Twist1 induces the expression of microRNA-29 to suppress SIN3A in head and neck cancer cells

Abstract Background In head and neck squamous cell carcinoma (HNSCC), invasiveness and metastasis of cancer cells contribute to make this insidious disease a major cause of mortality. Epithelial-mesenchymal transition (EMT) is generally considered to be the major mechanism of cancer metastasis. We p...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of cancer research and practice 2016-12, Vol.3 (4), p.113-117
Hauptverfasser: Chou, Chun-Hung, Yang, Muh-Hwa, M.D., Ph.D
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Abstract Background In head and neck squamous cell carcinoma (HNSCC), invasiveness and metastasis of cancer cells contribute to make this insidious disease a major cause of mortality. Epithelial-mesenchymal transition (EMT) is generally considered to be the major mechanism of cancer metastasis. We previously demonstrated the crucial role of the EMT regulator Twist1 in HNSCC. A growing body of evidence suggests that microRNAs play essential roles in cancer progression and metastasis. The aim of this study was to investigate the role of microRNA in Twist1-mediated cancer metastasis. Materials and Methods The HNSCC cell lines FaDu, SAS, OECM1 and CAL-27, were used in this study. Quantitative RT-PCR for microRNAs and Western blot were performed on four HNSCC cell lines to study the molecular mechanisms involved. Results Expression of the miR-29 family, including miR-29a, b, and c were increased in Twist1-overexpressing HNSCC cells. Furthermore, we discovered that SIN3A, a co-repressor of another EMT regulator Snail, is a target of miR-29s. With our results, we demonstrated that Twist1 modifies the function of gene expression through microRNA machinery. Conclusion We herein have delineated the regulatory mechanism of the Twist1-miR29-SIN3A axis in HNSCC.
ISSN:2311-3006
2311-3006
DOI:10.1016/j.jcrpr.2016.03.002