Radiotherapy

Krause, Sonja; Debus, Jürgen; Neuhof, Dirk

doi:10.1007/978-3-540-85772-3_13

Cited by 6 publications

(5 citation statements)

References 34 publications

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“… 1 – 3 Radiotherapy coupled with surgery and chemotherapy is the most important method of contemporary NSCLC treatment. 4 However, the use of this therapy is also confronted with challenges due to the intrinsic radioresistance of tumor cells. Hence, enhancing the radiosensitivity of resistant tumor cells is a common strategy in the clinical application of radiotherapy.…”

Section: Introductionmentioning

confidence: 99%

Small interfering RNA targeting S100A4 sensitizes non-small-cell lung cancer cells (A549) to radiation treatment

Qiao

Zhuang

2016

OTT

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ObjectiveThis study aimed to investigate the impact of S100A4-small interfering RNA (S100A4-siRNA) on apoptosis and enhanced radiosensitivity in non-small-cell lung cancer (A549) cells. We also explored the mechanisms of radiosensitization and identified a new target to enhance radiosensitivity and gene therapy for non-small-cell lung cancer.MethodsRNA interference is a powerful tool for gene silencing. In this study, we constructed an effective siRNA to knock down S100A4. A549 cells were randomly divided into three groups: blank, negative control, and S100A4-siRNA. To investigate the effect of S100A4-siRNA, the expression of S100A4, E-cadherin, and p53 proteins and their messenger RNA (mRNA) was detected by Western blot and quantitative real-time polymerase chain reaction. Transwell chambers were used to assess cell invasion. Cell cycle and apoptosis were analyzed by flow cytometry. Radiosensitivity was determined by colony formation ability.ResultsOur results demonstrate that S100A4-siRNA effectively silenced the S100A4 gene. When siRNA against S100A4 was used, S100A4 protein expression was downregulated, whereas the expressions of E-cadherin and p53 were upregulated. In addition, a clear reduction in S100A4 mRNA levels was noted compared with the blank and negative control groups, whereas E-cadherin and p53 mRNA levels increased. Transfection with S100A4-siRNA significantly reduced the invasiveness of A549 cells. S100A4 silencing induced immediate G2/M arrest in cell cycle studies and increased apoptosis rates in A549 cells. In clonogenic assays, we used a multitarget, single-hit model to detect radiosensitivity after S100A4 knockdown. All parameters (D0, Dq, α, β) indicated that the downregulation of S100A4 enhanced radiosensitivity in A549 cells. Furthermore, S100A4-siRNA upregulated p53 expression, suggesting that S100A4 may promote A549 cell proliferation, invasion, and metastasis by regulating the expression of other proteins. Therefore, siRNA-directed S100A4 knockdown may represent a viable clinical therapy for lung cancer.ConclusionS100A4 downregulation potentially enhances the sensitivity of human A549 cells to radiotherapy.

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Section: Introductionmentioning

confidence: 99%

Small interfering RNA targeting S100A4 sensitizes non-small-cell lung cancer cells (A549) to radiation treatment

Qiao

Zhuang

2016

OTT

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“…However, radiotherapy leads to a considerable number of difficulties in implant treatment. For example, the tissue in the irradiated area usually leads to a reduction of the vascular portion and cells and to hypoxia [3-5]. These changes lead to the destruction of osteoblasts and impaired bone modelling and remodelling which even cause osteoradionecrosis (ORN) [6,7].…”

Section: Introductionmentioning

confidence: 99%

How to improve the survival rate of implants after radiotherapy for head and neck cancer?

Zheng

Tang

et al. 2014

J Periodontal Implant Sci

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Implants have been widely used in restorative treatment for patients who have undergone head and neck cancer surgery. With the development of combination treatment of head and neck cancer, radiotherapy has been a common means of therapy. However, it could induce various changes in hard and soft tissues and reduce the success and survival rate of the implants. Some research, using either animal models or clinical studies, have shown that certain strategies could be used for improving the survival rate of implants. In this review, we discussed the changes in both hard and soft tissues, which may reduce the survival rate of the implants, and the proposed methods for improving the survival rate of patients after radiotherapy. Graphical Abstract

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“…Radiation therapy, often coupled with surgery and chemotherapy, is also one of the most important methods of contemporary cancer treatment [1]. More than 60% of all cancer patients will require radiotherapy at various stages over the course of their treatment.…”

Section: Introductionmentioning

confidence: 99%

Cell division cycle 25 homolog c effects on low-dose hyper-radiosensitivity and induced radioresistance at elevated dosage in A549 cells

Zhao

Cui

Han

et al. 2012

Journal of Radiation Research

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The underlying mechanisms behind both low-dose hyper-radiosensitivity (HRS) and induced radioresistance (IRR), generally occurring at elevated radiation levels, remain unclear; however, elucidation of the relationship between cell cycle division 25 homolog c (Cdc25c) phosphatase and HRS/IRR may provide important insights into this process. Two cell lines with disparate HRS status, A549 and SiHa cells, were selected as cell models for comparison of dose-dependent Cdc25c phosphatase expression subsequent to low-dose irradiation. Knockdown of Cdc25c in A549 cells was mediated by transfection with a pGCsi-RAN-U6neo vector containing hairpin siRNA sequences. S216-phosphorylated Cdc25c protein [p-Cdc25c (Ser216)], cell survival and mitotic ratio were measured by western blot, colony-forming assay and histone H3 phosphorylation analysis. Variant p-Cdc25c (Ser216) expression was observed in the two cell lines after irradiation. The p-Cdc25c (Ser216) expression noted in SiHa cells after administration of 0–1 Gy radiation was similar to the radioresistance model; however, in A549 cells, the dose response for the phosphorylation of the Cdc25c Ser216 residue overlapped the level required to overcome the HRS response. Furthermore, Cdc25c repression prior to low-dose radiation induced more distinct HRS and prevented the development of IRR. The dose required to overcome the HRS response coincided with the effect of early G2-phase checkpoint arrest in A549 cells (approximately 0.3 Gy), and Cdc25c knockdown in A549 cells (approximately 0.5 Gy) corresponded to the phosphorylation of the Cdc25c Ser216 residue. Resultant data confirmed that dose-dependent Cdc25c phosphatase does effectively act as an early G2-phase checkpoint, thus indicating mechanistic importance in the HRS to IRR transition in A549 cells.

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Radiotherapy

Cited by 6 publications

References 34 publications

Small interfering RNA targeting S100A4 sensitizes non-small-cell lung cancer cells (A549) to radiation treatment

Small interfering RNA targeting S100A4 sensitizes non-small-cell lung cancer cells (A549) to radiation treatment

How to improve the survival rate of implants after radiotherapy for head and neck cancer?

Cell division cycle 25 homolog c effects on low-dose hyper-radiosensitivity and induced radioresistance at elevated dosage in A549 cells

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