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The significance of homeodomain transcription factor 2 in colon cancer cells

BACKGROUND: Colon cancer is a serious malignant tumor. It has been reported that paired-like homeodomain transcription factor 2 (PITX2) can promote the progression of several types of cancer via regulating the Wnt/β-catenin pathway. It has also been demonstrated that high levels of long non-coding R...

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Detalles Bibliográficos
Autores principales: He, Yang, Gong, Peng, Wang, Sitong, Xu, Qing, Chen, Jianhua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8351361/
https://www.ncbi.nlm.nih.gov/pubmed/34372865
http://dx.doi.org/10.1186/s12938-021-00912-5
Descripción
Sumario:BACKGROUND: Colon cancer is a serious malignant tumor. It has been reported that paired-like homeodomain transcription factor 2 (PITX2) can promote the progression of several types of cancer via regulating the Wnt/β-catenin pathway. It has also been demonstrated that high levels of long non-coding RNA (lncRNA) gastric carcinoma high expressed transcript 1 (GHET1) can also promote the development of cervical cancer via activating the Wnt/β-catenin pathway. However, whether PITX2 can affect the development of colon cancer via regulating the expression of lncRNA GHET1 remains unclear. RESULTS: The results demonstrated that PITX2 knockdown attenuated the proliferation, migration and invasion abilities of colon cancer cells. Additionally, PITX2 promoted the expression of lncRNA GHET1 via binding to its promoter. Overexpression of lncRNA GHET1 induced the expression of Wnt/β-catenin signaling-related proteins, cyclin D1, c-Myc and MMP-7. Furthermore, lncRNA GHET1 overexpression abrogated the PITX2 silencing-mediated decreased proliferation, migration and invasion abilities of colon cancer cells. CONCLUSION: The findings of the present study suggested that PITX2 could enhance the proliferation, migration and invasion abilities of colon cancer cells via upregulating lncRNA GHET1 and activating the Wnt/β-catenin pathway.