Journal
CANCER CELL
Volume 38, Issue 6, Pages 844-+Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2020.10.009
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Funding
- National Key Research and Development Program of China [2019YFA0802002, 2017YF0503600]
- CAS Strategic Priority Research Program [XDB19030000]
- National Natural Science Foundation of China [31530094, 31571456]
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Ependymoma is the third most common pediatric tumor with posterior fossa group A (PFA) being its most aggressive subtype. Ependymomas are generally refractory to chemotherapies and thus lack any effective treatment. Here, we report that elevated expression of CXorf67 (chromosome X open reading frame 67), which frequently occurs in PFA ependymomas, suppresses homologous recombination (HR)-mediated DNA repair. Mechanistically, CXorf67 interacts with PALB2 and inhibits PALB2-BRCA2 interaction, thereby inhibiting HR repair. Concordantly, tumor cells with high CXorf67 expression levels show increased sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors, especially when combined with radiotherapy. Thus, our findings have revealed a role of CXorf67 in HR repair and suggest that combination of PARP inhibitors with radiotherapy could be an effective treatment option for PFA ependymomas.
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