Low-dose radiation-induced epithelial-mesenchymal transition through NF-κB in cervical cancer cells

Shi, Yan; Wang, Yu; Yang, Qifeng; Li, Xiaoyan; Kong, Xiaoli; Zhang, Ning; Yuan, Cunzhong; Yang, Ning; Kong, Beihua

doi:10.3892/ijo.2013.1852

Cited by 46 publications

(48 citation statements)

References 24 publications

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“…Low-dose radiation-induces EMT via NF-κB p65 signalling by enhancing the migration and invasion of cervical cancer cells. This change is evidenced by the morphological changes in cells that express changed levels of epithelial (down-regulated) and mesenchymal markers (upregulated) [37]. Hence, the inhibition of EMT could improve the effectiveness of ionizing radiation for the treatment of cervical cancer.…”

Section: Low Dose Radiation and Emtmentioning

confidence: 99%

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EMT in cervical cancer: Its role in tumour progression and response to therapy

2015

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Section: Low Dose Radiation and Emtmentioning

confidence: 99%

“…However, some patients develop resistance to radiotherapy [37]. Low-dose radiation-induces EMT via NF-κB p65 signalling by enhancing the migration and invasion of cervical cancer cells.…”

Section: Low Dose Radiation and Emtmentioning

confidence: 99%

EMT in cervical cancer: Its role in tumour progression and response to therapy

2015

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“…Expression analysis shows that the loss and the resulting migration property are regulated by ZEB1 [73]. Low-dose radiation treatment will suppress E-cadherin expression in cervical cancer cell lines [74]. Although hypoxic has been suggested to be involved in E-cadherin suppression in solid tumors, the oxygenation status (measured by microelectrodes) has no direct correlation with the tumor E-cadherin levels in the squamous cell carcinoma of uterine cervix [75].…”

Section: Cervical Cancermentioning

confidence: 99%

Transcription Regulation of E-Cadherin by Zinc Finger E-Box Binding Homeobox Proteins in Solid Tumors

Wong

Gao

Chan

2014

BioMed Research International

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Downregulation of E-cadherin in solid tumors with regional migration and systematic metastasis is well recognized. In view of its significance in tumorigenesis and solid cancer progression, studies on the regulatory mechanisms are important for the development of target treatment and prediction of clinical behavior for cancer patients. The vertebrate zinc finger E-box binding homeobox (ZEB) protein family comprises 2 major members: ZEB1 and ZEB2. Both contain the motif for specific binding to multiple enhancer boxes (E-boxes) located within the short-range transcription regulatory regions of the E-cadherin gene. Binding of ZEB1 and ZEB2 to the spaced E-cadherin E-boxes has been implicated in the regulation of E-cadherin expression in multiple human cancers. The widespread functions of ZEB proteins in human malignancies indicate their significance. Given the significance of E-cadherin in the solid tumors, a deeper understanding of the functional role of ZEB proteins in solid tumors could provide insights in the design of target therapy against the migratory nature of solid cancers.

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“…15 Previous findings indicate that ionizing radiation (IR) is able to affect abundance of proteases and transcription factors involving in multiple signaling pathways participating in this complex pathogenesis. [16][17][18] Thus, utilizing this knowledge and identifying novel pathways for therapeutic targets is the first goal in research on pulmonary neoplasms.…”

mentioning

confidence: 99%

Inhibition of TBK1 attenuates radiation-induced epithelial–mesenchymal transition of A549 human lung cancer cells via activation of GSK-3β and repression of ZEB1

Huang

et al. 2014

Laboratory Investigation

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Radiotherapy is an effective treatment method for lung cancer, particularly when the disease is at an advanced stage. However, previous researchers have observed that the majority of patients with conventional radiation therapy develop distant metastases and succumb to the disease. Thus, identifying and understanding novel pathways for the development of new therapeutic targets is a major goal in research on pulmonary neoplasms. Recent studies suggest that epithelial-mesenchymal transition (EMT) is the most important contributor to cancer metastasis. Induction of this complex process requires endogenously produced microRNAs; specifically, downregulation of the miRNA-200c causes an induction of EMT. We recently identified the tank-binding kinase-1 (TBK1) as a downstream effector of the miR-200c-driven pathway, but the biological function of TBK1 in EMT remains unknown. In this study, we tested whether TBK1 has a role in radiation-induced EMT and identified associated potential mechanisms. Human alveolar type II epithelial carcinoma A549 cells were irradiated with 60 Co g-rays. Western blotting revealed a time-and dose-dependent decrease in E-cadherin with a concomitant increase in vimentin after radiation, suggesting that the epithelial cells acquired a mesenchymal-like morphology. TBK1 siRNA significantly inhibited radiationinduced suppression of the epithelial marker E-cadherin and upregulation of the mesenchymal marker vimentin. The invasion and migratory potential of lung cancer cells upon radiation treatment was also reduced by TBK1 knockdown. Furthermore, radiation-induced EMT attenuated by TBK1 depletion was partially dependent on transcriptional factor ZEB1 expression. Finally, we found glycogen synthase kinase-3b (GSK-3b) is involved in regulation of radiation-induced EMT by TBK1. Thus, our findings reveal that TBK1 signaling regulates radiation-induced EMT by controlling GSK-3b phosphorylation and ZEB1 expression. TBK1 may therefore constitute a useful target for treatment of radiotherapy-induced metastasis diseases.

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Low-dose radiation-induced epithelial-mesenchymal transition through NF-κB in cervical cancer cells

Cited by 46 publications

References 24 publications

EMT in cervical cancer: Its role in tumour progression and response to therapy

EMT in cervical cancer: Its role in tumour progression and response to therapy

Transcription Regulation of E-Cadherin by Zinc Finger E-Box Binding Homeobox Proteins in Solid Tumors

Inhibition of TBK1 attenuates radiation-induced epithelial–mesenchymal transition of A549 human lung cancer cells via activation of GSK-3β and repression of ZEB1

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