Next Article in Journal
Biobanking of Exosomes in the Era of Precision Medicine: Are We There Yet?
Next Article in Special Issue
Targeted Radionuclide Therapy of Human Tumors
Previous Article in Journal
Enzymatic Kinetic Resolution of 2-Piperidineethanol for the Enantioselective Targeted and Diversity Oriented Synthesis
Previous Article in Special Issue
Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells
Article Menu
Issue 1 (January) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2016, 17(1), 18;

CHMP4C Disruption Sensitizes the Human Lung Cancer Cells to Irradiation

Key Laboratory of Radiological Protection and Nuclear Emergency, China CDC, National Institute for Radiological Protection, Chinese Center for Disease Control and Prevention, 2 Xinkang Street, Dewai, Beijing 10088, China
Author to whom correspondence should be addressed.
Academic Editor: William Chi-shing Cho
Received: 17 November 2015 / Revised: 17 December 2015 / Accepted: 18 December 2015 / Published: 24 December 2015
(This article belongs to the Special Issue Molecular Classification of Human Cancer: Diagnosis and Treatment)
Full-Text   |   PDF [4463 KB, uploaded 24 December 2015]   |  


Human lung cancer is highly invasive and the most malignant among human tumors. Adenocarcinoma as a specific type of non-small cell lung cancer occurs with high frequency and is also highly resistant to radiation therapy. Thus, how to avoid radiation resistance and improve radiotherapy effectiveness is a crucial question. In the present study, human lung cancer A549 and H1299 cells were irradiated using γ-rays from a Co60 irradiator. Protein expression was detected by Western blotting. Cell cycle and apoptosis were measured by flow cytometry. Surviving fraction was determined by colony formation assay. γH2AX and 53BP1 foci formation were examined by fluorescence microscopy. In the results, we show that CHMP4C, a subunit of Endosomal sorting complex-III (ESCRT-III), is involved in radiation-induced cellular response. Radiation-induced Aurora B expression enhances CHMP4C phosphorylation in non-small cell lung cancer (NSCLC) cells, maintaining cell cycle check-point and cellular viability as well as resisting apoptosis. CHMP4C depletion enhances cellular sensitivity to radiation, delays S-phase of cell cycle and reduces ionizing radiation (IR)-induced γH2AX foci formation. We found that Aurora B targets CHMP4C and inhibition of Aurora B exhibits similar effects with silencing of CHMP4C in radioresistance. We also confirm that CHMP4C phosphorylation is elevated after IR both in p53-positive and-negative cells, indicating that the close correlation between CHMP4C and Aurora B signaling pathway in mediating radiation resistance is not p53 dependent. Together, our work establishes a new function of CHMP4C in radiation resistance, which will offer a potential strategy for non-small cell lung cancer by disrupting CHMP4C. View Full-Text
Keywords: CHMP4C; Aurora B; human non-small lung cancer cells; radiation CHMP4C; Aurora B; human non-small lung cancer cells; radiation

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Li, K.; Liu, J.; Tian, M.; Gao, G.; Qi, X.; Pan, Y.; Ruan, J.; Liu, C.; Su, X. CHMP4C Disruption Sensitizes the Human Lung Cancer Cells to Irradiation. Int. J. Mol. Sci. 2016, 17, 18.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top