Papers

Peer-reviewed
Oct, 2013

STK10 missense mutations associated with anti-apoptotic function

Oncology Reports
  • Kazutaka Fukumura
  • Yoshihiro Yamashita
  • Masahito Kawazu
  • Eirin Sai
  • Shin-Ichiro Fujiwara
  • Naoya Nakamura
  • Kengo Takeuchi
  • Mizuo Ando
  • Kohei Miyazono
  • Toshihide Ueno
  • Keiya Ozawa
  • Hiroyuki Mano
  • Display all

Volume
30
Number
4
First page
1542
Last page
1548
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.3892/or.2013.2605
Publisher
4

Peripheral T-cell lymphoma (PTCL) is an aggressive lymphoma with a 5-year overall survival rate of &lt
30%. To identify carcinogenesis-related genes in PTCL, we conducted high-throughput resequencing of target-captured cDNA in a PTCL specimen, revealing a total of 19 missense mutations among 18 independent genes. One of such substitutions, c.2201G&gt
A in STK10 cDNA, replaces an arginine residue to a histidine (R634H) in the encoded protein. Of note, while wild-type STK10 suppresses NF-κ
B activity and potentiates dexamethasone-induced apoptosis, the R634H change significantly decreases such pro-apoptotic activity. This c.2201G&gt
A change of STK10 was also identified in another PTCL specimen, but now registered as a single nucleotide polymorphism in the latest dbSNP database. Furthermore, other somatic mutations of STK10 have been reported, and we now reveal that some of them (L85P and K277E) have more profound anti-apoptotic effects compared to R634H. These results suggest that STK10 functions as a tumor suppressor gene, and that dysfunction of STK10 activity either through polymorphism or somatic mutations may confer anti-apoptotic effects contributing to carcinogenesis.

Link information
DOI
https://doi.org/10.3892/or.2013.2605
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/23842845
ID information
  • DOI : 10.3892/or.2013.2605
  • ISSN : 1021-335X
  • ISSN : 1791-2431
  • Pubmed ID : 23842845
  • SCOPUS ID : 84882578901

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