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High throughput RNAi screening identifies ID1 as a synthetic sick/lethal gene interacting with the common TP53

Hiroo Imai1, Shunsuke Kato1, Yasuhiro Sakamoto1

  • 1Department of Clinical Oncology, IDAC, Tohoku University, Sendai, Miyagi 980-8575, Japan.

Oncology Reports
|January 1, 2014
PubMed

Insights

Researchers identified Inhibitor of differentiation 1 (ID1) as a synthetic sick/lethal gene interacting with the TP53 R175H mutation. Suppressing ID1 selectively inhibits R175H-expressing cancer cell growth, offering a potential new cancer therapy target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The TP53 R175H mutation is prevalent in human cancers.
  • Targeting genes synthetic sick/lethal with R175H is a promising cancer therapy strategy.

Purpose of the Study:

  • To identify genes that induce synthetic sickness/lethality in R175H-expressing cancer cells.
  • To evaluate Inhibitor of differentiation 1 (ID1) as a potential therapeutic target.

Main Methods:

  • High-throughput screening using a lentiviral bar-coded shRNA library.
  • Utilized a tetracycline-inducible R175H glioblastoma cell line (SF126-tet-R175H).
  • Validated candidate genes, including ID1, using siRNA and flow cytometry.

Main Results:

  • Identified 906 candidate gene suppressions causing growth inhibition in R175H-expressing cells.
  • ID1 suppression accelerated growth inhibition in R175H-expressing cells, but not in TP53-null or other p53 mutant cells.
  • ID1 suppression induced G1 cell cycle arrest, potentiated by R175H expression.

Conclusions:

  • ID1 acts as a synthetic sick/lethal gene interacting with TP53 R175H.
  • ID1 represents a novel molecular target for cancer therapy in R175H-expressing cancers.

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