohistochemistry, Western blot, and transfection were applied to evaluate the expression and clinical significance of KLF17 in esophageal cancer. RESULTS: In this study, we showed that KLF17 was overexpressed in esophageal normal samples compared to the cancer. Moreover, KLF17 was upregulated at lymph node non-metastatic cancer tissues when compared to metastatic cancer tissues. KLF17 overexpression decreased EC cell proliferation, migration and invasion ability. In contrast, the knockdown of KLF17 increased EC cell proliferation, migration and invasion ability. CONCLUSION: These results suggest that KLF17 inhibits tumor development and may serve as a potential therapeutic target.
Authors: Amr M Ghaleb; Mandayam O Nandan; Sengthong Chanchevalap; W Brian Dalton; Irfan M Hisamuddin; Vincent W Yang Journal: Cell Res Date: 2005-02 Impact factor: 25.617
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