Cancer Cell Response to Radiation Therapy

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 11381

Special Issue Editors


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Guest Editor
Radiation Oncology Erlangen, Universitätsklinikum Erlangen, Friedrich-Alexander Universität Erlangen, 91054 Erlangen, Germany
Interests: cell biology; immunology; cancer research; cancer biology; radiation biology
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Guest Editor
Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsklinikum Erlangen, Strahlenklinik, Germany
Interests: radiation therapy and targeted therapy; immune modulating effects of radiotherapy; head and neck cancer

Special Issue Information

Dear Colleagues,

Radiotherapy is an effective method in the treatment of various tumor entities. The aim of radiotherapy is to inhibit the ongoing proliferation of tumor cells. The main biological goal of radiotherapy is the induction of DNA damage in tumor cells. Depending on the radiation dose, oxygenation, ability to repair DNA damage, the cell cycle and the microenvironment of the tumor, different cellular responses can occur. Cells with at least partially functional DNA damage response induce cell cycle arrest and activate DNA damage repair by homologous recombination (HR) or non-homologous end compound (NHEJ). If this is successful, the cells re-enter the cell cycle. If this is not successful, the cells can enter a permanent cell cycle block and induce senescence. In the case of more severe damage, the primary mechanism of radiation-induced cell death in solid tumours is mitotic catastrophe, a pathway that leads to cell death after a disrupted mitosis process. Another form of cell death is apoptosis, which occurs mainly after radiotherapy of haematological malignancies. The expansion of knowledge about the signalling pathways involved and the factors that influence the type of cell death will become increasingly important in the future, as a large number of targeted drugs against the response to DNA damage are currently being studied in clinical trials. These new drugs, known as DNA damage response inhibitors (DDRi), were developed as combination drugs for immune-oncology, but will have a strong influence on the effect of radiotherapy and open up the possibility of new treatment strategies.

We are looking forward to your contributions to this Special Issue.

Prof. Dr. Luitpold Valentin R. Distel
Dr. Markus Hecht
Guest Editors

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Keywords

  • radiation
  • DNA damage response
  • homologous recombination
  • non-homologous end joining
  • cell death
  • mitotic catastrophe
  • senescence
  • targeted therapy
DDRi

Published Papers (3 papers)

