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4. BLM helicase inhibition synergizes with PARP inhibition to improve the radiosensitivity of olaparib resistant non-small cell lung cancer cells by inhibiting homologous recombination repair

Author

Kong, Yangyang, primary, Xu, Chang, additional, Sun, Xiaohui, additional, Sun, Hao, additional, Zhao, Xiaotong, additional, He, Ningning, additional, Ji, Kaihua, additional, Wang, Qin, additional, Du, Liqing, additional, Wang, Jinhan, additional, Zhang, Manman, additional, Liu, Yang, additional, Wang, Yan, additional, and Liu, Qiang, additional

Published
2022
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5. Synthesis, crystal structure and spectral properties of a copper(II) complex with flavonoxylacetate ligand

Author

Yu, Hui, Song, Rong, Kong, Yangyang, Cao, Ting, and Chen, Yun

Abstract

A new Cu(II) complex with flavonoxylacetate ligand was synthesized and characterized. The structure of the complex was determined by X-ray single crystal diffraction technique. In the crystal structure, flavonoxylacetate coordinates Cu(II) ion in bidentate mode resulting in a chelating pentagonal coordination structure. Central Cu(II) has an elongated octahedral coordination showing a strong Jahn-Teller effect. The stability of the crystal structure was investigated by thermal gravimetric analyses. The loss of coordination water in crystals occurs above 150 °C. Fluorescence spectra are affected by pH value and coordination metal ion as well as the substitution pattern of the carboxymethoxy on the flavone skeleton. Furthermore, the fluorescence quenched in the Cu(II) complex recovered with increase of S2- ion concentration.

Published
2020
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8. BLM helicase inhibition synergizes with PARP inhibition to improve the radiosensitivity of olaparib resistant non-small cell lung cancer cells by inhibiting homologous recombination repair.

Author

Kong Y, Xu C, Sun X, Sun H, Zhao X, He N, Ji K, Wang Q, Du L, Wang J, Zhang M, Liu Y, Wang Y, and Liu Q

Subjects
Adenosine Diphosphate Ribose therapeutic use, Cell Line, Tumor, Humans, Phthalazines, Piperazines, Poly(ADP-ribose) Polymerase Inhibitors pharmacology, Poly(ADP-ribose) Polymerase Inhibitors therapeutic use, Radiation Tolerance, RecQ Helicases genetics, Recombinational DNA Repair, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung radiotherapy, Lung Neoplasms drug therapy, Lung Neoplasms radiotherapy, Radiation-Sensitizing Agents pharmacology, Radiation-Sensitizing Agents therapeutic use
Abstract

Objective: We aimed to investigate the radiosensitizing efficacy of the poly-ADP-ribose polymerase (PARP) inhibitor, olaparib, and the Bloom syndrome protein (BLM) helicase inhibitor, ML216, in non-small cell lung cancer (NSCLC) cells., Methods: Radiosensitization of NSCLC cells was assessed by colony formation and tumor growth assays. Mechanistically, the effects of ML216, olaparib, and radiation on cell and tumor proliferation, DNA damage, cell cycle, apoptosis, homologous recombination (HR) repair, and non-homologous end joining (NHEJ) repair activity were determined., Results: Both olaparib and ML216 enhanced the radiosensitivities of olaparib-sensitive H460 and H1299 cells, which was seen as decreased surviving fractions and Rad51 foci, increased total DNA damage, and γH2AX and 53BP1 foci ( P < 0.05). The expressions of HR repair proteins were remarkably decreased in olaparib-treated H460 and H1299 cells after irradiation ( P < 0.05), while olaparib combined with ML216 exerted a synergistic radiosensitization effect on olaparib-resistant A549 cells. In addition to increases of double strand break (DSB) damage and decreases of Rad51 foci, olaparib combined with ML216 also increased pDNA-PKcs (S2056) foci, abrogated G2 cell cycle arrest, and induced apoptosis in A549 lung cancer after irradiation in vitro and in vivo ( P < 0.05). Moreover, Western blot showed that olaparib combined with ML216 and irradiation inhibited HR repair, promoted NHEJ repair, and inactivated cell cycle checkpoint signals both in vitro and in vivo ( P < 0.05)., Conclusions: Taken together, these results showed the efficacy of PARP and BLM helicase inhibitors for radiosensitizing NSCLC cells, and supported the model that BLM inhibition sensitizes cells to PARP inhibitor-mediated radiosensitization, as well as providing the basis for the potential clinical development of this combination for tumors intrinsically resistant to PARP inhibitors and radiotherapy., Competing Interests: No potential conflicts of interest are disclosed., (Copyright © 2022 Cancer Biology & Medicine.)

Published
2021
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