Jing Liu1, Ying Zuo2, Gui-Mei Qu1, Xiao Song3, Zhong-Hui Liu4, Ting-Guo Zhang5, Zhu-Hua Zheng6, Hong-Kun Wang7. 1. Department of Pathology, Affiliated Yantai Yuhuangding Hospital, Medical College of Qingdao University, Yantai, China. 2. Department of Gynecology, Affiliated Yantai Yuhuangding Hospital, Medical College of Qingdao University, Yantai, China. 3. Department of Pathology, People's Hospital of Rong cheng, Weihai, China. 4. Department of Pathology, Yantai Muping District Traditional Chinese Medicine Hospital, Yantai, China. 5. Department of Pathology, School of Medicine, Shandong University, Jinan, Shandong, China. 6. Department of Pediatrics, Traditional Chinese Medicine Hospital of Rushan, Weihai, China. 7. Department of Gynaecology and Obstetrics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. annie_coco@163.com.
Abstract
BACKGROUND: The molecular pathogenesis of endometrial cancer is not completely understood. CypB upregulated in many cancers, however, its role in endometrial carcinoma has not been studied. Here, we determine the effect of CypB on the growth of endometrial cancer. METHODS: In this study, we examined the expression of CypB in endometrial cancer tissues using immunohistochemistry. CypB silenced in HEC-1-B cell line by shRNA. CCK-8, colony formation assays, wound healing assays, and transwell analysis were performed to assess its effect on tumor cell proliferation and metastasis. Furthermore, microarray analysis was carried out to compare the global mRNA expression profile between the HEC-1-B and CypB-silenced HEC-1-B cells. Gene ontology and KEGG pathway enrichment analysis were performed to determine the potential function of differentially expressed genes related to CypB. RESULTS: We found that CypB was upregulated in endometrial cancer, inhibit CypB expression could significantly suppress cell proliferation, metastasis, and migration. We identified 1536 differentially expressed genes related to CypB (onefold change, p < 0.05), among which 652 genes were upregulated and 884 genes were downregulated. The genes with significant difference in top were mainly enriched in the cell cycle, glycosphingolipid biosynthesis, adherens junctions, and metabolism pathways. CONCLUSION: The results of our study suggest that CypB may serve as a novel regulator of endometrial cell proliferation and metastasis, thus representing a novel target for gene-targeted endometrial therapy. TRIAL REGISTRATION: YLYLLS [2018] 008. Registered 27 November 2017.
BACKGROUND: The molecular pathogenesis of endometrial cancer is not completely understood. CypB upregulated in many cancers, however, its role in endometrial carcinoma has not been studied. Here, we determine the effect of CypB on the growth of endometrial cancer. METHODS: In this study, we examined the expression of CypB in endometrial cancer tissues using immunohistochemistry. CypB silenced in HEC-1-B cell line by shRNA. CCK-8, colony formation assays, wound healing assays, and transwell analysis were performed to assess its effect on tumor cell proliferation and metastasis. Furthermore, microarray analysis was carried out to compare the global mRNA expression profile between the HEC-1-B and CypB-silenced HEC-1-B cells. Gene ontology and KEGG pathway enrichment analysis were performed to determine the potential function of differentially expressed genes related to CypB. RESULTS: We found that CypB was upregulated in endometrial cancer, inhibit CypB expression could significantly suppress cell proliferation, metastasis, and migration. We identified 1536 differentially expressed genes related to CypB (onefold change, p < 0.05), among which 652 genes were upregulated and 884 genes were downregulated. The genes with significant difference in top were mainly enriched in the cell cycle, glycosphingolipid biosynthesis, adherens junctions, and metabolism pathways. CONCLUSION: The results of our study suggest that CypB may serve as a novel regulator of endometrial cell proliferation and metastasis, thus representing a novel target for gene-targeted endometrial therapy. TRIAL REGISTRATION: YLYLLS [2018] 008. Registered 27 November 2017.
Authors: A Yeramian; G Moreno-Bueno; X Dolcet; L Catasus; M Abal; E Colas; J Reventos; J Palacios; J Prat; X Matias-Guiu Journal: Oncogene Date: 2012-03-19 Impact factor: 9.867
Authors: M Carpentier; L Descamps; F Allain; A Denys; S Durieux; L Fenart; C Kieda; R Cecchelli; G Spik Journal: J Neurochem Date: 1999-07 Impact factor: 5.372
Authors: Sebastian Daum; Michael Schumann; Sebastian Mathea; Tobias Aumüller; Molly A Balsley; Stephanie L Constant; Boris Féaux de Lacroix; Fabian Kruska; Manfred Braun; Cordelia Schiene-Fischer Journal: Biochemistry Date: 2009-07-07 Impact factor: 3.162
Authors: Kyu Jin Choi; Yu Ji Piao; Min Jin Lim; Jin Hwan Kim; Joohun Ha; Wonchae Choe; Sung Soo Kim Journal: Cancer Res Date: 2007-04-15 Impact factor: 12.701
Authors: Andrzej P Wojcieszynski; Craig R Hullett; Erin E Medlin; Neil K Taunk; Jacob E Shabason; Jeffrey V Brower; Shuai Chen; Justin E Bekelman; Lisa M Barroilhet; Kristin A Bradley Journal: Brachytherapy Date: 2018-04-22 Impact factor: 2.362
Authors: Peter A Sanderson; Hilary O D Critchley; Alistair R W Williams; Mark J Arends; Philippa T K Saunders Journal: Hum Reprod Update Date: 2017-03-01 Impact factor: 15.610
Authors: Naveena Singh; Lynn Hirschowitz; Richard Zaino; Isabel Alvarado-Cabrero; Maire A Duggan; Rouba Ali-Fehmi; Elizabeth Euscher; Jonathan L Hecht; Lars-Christian Horn; Olga Ioffe; Xavier Matias-Guiu; W Glenn McCluggage; Yoshiki Mikami; Jaume Ordi; Vinita Parkash; M Ruhul Quddus; Charles M Quick; Annette Staebler; Charles Zaloudek; Marisa Nucci; Anais Malpica; Esther Oliva Journal: Int J Gynecol Pathol Date: 2019-01 Impact factor: 2.762
Authors: Vicky Makker; Angela K Green; Robert M Wenham; David Mutch; Brittany Davidson; David Scott Miller Journal: Gynecol Oncol Res Pract Date: 2017-12-02