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Research

17 pages, 8969 KiB  
Article
Radiation-Induced Overexpression of TGFβ and PODXL Contributes to Colorectal Cancer Cell Radioresistance through Enhanced Motility
by Hyunjung Lee, Joon-Seog Kong, Seung-Sook Lee and Areumnuri Kim
Cells 2021, 10(8), 2087; https://doi.org/10.3390/cells10082087 - 13 Aug 2021
Cited by 5 | Viewed by 2478
Abstract
The primary cause of colorectal cancer (CRC) recurrence is increased distant metastasis after radiotherapy, so there is a need for targeted therapeutic approaches to reduce the metastatic-relapse risk. Dysregulation of the cell-surface glycoprotein podocalyxin-like protein (PODXL) plays an important role in promoting cancer-cell [...] Read more.
The primary cause of colorectal cancer (CRC) recurrence is increased distant metastasis after radiotherapy, so there is a need for targeted therapeutic approaches to reduce the metastatic-relapse risk. Dysregulation of the cell-surface glycoprotein podocalyxin-like protein (PODXL) plays an important role in promoting cancer-cell motility and is associated with poor prognoses for many malignancy types. We found that CRC cells exposed to radiation demonstrated increased TGFβ and PODXL expressions, resulting in increased migration and invasiveness due to increased extracellular matrix deposition. In addition, both TGFβ and PODXL were highly expressed in tissue samples from radiotherapy-treated CRC patients compared to those from patients without this treatment. However, it is unclear whether TGFβ and PODXL interactions are involved in cancer-progression resistance after radiation exposure in CRC. Here, using CRC cells, we showed that silencing PODXL blocked radiation-induced cell migration and invasiveness. Cell treatment with galunisertib (a TGFβ-pathway inhibitor) also led to reduced viability and migration, suggesting that its clinical use may enhance the cytotoxic effects of radiation and lead to the effective inhibition of CRC progression. Overall, the results demonstrate that downregulation of TGFβ and its-mediated PODXL may provide potential therapeutic targets for patients with radiotherapy-resistant CRC. Full article
(This article belongs to the Special Issue Cancer Cell Response to Radiation Therapy)
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14 pages, 5866 KiB  
Article
Downregulation of Mcl-1 by Panobinostat Potentiates Proton Beam Therapy in Hepatocellular Carcinoma Cells
by Changhoon Choi, Ga Haeng Lee, Arang Son, Gyu Sang Yoo, Jeong Il Yu and Hee Chul Park
Cells 2021, 10(3), 554; https://doi.org/10.3390/cells10030554 - 4 Mar 2021
Cited by 7 | Viewed by 2470
Abstract
Epigenetic modulation by histone deacetylase (HDAC) inhibitors is an attractive anti-cancer strategy for diverse hematological and solid cancers. Herein, we explored the relative effectiveness of the pan-HDAC inhibitor panobinostat in combination with proton over X-ray irradiation in HCC cells. Clonogenic survival assays revealed [...] Read more.
Epigenetic modulation by histone deacetylase (HDAC) inhibitors is an attractive anti-cancer strategy for diverse hematological and solid cancers. Herein, we explored the relative effectiveness of the pan-HDAC inhibitor panobinostat in combination with proton over X-ray irradiation in HCC cells. Clonogenic survival assays revealed that radiosensitization of Huh7 and Hep3B cells by panobinostat was more evident when combined with protons than X-rays. Panobinostat increased G2/M arrest and production of intracellular reactive oxygen species, which was further enhanced by proton irradiation. Immunofluorescence staining of γH2AX showed that panobinostat enhanced proton-induced DNA damage. Panobinostat dose-dependently decreased expression of an anti-apoptotic protein, Mcl-1, concomitant with increasing acetylation of histone H4. The combination of panobinostat with proton irradiation enhanced apoptotic cell death to a greater extent than that with X-ray irradiation. Depletion of Mcl-1 by RNA interference enhanced proton-induced apoptosis and proton radiosensitization, suggesting a potential role of Mcl-1 in determining proton sensitivity. Together, our findings suggest that panobinostat may be a promising combination agent for proton beam therapy in HCC treatment. Full article
(This article belongs to the Special Issue Cancer Cell Response to Radiation Therapy)
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18 pages, 3999 KiB  
Article
Focused Ultrasound-Induced Cavitation Sensitizes Cancer Cells to Radiation Therapy and Hyperthermia
by Shaonan Hu, Xinrui Zhang, Michael Unger, Ina Patties, Andreas Melzer and Lisa Landgraf
Cells 2020, 9(12), 2595; https://doi.org/10.3390/cells9122595 - 3 Dec 2020
Cited by 24 | Viewed by 5625
Abstract
Focused ultrasound (FUS) has become an important non-invasive therapy for solid tumor ablation via thermal effects. The cavitation effect induced by FUS is thereby avoided but applied for lithotripsy, support drug delivery and the induction of blood vessel destruction for cancer therapy. In [...] Read more.
Focused ultrasound (FUS) has become an important non-invasive therapy for solid tumor ablation via thermal effects. The cavitation effect induced by FUS is thereby avoided but applied for lithotripsy, support drug delivery and the induction of blood vessel destruction for cancer therapy. In this study, head and neck cancer (FaDu), glioblastoma (T98G), and prostate cancer (PC-3) cells were exposed to FUS by using an in vitro FUS system followed by single-dose X-ray radiation therapy (RT) or water bath hyperthermia (HT). Sensitization effects of short FUS shots with cavitation (FUS-Cav) or without cavitation (FUS) to RT or HT (45 °C, 30 min) were evaluated. FUS-Cav significantly increases the sensitivity of cancer cells to RT and HT by reducing long-term clonogenic survival, short-term cell metabolic activity, cell invasion, and induction of sonoporation. Our results demonstrated that short FUS treatment with cavitation has good potential to sensitize cancer cells to RT and HT non-invasively. Full article
(This article belongs to the Special Issue Cancer Cell Response to Radiation Therapy)
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