Thyroid Hormone Promotes β-Catenin Activation and Cell Proliferation in Colorectal Cancer

Yee Shin Lee, Yu Tang Chin, Ya Jung Shih, André Wendindondé Nana, Yi Ru Chen, Han Chung Wu, Yu Chen S.H. Yang, Hung Yun Lin, Paul J. Davis

研究成果: 雜誌貢獻文章同行評審

19 引文 斯高帕斯(Scopus)

摘要

Thyroid hormone status has long been implicated in cancer development. Here we investigated the role of thyroxine (T4) in colorectal cancer cell lines HCT 116 (APC wild type) and HT-29 (APC mutant), as well as the primary cultures of cancer cells derived from patients. Cell proliferation was evaluated with standard assay and proliferation marker expression. β-Catenin activation was examined according to nuclear β-catenin accumulation and β-catenin target gene expression. The results showed that T4 increased colorectal cancer cell proliferation while cell number and viability were elevated by T4 in both established cell lines and primary cells. Moreover, the transcriptions of proliferative genes PCNA, CCND1, and c-Myc were enhanced by T4 in the primary cells. T4 induced nuclear β-catenin accumulation, as well as high cyclin D1 and c-Myc levels compared to the untreated cells. In addition, the β-catenin-directed transactivation of CCND1 and c-Myc promoters was also upregulated by T4. CTNNB1 transcription was raised by T4 in HCT 116, but not in HT-29, while the boosted β-catenin levels were observed in both. Lastly, the T4-mediated gene expression could be averted by the knockdown of β-catenin. These results suggested that T4 promotes β-catenin activation and cell proliferation in colorectal cancer, indicating that an applicable therapeutic strategy should be considered.
原文英語
頁(從 - 到)156-165
頁數10
期刊Hormones and Cancer
9
發行號3
DOIs
出版狀態已發佈 - 六月 1 2018

ASJC Scopus subject areas

  • 內分泌學、糖尿病和代謝
  • 腫瘤科
  • 內分泌
  • 內分泌和自主系統
  • 癌症研究

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