Yiyu Qin1, Yang Zhou2, Anxing Ge3, Li Chang4, Haiyan Shi5, Yang Fu6, Qiong Luo7. 1. Clinical Medical College, Jiangsu Vocational College of Medicine, Yancheng, Jiangsu, 224005, PR China. Electronic address: qyy128@163.com. 2. Clinical Medical College, Jiangsu Vocational College of Medicine, Yancheng, Jiangsu, 224005, PR China. Electronic address: 13512205109@163.com. 3. Department of Science and Technology, Jiangsu Vocational College of Medicine, Yancheng, Jiangsu, 224005, PR China. Electronic address: geanxing@163.com. 4. Clinical Medical College, Jiangsu Vocational College of Medicine, Yancheng, Jiangsu, 224005, PR China. Electronic address: clhhyxyjs@163.com. 5. Clinical Medical College, Jiangsu Vocational College of Medicine, Yancheng, Jiangsu, 224005, PR China. Electronic address: 491815948@qq.com. 6. Department of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, PR China. Electronic address: fytougao@126.com. 7. Clinical Medical College, Jiangsu Vocational College of Medicine, Yancheng, Jiangsu, 224005, PR China. Electronic address: nn9520@163.com.
Abstract
BACKGROUND: Gallbladder cancer (GBC) ranks fifth in the most common malignancy of the gastrointestinal tract worldwide. It is reported many small nucleolar RNAs (SNORNs) could regulate the progression of GBC. To identify potential therapeutic targets for GBC, we conducted microarray analysis in GBC tissues and adjacent normal tissues. We found that SNORA21 was downregulated most in gallbladder tumor samples. Therefore, this research aimed to investigate the role of SNORA21 during the tumorigenesis of GBC. METHODS: The differential expression of SNORNs between GBC tissues and para-carcinoma tissues were examined by microarray analysis and that were confirmed by qRT-PCR. Cell proliferation was tested by CCK-8 and immunofluorescence. Cell apoptosis and cell cycle in GBC were detected by flow cytometry. Expression of proteins in GBC cells was measured by Western-blot. Transwell assay was used for testing the cell migration and invasion. Xenograft tumor model was established to verify the effect of SNORA21 overexpression on GBC in vivo. RESULTS: The results revealed that SNORA21 overexpression inhibited the proliferation, migration and invasion of GBC cells. Moreover, overexpression of SNORA21 significantly increased the expression of E-cadherin and decreased the levels of N-cadherin and vimentin. Meanwhile, overexpression of SNORA21 significantly induced apoptosis and G1 arrest of GBC cells. Finally, SNORA21 overexpression significantly suppressed the growth of gallbladder tumors in vivo. CONCLUSION: Overexpression of SNORA21 significantly suppressed the tumorigenesis of GBC in vitro and in vivo, which may serve as a potential novel target for the treatment of GBC.
BACKGROUND: Gallbladder cancer (GBC) ranks fifth in the most common malignancy of the gastrointestinal tract worldwide. It is reported many small nucleolar RNAs (SNORNs) could regulate the progression of GBC. To identify potential therapeutic targets for GBC, we conducted microarray analysis in GBC tissues and adjacent normal tissues. We found that SNORA21 was downregulated most in gallbladder tumor samples. Therefore, this research aimed to investigate the role of SNORA21 during the tumorigenesis of GBC. METHODS: The differential expression of SNORNs between GBC tissues and para-carcinoma tissues were examined by microarray analysis and that were confirmed by qRT-PCR. Cell proliferation was tested by CCK-8 and immunofluorescence. Cell apoptosis and cell cycle in GBC were detected by flow cytometry. Expression of proteins in GBC cells was measured by Western-blot. Transwell assay was used for testing the cell migration and invasion. Xenograft tumor model was established to verify the effect of SNORA21 overexpression on GBC in vivo. RESULTS: The results revealed that SNORA21 overexpression inhibited the proliferation, migration and invasion of GBC cells. Moreover, overexpression of SNORA21 significantly increased the expression of E-cadherin and decreased the levels of N-cadherin and vimentin. Meanwhile, overexpression of SNORA21 significantly induced apoptosis and G1 arrest of GBC cells. Finally, SNORA21 overexpression significantly suppressed the growth of gallbladder tumors in vivo. CONCLUSION: Overexpression of SNORA21 significantly suppressed the tumorigenesis of GBC in vitro and in vivo, which may serve as a potential novel target for the treatment of GBC.