Search Results
You are looking at 1 - 2 of 2 items for
- Author: Xi Wei x
- Refine by access: All content x
Search for other papers by Xianhui Ruan in
Google Scholar
PubMed
Search for other papers by Xianle Shi in
Google Scholar
PubMed
Search for other papers by Qiman Dong in
Google Scholar
PubMed
Search for other papers by Yang Yu in
Google Scholar
PubMed
Search for other papers by Xiukun Hou in
Google Scholar
PubMed
Search for other papers by Xinhao Song in
Google Scholar
PubMed
Search for other papers by Xi Wei in
Google Scholar
PubMed
Search for other papers by Lingyi Chen in
Google Scholar
PubMed
Search for other papers by Ming Gao in
Google Scholar
PubMed
There is no effective treatment for patients with poorly differentiated papillary thyroid cancer or anaplastic thyroid cancer (ATC). Anlotinib, a multi-kinase inhibitor, has already shown antitumor effects in various types of carcinoma in a phase I clinical trial. In this study, we aimed to better understand the effect and efficacy of anlotinib against thyroid carcinoma cells in vitro and in vivo. We found that anlotinib inhibits the cell viability of papillary thyroid cancer and ATC cell lines, likely due to abnormal spindle assembly, G2/M arrest, and activation of TP53 upon anlotinib treatment. Moreover, anlotinib suppresses the migration of thyroid cancer cells in vitro and the growth of xenograft thyroid tumors in mice. Our data demonstrate that anlotinib has significant anticancer activity in thyroid cancer, and potentially offers an effective therapeutic strategy for patients of advanced thyroid cancer type.
Search for other papers by Xi Wei in
Google Scholar
PubMed
Department of Radiotherapy and Oncology, the Second Affiliated Hospital of Soochow University, Suzhou, China
Search for other papers by Shang Cai in
Google Scholar
PubMed
Search for other papers by Rebecca J Boohaker in
Google Scholar
PubMed
Search for other papers by Joshua Fried in
Google Scholar
PubMed
Search for other papers by Ying Li in
Google Scholar
PubMed
Search for other papers by Linfei Hu in
Google Scholar
PubMed
Search for other papers by Yi Pan in
Google Scholar
PubMed
Search for other papers by Ruifen Cheng in
Google Scholar
PubMed
Search for other papers by Sheng Zhang in
Google Scholar
PubMed
Search for other papers by Ye Tian in
Google Scholar
PubMed
Search for other papers by Ming Gao in
Google Scholar
PubMed
Department of Molecular Radiation Oncology, Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China
Search for other papers by Bo Xu in
Google Scholar
PubMed
Anaplastic thyroid cancer (ATC) is an aggressive cancer with poor clinical prognosis. However, mechanisms driving ATC aggressiveness is not well known. Components of the DNA damage response (DDR) are frequently found mutated or aberrantly expressed in ATC. The goal of this study is to establish the functional link between histone acetyltransferase lysine (K) acetyltransferase 5 (KAT5, a critical DDR protein) and ATC invasiveness using clinical, in vitro and in vivo models. We analyzed the expression of KAT5 by immunohistochemistry and assessed its relationship with metastasis and overall survival in 82 ATC patients. Using cellular models, we established functional connection of KAT5 expression and C-MYC stabilization. We then studied the impact of genetically modified KAT5 expression on ATC metastasis in nude mice. In clinical samples, there is a strong correlation of KAT5 expression with ATC metastasis (P = 0.0009) and overall survival (P = 0.0017). At the cellular level, upregulation of KAT5 significantly promotes thyroid cancer cell proliferation and invasion. We also find that KAT5 enhances the C-MYC protein level by inhibiting ubiquitin-mediated degradation. Further evidence reveals that KAT5 acetylates and stabilizes C-MYC. Finally, we prove that altered KAT5 expression influences ATC lung metastases in vivo. KAT5 promotes ATC invasion and metastases through stabilization of C-MYC, demonstrating it as a new biomarker and therapeutic target for ATC.
