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. 2021 Aug 23;9:719192. doi: 10.3389/fcell.2021.719192

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Copyright © 2021 Li, Wang, Lan, Wu, Evans, Ruiz, Yan, Zhou, Oliveira, Reis, Hu, Chen, Behrens, He and Zhang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Treatment of Oxaliplatin inhibits HR repair pathways via blocking CDK1-BRCA1 activities in Oxaliplatin resistance gastric cancer Organoid and PDOX. (A) Representative images of immunofluorescent staining comparison of CDK1 phosphorylation and BRCA1 phosphorylation in öxaliplatin resistance gastric cancer organoids under the effects of Olaparib + Oxaliplatin, Oxaliplatin, Olaparib, and the blank control group. The scale represents 20 μm. Drug action time was 36 h. (B,C) Proportion of CDK1 phosphorylation and BRCA1 phosphorylation positive cells (A), respectively. (D) Representative images of comparison of IHC staining of CDK1 and its phosphorylation and BRCA1 and its phosphorylation in BALB/C NUDE mice after tumorigenesis under the effects of Olaparib + Oxaliplatin, Oxaliplatin, Olaparib, and blank control group. The scale represents 200 um. (E,F) Proportion of CDK1 phosphorylation and BRCA1 phosphorylation positive cells in (D), respectively. The Student’s t test was used for statistical analysis. Error bars indicate mean ± standard deviation. OXA, Oxaliplatin. OLP, Olaparib. CON, control group. CISP, cisplatin. PCDK1, CDK1 phosphorylation antibody. PBRCA1, BRCA1 phosphorylation antibody. PDOX, patient-derived organotipic culture xenograft. **< 0.01, and ***< 0.001. All experiments were repeated three times.