Impaired DNA double‐strand breaks repair by kinesin family member 4A inhibition renders human H1299 non‐small‐cell lung cancer cells sensitive to cisplatin-Reference-Cited by-同舟云学术

Impaired DNA double‐strand breaks repair by kinesin family member 4A inhibition renders human H1299 non‐small‐cell lung cancer cells sensitive to cisplatin

Published:2018-11-11 Issue:7 Volume:234 Page:10360-10371
ISSN:0021-9541
Container-title:Journal of Cellular Physiology
language:en
Short-container-title:J Cell Physiol

Author:

Wan Qing¹²,Shen Yong¹,Zhao Huzi¹,Wang Bei¹,Zhao Lei¹,Zhang Yongchen¹,Bu Xiaodong¹,Wan Meiling¹,Shen Chuanlu¹^ORCID

Affiliation:

1. Department of Pathology and Pathophysiology Medical School, Southeast University Nanjing China

2. Center of Clinical Laboratory Medicine, Zhongda Hospital, Southeast University Nanjing China

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Cell Biology,Clinical Biochemistry,Physiology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcp.27703

Reference68 articles.

1. Increased Sensitivity to Cisplatin in Non-Small Cell Lung Cancer Cell Lines after FHIT Gene Transfer

2. Involvement of Poly(ADP-ribose) Polymerase-1 and XRCC1/DNA Ligase III in an Alternative Route for DNA Double-strand Breaks Rejoining

3. Stimulation of β‐adrenoceptor enhances sensitivity to cisplatin in non‐small cell lung cancer cell lines;Bando T.;International Journal of Oncology,1997

4. KIF4A and PP2A–B56 form a spatially restricted feedback loop opposing Aurora B at the anaphase central spindle

5. RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection

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