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Sato, Hiro; Niimi, Atsuko; Yasuhara, Takaaki; Permata, Tiara Bunga Mayang; Hagiwara, Yoshihiko; Isono, Mayu; Nuryadi, Endang; Sekine, Ryota; Oike, Takahiro; Kakoti, Sangeeta; Yoshimoto, Yuya; Held, Kathryn D; Suzuki, Yoshiyuki; Kono, Koji; Miyagawa, Kiyoshi; Nakano, Takashi; Shibata, Atsushi
Nature communications, 11/2017, Volume: 8, Issue: 1Journal Article
Accumulating evidence suggests that exogenous cellular stress induces PD-L1 upregulation in cancer. A DNA double-strand break (DSB) is the most critical type of genotoxic stress, but the involvement of DSB repair in PD-L1 expression has not been investigated. Here we show that PD-L1 expression in cancer cells is upregulated in response to DSBs. This upregulation requires ATM/ATR/Chk1 kinases. Using an siRNA library targeting DSB repair genes, we discover that BRCA2 depletion enhances Chk1-dependent PD-L1 upregulation after X-rays or PARP inhibition. In addition, we show that Ku70/80 depletion substantially enhances PD-L1 upregulation after X-rays. The upregulation by Ku80 depletion requires Chk1 activation following DNA end-resection by Exonuclease 1. DSBs activate STAT1 and STAT3 signalling, and IRF1 is required for DSB-dependent PD-L1 upregulation. Thus, our findings reveal the involvement of DSB repair in PD-L1 expression and provide mechanistic insight into how PD-L1 expression is regulated after DSBs.
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