Expression of Hqk Encoding a KH RNA Binding Protein Is Altered in Human Glioma

The quaking gene family encodes single KH domain RNA‐binding proteins that play vital roles in cell differentiation, proliferation, and apoptotic processes. The human quaking gene, Hqk, maps to 6q25–q26, where cytogenetic alterations associated with a variety of human malignancies, including gliomas...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Cancer science 2002-02, Vol.93 (2), p.167-177
Hauptverfasser: Li, Zheng Zhe, Kondo, Tatsuya, Murata, Tomoaki, Ebersole, Thomas A., Nishi, Torn, Tada, Kenji, Ushio, Yukitaka, Yamamura, Ken‐ichi, Abe, Kuniya
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The quaking gene family encodes single KH domain RNA‐binding proteins that play vital roles in cell differentiation, proliferation, and apoptotic processes. The human quaking gene, Hqk, maps to 6q25–q26, where cytogenetic alterations associated with a variety of human malignancies, including gliomas have been reported. To assess possible relationships of Hqk with human diseases such as glial tumors, we first isolated the Hqk gene, characterized its structure and expression pattern, and carried out mutational analysis of Hqk in primary tumor samples. The Hqk gene contains 8 exons spanning a ∼200 kb genomic region, and generating at least four alternatively spliced transcripts, Hqk–5, Hqk–6, Hqk–7 and Hqk–7B, of which Hqk–7 is abundantly expressed in brain. Analysis of primary tumors demonstrated a high incidence of expression alterations of Hqk in gliomas (30%; 6/20), but not in other tumors such as schwannomas (0/3), or meningiomas (0/8). Among the tumor samples showing expression alterations, two were devoid of all three major transcripts, one was missing only the Hqk–5 message, and only the Hqk–7 message was absent in two cases. Our results thus imply the involvement of Hqk in human glial tumor progression.
ISSN:0910-5050
1347-9032
1349-7006
1876-4673
DOI:10.1111/j.1349-7006.2002.tb01255.x