Hypoxia-Induced Tumour Cell Migration in an in vivo Chicken Model

Plaßwilm, Ludwig; Tannapfel, Andrea; Cordes, Nils; Demir, Resit; Höper, K.; Bauer, Joseph A.; Höper, J.

doi:10.1159/000055909

Cited by 26 publications

(18 citation statements)

References 30 publications

(38 reference statements)

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“…The differences in stem potential of those cells describe the characteristics of primary and metastatic cells rather than the contribution of CD105+. Also, in contrast to other studies, we have shown that in the case of pRCC, hypoxic conditions in vitro diminish the stem-like properties of cell lines [79–85]. …”

Section: Discussioncontrasting

confidence: 99%

Functional significance of CD105-positive cells in papillary renal cell carcinoma

Matak

Brodaczewska²,

Szczylik³

et al. 2017

BMC Cancer

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BackgroundCD105 was postulated as a renal cell carcinoma (RCC) stem cell marker, and CD133 as a putative RCC progenitor. Hypoxia, a natural microenvironment that prevails in tumors, was also incorporated into the study, especially in terms of the promotion of hypothetical stem-like cell properties.MethodsWithin this study, we verify the existence of CD105+ and CD133+ populations in selected papillary subtype RCC (pRCC) cell lines. Both populations were analyzed for correlation with stem-like cell properties, such as stemness gene expression, and sphere and colony formation. For the preliminary analysis, several RCC cell lines were chosen (786-O, SMKT-R2, Caki-2, 796-P, ACHN, RCC6) and the control was human kidney cancer stem cells (HKCSC) and renal cells of embryonic origin (ASE-5063). Four cell lines were chosen for further investigation: Caki-2 (one of the highest numbers of CD105+ cells; primary origin), ACHN (a low number of CD105+ cells; metastatic origin), HKCSC (putative positive control), and ASE-5063 (additional control).ResultsIn 769-P and RCC6, we could not detect a CD105+ population. Hypoxia variously affects pRCC cell growth, and mainly diminishes the stem-like properties of cells. Furthermore, we could not observe the correlation of CD105 and/or CD133 expression with the enhancement of stem-like properties.ConclusionsBased on this analysis, CD105/CD133 cannot be validated as cancer stem cell markers of pRCC cell lines.

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Section: Discussioncontrasting

confidence: 99%

Functional significance of CD105-positive cells in papillary renal cell carcinoma

Matak

Brodaczewska²,

Szczylik³

et al. 2017

BMC Cancer

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“…Another transcription factor that can activate the c-Met promoter under normoxic as Previous studies suggested that hypoxia can stimulate glioma cell migration and invasion, although the responsible mechanisms have so far remained unclear. [18][19][20] In this study we analyzed 3 glioblastoma cell lines in which c-Met was inducible by hypoxia. We found that hypoxia by itself stimulated the migration of only 1 of these cell lines (U87), but enhanced the motogenic effects of SF/HGF on all 3 cell lines.…”

Section: Hypoxia Synergizes With Sf/hgf In Inducing Glioma Cell Migramentioning

confidence: 99%

“…14 Hypoxia has been found to also increase the migration of glioma cells, although the mechanisms of this stimulation have so far remained unclear. [18][19][20] We hypothesized that the induction of cMet via HIF-1 might be one such mechanism. We therefore analyzed (i) whether c-Met protein and mRNA are inducible by hypoxia in glioma cells, (ii) whether the hypoxic induction of c-Met is mediated through HIF-1a and (iii) whether hypoxia can enhance the effect of SF/HGF on glioma cell migration in vitro.…”

mentioning

confidence: 99%

Hypoxia can induce c‐Met expression in glioma cells and enhance SF/HGF‐induced cell migration

Eckerich

Zapf

Fillbrandt

et al. 2007

Intl Journal of Cancer

120

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The c-Met receptor and its ligand scatter factor/hepatocyte growth factor (SF/HGF) are strongly overexpressed in malignant gliomas. Signaling through c-Met as well as exposure to hypoxia can stimulate glioma cell migration and invasion. In several cancer cell types, hypoxia was shown to activate the c-met promoter, which contains hypoxia inducible factor-1 (HIF-1) binding sites. We hypothesized that hypoxia might upregulate c-Met also in glioma cells. Analyzing 18 different glioblastoma cell lines and 10 glioblastoma primary cultures, we found that in 50% of both the cell lines and the primary cultures c-Met protein levels were increased following exposure to hypoxia. Upregulation of c-met in response to hypoxia was also detected at the transcriptional level. In all primary cultures and in 16 of the 18 cell lines (89%), HIF1a levels were increased by hypoxia. Transfection of siRNA against HIF-1a abgrogated the hypoxic induction of c-Met, suggesting that c-Met expression is upregulated by a HIF-1a-dependent mechanism. Hypoxia sensitized glioblastoma cell lines which showed hypoxic induction of c-Met to the motogenic effects of SF/ HGF. These findings suggest that approximately half of all human glioblastomas respond to hypoxia with an induction of c-Met, which can enhance the stimulating effect of SF/HGF on tumor cell migration. ' 2007 Wiley-Liss, Inc.

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“…This results in additional resistance to radiotherapy and chemotherapy (2) and further increase in angiogenesis and a more aggressive tumor potential (3–5). …”

Section: Introductionmentioning

confidence: 99%

Ozone Therapy for Tumor Oxygenation: a Pilot Study

Clavo

Pérez

Mora

et al. 2004

Evidence-Based Complementary and Alternative Medicine

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Tumor hypoxia is an adverse factor for chemotherapy and radiotherapy. Ozone therapy is a non-conventional form of medicine that has been used successfully in the treatment of ischemic disorders. This prospective study was designed to assess the effect of ozone therapy on tumor oxygenation. Eighteen subjects were recruited for the study. Systemic ozone therapy was administered by autohemotransfusion on three alternate days over one week. Tumor oxygenation levels were measured using polarographic needle probes before and after the first and the third ozone therapy session. Overall, no statistically significant change was observed in the tumor oxygenation in the 18 patients. However, a significant decrease was observed in hypoxic values ≤10 and ≤5 mmHg of pO2. When individually assessed, a significant and inverse non-linear correlation was observed between increase in oxygenation and the initial tumor pO2 values at each measuring time-point, thus indicating that the more poorly-oxygenated tumors benefited most (rho = −0.725; P = 0.001). Additionally, the effect of ozone therapy was found to be lower in patients with higher hemoglobin concentrations (rho = −0.531; P < 0.034). Despite being administered over a very short period, ozone therapy improved oxygenation in the most hypoxic tumors. Ozone therapy as adjuvant in chemo-radiotherapy warrants further research.

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Hypoxia-Induced Tumour Cell Migration in an in vivo Chicken Model

Cited by 26 publications

References 30 publications

Functional significance of CD105-positive cells in papillary renal cell carcinoma

Functional significance of CD105-positive cells in papillary renal cell carcinoma

Hypoxia can induce c‐Met expression in glioma cells and enhance SF/HGF‐induced cell migration

Ozone Therapy for Tumor Oxygenation: a Pilot Study

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