論文

査読有り 国際誌
2020年12月

SIX6 is a TAL1-regulated transcription factor in T-ALL and associated with inferior outcome.

Leukemia & lymphoma
  • Saara Laukkanen
  • Laura Oksa
  • Atte Nikkilä
  • Mari Lahnalampi
  • Mataleena Parikka
  • Masafumi Seki
  • Junko Takita
  • Sofie Degerman
  • Charles E de Bock
  • Merja Heinäniemi
  • Olli Lohi
  • 全て表示

61
13
開始ページ
3089
終了ページ
3100
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1080/10428194.2020.1804560

T-cell acute lymphoblastic leukemia (T-ALL) is a hematological malignancy driven by abnormal activity of transcription factors. Here we report an aberrant expression of the developmental transcription factor SIX6 in the TAL1-subtype of T-ALL. Our results demonstrate that the binding of TAL1 and GATA3 transcription factors into an upstream enhancer element directly regulates SIX6 expression. High expression of SIX6 was associated with inferior event-free survival within three independent patient cohorts. At a functional level, CRISPR-Cas9-mediated knockout of the SIX6 gene in TAL1 positive Jurkat cells induced changes in genes associated with the mTOR-, K-RAS-, and TNFα-related molecular signatures but did not impair cell proliferation or viability. There was also no acceleration of T-ALL development within a Myc driven zebrafish tumor model in vivo. Taken together, our results show that SIX6 belongs to the TAL1 regulatory gene network in T-ALL but is alone insufficient to influence the development or maintenance of T-ALL.

リンク情報
DOI
https://doi.org/10.1080/10428194.2020.1804560
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32835548
ID情報
  • DOI : 10.1080/10428194.2020.1804560
  • PubMed ID : 32835548

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