Literature DB >> 26463629

HPIP promotes thyroid cancer cell growth, migration and EMT through activating PI3K/AKT signaling pathway.

Shun-chang Wang1, Da-sen Chai2, Chuan-bo Chen2, Zheng-ye Wang2, Lei Wang2.   

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.
Copyright © 2015 Elsevier Masson SAS. All rights reserved.

Entities:  

Keywords:  Epithelial–mesenchymal transition (EMT); Hematopoietic pre-B cell leukemia transcription factor (PBX)-interacting protein (HPIP); Migration; Proliferation; Thyroid carcinoma

Mesh:

Substances:

Year:  2015        PMID: 26463629     DOI: 10.1016/j.biopha.2015.08.027

Source DB:  PubMed          Journal:  Biomed Pharmacother        ISSN: 0753-3322            Impact factor:   6.529


  26 in total

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