WEE1 inhibition enhances sensitivity to hypoxia/reoxygenation in HeLa cells | Zendy

Tatsuaki Goto | Zendy; Hisao Homma | Zendy; Atsushi Kaida | Zendy; Masahiko Miura | Zendy

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WEE1 inhibition enhances sensitivity to hypoxia/reoxygenation in HeLa cells

Author(s) -

Tatsuaki Goto,

Hisao Homma,

Atsushi Kaida,

Masahiko Miura

Publication year - 2019

Publication title -

journal of radiation research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.643

H-Index - 60

eISSN - 1349-9157

pISSN - 0449-3060

DOI - 10.1093/jrr/rrz045

Subject(s) - wee1 , mitotic catastrophe , mitosis , hela , homologous recombination , clonogenic assay , microbiology and biotechnology , dna damage , hypoxia (environmental) , g2 m dna damage checkpoint , chemistry , cell cycle checkpoint , cell cycle , biology , cancer research , cell , dna , biochemistry , cyclin dependent kinase 1 , organic chemistry , oxygen

Hypoxia/reoxygenation (H/R) treatment reportedly induces DNA damage response (DDR), including DNA double-strand break (DSB) repair and G2 arrest, resulting in reduction of clonogenic survival. Because WEE1 plays a key role in the G2/M checkpoint along with CHK1/2, we investigated the effect of WEE1 inhibition on H/R-induced DDR using HeLa cells. The H/R treatment combined with WEE1 inhibitor abrogated G2 arrest, subsequently leading to the cells entering the M phase, and finally resulting in mitotic catastrophe after prolonged mitosis. Colony-forming assay showed an enhanced decrease in the surviving fraction and the focus formation of BRCA1 was significantly reduced. We demonstrate for the first time that WEE1 inhibition enhances H/R-induced cell death accompanied by mitotic catastrophe and that the process may be mediated by homologous recombination.

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