Radiation up-regulates the expression of VEGF in a canine oral melanoma cell line

Flickinger, Irene; Rütgen, Barbara C.; Gerner, Wilhelm; Calice, Ivana; Tichy, Alexander; Saalmüller, Armin; Kleiter, Miriam

doi:10.4142/jvs.2013.14.2.207

Cited by 9 publications

(6 citation statements)

References 24 publications

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“…VEGF, a heparin-binding glycoprotein, has five known isoforms, and is an important growth factor in the progression and angiogenesis of malignant tumors (34). It was demonstrated that radiation induces VEGF expression in a range of tumor cell lines (35), and that certain tumor cells protect themselves against radiotherapy via the release of VEGF (36).…”

Section: Discussionmentioning

confidence: 99%

Heavy‑ion beam irradiation inhibits invasion of tongue squamous cell carcinoma Tca8113 cells

Feng

Zheng

et al. 2019

Oncol Lett

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Tongue squamous cell carcinoma (TSCC) is a common malignant tumor type with aggressive biological characteristics, located in the oral and maxillofacial region. Vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) have been implicated in the invasion and metastasis of various malignant tumor types, such as lung cancer and gastric carcinoma. High linear energy transfer (LET) particle irradiation has several advantages over conventional X-rays in suppressing the invasion and metastasis of malignant tumors. The objective of the present study was to investigate the effects of high-LET carbon ions and low-LET X-rays on the expression of VEGF and MMPs, and to identify the associated mechanisms in the Tca8113 TSCC cell line. Tca8113 cells were irradiated with carbon ions or X-rays at doses of 1 and 4 Gy. An immunofluorescence assay indicated that VEGF expression was notably decreased at 24 and 48 h after heavy ion irradiation compared with irradiation with conventional X-rays. The expression of MMP-2 and MMP-9 also decreased in a dose-dependent manner following heavy ion irradiation. These findings indicate that compared with low-LET X-ray irradiation, high-LET carbon ions possess higher biological efficacy in inhibiting the invasive ability of Tca8113 cells via reduction of VEGF, MMP-2 and MMP-9 expression.

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Section: Discussionmentioning

confidence: 99%

Heavy‑ion beam irradiation inhibits invasion of tongue squamous cell carcinoma Tca8113 cells

Feng

Zheng

et al. 2019

Oncol Lett

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“…Dose-dependent increases in VEGF levels after RT have been documented in human glioblastoma cells and in lung cancer mouse xenografts [ 36 , 37 ], and proposed to be associated with radioresistance. In the veterinary literature, RT up-regulated VEGF production in a melanoma cell line in a dose-dependent manner [ 38 ], but no changes in VEGF levels post- radiation were seen in a mast cell tumor cell line [ 39 ]. There are also correlations between the EGFR and VEGF pathways, as these share parallel and reciprocal downstream signaling mechanisms, and exert direct and indirect effects on tumor cells that contribute to cancer progression [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of epidermal growth factor receptor kinase inhibition on radiation response in canine osteosarcoma cells

2016

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BackgroundRadiation therapy is a palliative treatment modality for canine osteosarcoma, with transient improvement in analgesia observed in many cases. However there is room for improvement in outcome for these patients. It is possible that the addition of sensitizing agents may increase tumor response to radiation therapy and prolong quality of life. Epidermal growth factor receptor (EGFR) expression has been documented in canine osteosarcoma and higher EGFR levels have been correlated to a worse prognosis. However, effects of EGFR inhibition on radiation responsiveness in canine osteosarcoma have not been previously characterized. This study examined the effects of the small molecule EGFR inhibitor erlotinib on canine osteosarcoma radiation responses, target and downstream protein expression in vitro. Additionally, to assess the potential impact of treatment on tumor angiogenesis, vascular endothelial growth factor (VEGF) levels in conditioned media were measured.ResultsErlotinib as a single agent reduced clonogenic survival in two canine osteosarcoma cell lines and enhanced the impact of radiation in one out of three cell lines investigated. In cell viability assays, erlotinib enhanced radiation effects and demonstrated single agent effects. Erlotinib did not alter total levels of EGFR, nor inhibit downstream protein kinase B (PKB/Akt) activation. On the contrary, erlotinib treatment increased phosphorylated Akt in these osteosarcoma cell lines. VEGF levels in conditioned media increased after erlotinib treatment as a single agent and in combination with radiation in two out of three cell lines investigated. However, VEGF levels decreased with erlotinib treatment in the third cell line.ConclusionsErlotinib treatment promoted modest enhancement of radiation effects in canine osteosarcoma cells, and possessed activity as a single agent in some cell lines, indicating a potential role for EGFR inhibition in the treatment of a subset of osteosarcoma patients. The relative radioresistance of osteosarcoma cells does not appear to be related to EGFR signalling exclusively. Angiogenic responses to radiation and kinase inhibitors are similarly likely to be multifactorial and require further investigation.

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“…A well-known driver of neovascularisation is vascular endothelial growth factor (VEGF), a heparin glycoprotein that binds to receptors VEGFR1 and VEGFR2 on endothelial cells. Up to 95% of COMs express VEGF [13], with VEGF secretion recorded from a canine oral melanoma cell line [106], and genetic copy number imbalances in Vegfr2 also documented [47]. Plasma levels of angiogenic factors such as VEGF are a negative prognostic factor in human cutaneous melanoma patients, and both serum and plasma levels of VEGF are significantly elevated in COM patients relative to geriatric control dogs.…”

Section: Angiogenesismentioning

confidence: 92%

A Comparative View on Molecular Alterations and Potential Therapeutic Strategies for Canine Oral Melanoma

Hardwick

2021

Veterinary Sciences

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Canine oral melanoma (COM) is a highly aggressive tumour associated with poor prognosis due to metastasis and resistance to conventional anti-cancer therapies. As with human mucosal melanoma, the mutational landscape is predominated by copy number aberrations and chromosomal structural variants, but differences in study cohorts and/or tumour heterogeneity can lead to discordant results regarding the nature of specific genes affected. This review discusses somatic molecular alterations in COM that result from single nucleotide variations, copy number changes, chromosomal rearrangements, and/or dysregulation of small non-coding RNAs. A cross-species comparison highlights notable recurrent aberrations, and functionally grouping dysregulated proteins reveals unifying biological pathways that may be critical for oncogenesis and metastasis. Finally, potential therapeutic strategies are considered to target these pathways in canine patients, and the benefits of collaboration between science, medical, and veterinary communities are emphasised.

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Radiation up-regulates the expression of VEGF in a canine oral melanoma cell line

Cited by 9 publications

References 24 publications

Heavy‑ion beam irradiation inhibits invasion of tongue squamous cell carcinoma Tca8113 cells

Heavy‑ion beam irradiation inhibits invasion of tongue squamous cell carcinoma Tca8113 cells

Effects of epidermal growth factor receptor kinase inhibition on radiation response in canine osteosarcoma cells

A Comparative View on Molecular Alterations and Potential Therapeutic Strategies for Canine Oral Melanoma

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