Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest in human endometrioid endometrial adenocarcinoma
Endometrial cancer is the most common gynecologic malignancy, about 80% of which is endometrial endometrioid carcinoma. Dysregulation of spindle assembly checkpoint plays a vital role in endometrial endometrioid carcinoma tumorigenesis and progression. The purpose of this study was to explore how ty...
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| Format: | Article |
| Language: | English |
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SAGE Publishing
2017-07-01
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| Series: | Tumor Biology |
| Online Access: | https://doi.org/10.1177/1010428317712444 |
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| author | Jiamiao Zhang Yan Jiang Yu Zhao Wanxue Wang Yiran Xie Huating Wang Yihua Yang |
| author_facet | Jiamiao Zhang Yan Jiang Yu Zhao Wanxue Wang Yiran Xie Huating Wang Yihua Yang |
| author_sort | Jiamiao Zhang |
| collection | DOAJ |
| description | Endometrial cancer is the most common gynecologic malignancy, about 80% of which is endometrial endometrioid carcinoma. Dysregulation of spindle assembly checkpoint plays a vital role in endometrial endometrioid carcinoma tumorigenesis and progression. The purpose of this study was to explore how tyrosine threonine kinase, a spindle assembly checkpoint–related protein, promotes the endometrial endometrioid carcinoma progression. We found that both messenger RNA and protein levels of tyrosine threonine kinase in endometrial endometrioid carcinoma tissues are higher than those in normal endometrial tissues, and its expression is associated with tumor stages. Genetic depletion of tyrosine threonine kinase by RNA interference in two endometrial endometrioid carcinoma cell lines significantly inhibits cell proliferation and induces apoptosis. Mechanistically, depletion of tyrosine threonine kinase induces G2/M cell cycle arrest and triggers caspase-dependent cell apoptosis. Collectively, tyrosine threonine kinase is significantly upregulated in endometrial endometrioid carcinoma, and downregulation of tyrosine threonine kinase can suppress endometrial endometrioid carcinoma cell proliferation and promote apoptosis via G2/M cell cycle arrest. Our study demonstrates that tyrosine threonine kinase can be a potential therapeutic target for endometrial endometrioid carcinoma treatment. |
| format | Article |
| id | doaj-art-fb760154a0444870be71b3b0ada2a263 |
| institution | DOAJ |
| issn | 1423-0380 |
| language | English |
| publishDate | 2017-07-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Tumor Biology |
| spelling | doaj-art-fb760154a0444870be71b3b0ada2a2632025-08-20T02:49:16ZengSAGE PublishingTumor Biology1423-03802017-07-013910.1177/1010428317712444Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest in human endometrioid endometrial adenocarcinomaJiamiao Zhang0Yan Jiang1Yu Zhao2Wanxue Wang3Yiran Xie4Huating Wang5Yihua Yang6Reproductive Medicine Center of the Affiliated Hospital, Guilin Medical University, Guilin, ChinaDepartment of Obstetrics and Gynecology of The Zhong Kang Hospital in Zhengzhou, Zhengzhou, ChinaLi Ka Shing Institute of Health Sciences and Prince of Wales Hospital, Chinese University of Hong Kong, Hong KongReproductive Medicine Center of the Affiliated Hospital, Guilin Medical University, Guilin, ChinaReproductive Medicine Center of the Affiliated Hospital, Guilin Medical University, Guilin, ChinaLi Ka Shing Institute of Health Sciences and Prince of Wales Hospital, Chinese University of Hong Kong, Hong KongReproductive Medicine Center of the Affiliated Hospital, Guilin Medical University, Guilin, ChinaEndometrial cancer is the most common gynecologic malignancy, about 80% of which is endometrial endometrioid carcinoma. Dysregulation of spindle assembly checkpoint plays a vital role in endometrial endometrioid carcinoma tumorigenesis and progression. The purpose of this study was to explore how tyrosine threonine kinase, a spindle assembly checkpoint–related protein, promotes the endometrial endometrioid carcinoma progression. We found that both messenger RNA and protein levels of tyrosine threonine kinase in endometrial endometrioid carcinoma tissues are higher than those in normal endometrial tissues, and its expression is associated with tumor stages. Genetic depletion of tyrosine threonine kinase by RNA interference in two endometrial endometrioid carcinoma cell lines significantly inhibits cell proliferation and induces apoptosis. Mechanistically, depletion of tyrosine threonine kinase induces G2/M cell cycle arrest and triggers caspase-dependent cell apoptosis. Collectively, tyrosine threonine kinase is significantly upregulated in endometrial endometrioid carcinoma, and downregulation of tyrosine threonine kinase can suppress endometrial endometrioid carcinoma cell proliferation and promote apoptosis via G2/M cell cycle arrest. Our study demonstrates that tyrosine threonine kinase can be a potential therapeutic target for endometrial endometrioid carcinoma treatment.https://doi.org/10.1177/1010428317712444 |
| spellingShingle | Jiamiao Zhang Yan Jiang Yu Zhao Wanxue Wang Yiran Xie Huating Wang Yihua Yang Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest in human endometrioid endometrial adenocarcinoma Tumor Biology |
| title | Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest in human endometrioid endometrial adenocarcinoma |
| title_full | Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest in human endometrioid endometrial adenocarcinoma |
| title_fullStr | Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest in human endometrioid endometrial adenocarcinoma |
| title_full_unstemmed | Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest in human endometrioid endometrial adenocarcinoma |
| title_short | Downregulation of tyrosine threonine kinase inhibits tumor growth via G2/M arrest in human endometrioid endometrial adenocarcinoma |
| title_sort | downregulation of tyrosine threonine kinase inhibits tumor growth via g2 m arrest in human endometrioid endometrial adenocarcinoma |
| url | https://doi.org/10.1177/1010428317712444 |
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