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Tweety homolog 3 promotes colorectal cancer progression through mutual regulation of histone deacetylase 7.
Lu, Pengyan; Deng, Shumin; Liu, Jiaxin; Xiao, Qing; Zhou, Zhengwei; Li, Shuojie; Xin, Jiaxuan; Shu, Guang; Yi, Bo; Yin, Gang.
Afiliación
  • Lu P; Department of Pathology Xiangya Hospital, School of Basic Medical Sciences, Central South University Changsha China.
  • Deng S; Department of Pathology Xiangya Hospital, School of Basic Medical Sciences, Central South University Changsha China.
  • Liu J; Department of Pathology Xiangya Hospital, School of Basic Medical Sciences, Central South University Changsha China.
  • Xiao Q; Department of Pathology The Third Xiangya Hospital, Central South University Changsha China.
  • Zhou Z; Department of Pathology Xiangya Hospital, School of Basic Medical Sciences, Central South University Changsha China.
  • Li S; Department of Pathology Xiangya Hospital, School of Basic Medical Sciences, Central South University Changsha China.
  • Xin J; Department of Gastrointestinal Surgery The Third Xiangya Hospital, Central South University Changsha China.
  • Shu G; Department of Pathology Xiangya Hospital, School of Basic Medical Sciences, Central South University Changsha China.
  • Yi B; Department of Pathology The Third Xiangya Hospital, Central South University Changsha China.
  • Yin G; Department of Pathology Xiangya Hospital, School of Basic Medical Sciences, Central South University Changsha China.
MedComm (2020) ; 5(6): e576, 2024 Jun.
Article en En | MEDLINE | ID: mdl-38827027
ABSTRACT
Colorectal cancer (CRC) is one of the leading cancers worldwide, with metastasis being a major cause of high mortality rates among patients. In this study, dysregulated gene Tweety homolog 3 (TTYH3) was identified by Gene Expression Omnibus database. Public databases were used to predict potential competing endogenous RNAs (ceRNAs) for TTYH3. Quantitative real-time polymerase chain reaction, western blot, and immunohistochemistry were utilized to analyze TTYH3 and histone deacetylase 7 (HDAC7) levels. Luciferase assays confirmed miR-1271-5p directly targeting the 3' untranslated regions of TTYH3 and HDAC7. In vitro experiments such as transwell and human umbilical vein endothelial cell tube formation, as well as in vivo mouse models, were conducted to assess the biological functions of TTYH3 and HDAC7. We discovered that upregulation of TTYH3 in CRC promotes cell migration by affecting the Epithelial-mesenchymal transition pathway, which was independent of its ion channel activity. Mechanistically, TTYH3 and HDAC7 functioned as ceRNAs, reciprocally regulating each other's expression. TTYH3 competes for binding miR-1271-5p, increasing HDAC7 expression, facilitating CRC metastasis and angiogenesis. This study reveals the critical role of TTYH3 in promoting CRC metastasis through ceRNA crosstalk, offering new insights into potential therapeutic targets for clinical intervention.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: MedComm (2020) Año: 2024 Tipo del documento: Article Pais de publicación: China
Texto completo
Añadir a Mi BVS
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PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: MedComm (2020) Año: 2024 Tipo del documento: Article Pais de publicación: China