HPIP promotes thyroid cancer cell growth, migration and EMT through activating PI3K/AKT signaling pathway - 12/10/15
, Da-sen Chai, Chuan-bo Chen, Zheng-ye Wang, Lei WangBienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Hematopoietic pre-B cell leukemia transcription factor (PBX)-interacting protein (HPIP), a co-repressor for the transcription factor PBX, is a nucleo-cytoplasmic shuttling protein. Increasing evidence suggests that HPIP is an oncogene which is frequently overexpressed in many human carcinomas. However, the role of HPIP in thyroid carcinoma is still unclear. Therefore, in this study, we investigated the role of HPIP in thyroid carcinoma, and explored the underling mechanism. We found that the expression of HPIP is upregulated in thyroid carcinoma cell lines. Knockdown of HPIP inhibits thyroid carcinoma cell proliferation, migration/invasion and epithelial–mesenchymal transition (EMT). HPIP knockdown also reduces thyroid tumor growth in nude mice. Furthermore, knockdown of HPIP significantly inhibits the expression of phosphorylated PI3K and AKT in thyroid carcinoma cells. Taken together, these results suggest that knockdown of HPIP inhibits the proliferation, migration and EMT by suppressing the PI3K/AKT pathway, and HPIP may be a potential therapeutic target for the treatment of thyroid carcinoma.
Le texte complet de cet article est disponible en PDF.Keywords : Hematopoietic pre-B cell leukemia transcription factor (PBX)-interacting protein (HPIP), Thyroid carcinoma, Proliferation, Migration, Epithelial–mesenchymal transition (EMT)
Plan
Vol 75
P. 33-39 - octobre 2015 Retour au numéro
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