Prognostic Impact of VEGF and VEGF Receptor 1 (FLT1) Expression in Patients Irradiated for Stage II/III Non-Small Cell Lung Cancer (NSCLC)

Rades, Dirk; Setter, Cornelia; Dunst, Juergen; Dahl, Olav; Schild, Steven E.; Noack, F.

doi:10.1007/s00066-010-2131-4

Cited by 15 publications

(8 citation statements)

References 28 publications

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“…The study of Checinska et al ( 41 ) suggested that caspase-9 may initiate a scaffold function and may serve as caspase substrate during NSCLC apoptosis. Additionally, therapy that targets VEGF has been demonstrated to be beneficial for the treatment of NSCLC ( 42 , 43 ). Furthermore, TRAIL-I-131 treatment markedly inhibited VEGF and AP-1 expression in A549 and H358 cells, which potentially contributed to the inhibitory efficacy of TRAIL-I-131 treatment for tumor growth in the NSCLC-bearing mouse model.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor‑related apoptosis‑inducing ligand additive with Iodine‑131 of inhibits non‑small cell lung cancer cells through promoting apoptosis

Yao

Liu

2018

Oncol Lett

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Non-small-cell lung cancer (NSCLC) accounts for ~80% of human lung cancer cases and is the most common cause of cancer-associated mortality worldwide. Reports have indicated that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Iodine-131 (I-131) can induce tumor cell apoptosis. The purpose of the present study was to investigate the additive efficacy of TRAIL and I-131 on NSCLC cells. The present study demonstrated that additive treatment of TRAIL and I-131 (TRAIL-I-131) significantly inhibited the growth and aggressiveness of NSCLC cells compared with single TRAIL or I-131 treatment. Results demonstrated that TRAIL-I-131 treatment induced apoptosis of NSCLC cells, with western blot analysis confirming that TRAIL-I-131 treatment increased proapoptotic Bad and Bax expression levels, while antiapoptotic Bcl-2 and Bcl-w protein levels were decreased in NSCLC cells. The present study demonstrated that TRAIL-I-131 treatment inhibited vascular endothelial growth factor (VEGF) and activator protein-1 (AP-1) in NSCLC cells. Potential mechanism analyses identified that TRAIL-I-131 treatment induced apoptosis of NSCLC cells through caspase-9 activation. In vivo assays revealed that TRAIL-I-131 treatment significantly inhibited NSCLC tumor growth and increased apoptotic bodies in tumor tissues. Immunohistology demonstrated that caspase-9 was upregulated and VEGF was downregulated in tumor tissues in TRAIL-I-131-treated tumors. In conclusion, these results indicate that TRAIL combined with I-131 promoted apoptosis of NSCLC through caspase-9 activation, which may be a promising anticancer therapeutic schedule for the treatment of NSCLC.

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor‑related apoptosis‑inducing ligand additive with Iodine‑131 of inhibits non‑small cell lung cancer cells through promoting apoptosis

Yao

Liu

2018

Oncol Lett

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“…Whether methods which can be applied in the clinic can predict outcome after radiotherapy in patients, e.g., the gH2AX foci assay to estimate intrinsic radiosensitivity [7,10], specific surface markers to assess the number of tumor stem cells [2,9], and endogenous hypoxia markers [3,6,12], requires further validation.…”

Section: Tumormentioning

confidence: 99%

Prognostic Value of Radiobiological Hypoxia during Fractionated Irradiation for Local Tumor Control

et al. 2011

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“…In response to the reduced O 2 availability, adaptative mechanisms such as increased glycolysis, glucose uptake, and survival factors, including HIFs and VEGF, are induced. These factors have miscellaneous effects on tumor progression and outcome of chemo-/ radiotherapy [2,13,15] .…”

Section: Introductionmentioning

confidence: 99%

Curcumin Decreases Survival of Hep3B Liver and MCF-7 Breast Cancer Cells

2011

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Prognostic Impact of VEGF and VEGF Receptor 1 (FLT1) Expression in Patients Irradiated for Stage II/III Non-Small Cell Lung Cancer (NSCLC)

Abstract: Tumor expression of VEGF and FLT1 appear to have no significant impact on LC, MFS, or OS in patients irradiated for NSCLC.

Cited by 15 publications

References 28 publications

Tumor necrosis factor‑related apoptosis‑inducing ligand additive with Iodine‑131 of inhibits non‑small cell lung cancer cells through promoting apoptosis

Tumor necrosis factor‑related apoptosis‑inducing ligand additive with Iodine‑131 of inhibits non‑small cell lung cancer cells through promoting apoptosis

Prognostic Value of Radiobiological Hypoxia during Fractionated Irradiation for Local Tumor Control

Curcumin Decreases Survival of Hep3B Liver and MCF-7 Breast Cancer Cells

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