Carbon dioxide, Hypoxia and Low pH Lead to Overexpression of<i>c-myc</i>and<i>HMGB-1</i>Oncogenes in Neuroblastoma Cells

Reismann, Marc; Wehrmann, Fabian; Schukfeh, Nagoud; Kuebler, Joachim F.; Ure, Benno M.; Glüer, S.

doi:10.1055/s-0029-1202778

Cited by 26 publications

(17 citation statements)

References 24 publications

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“…The activity of c-Myc may also drive the expression of proteins that promote glycolysis and tumor acidity of which include LDH-A and GLUT1 as well as enzymes that promote nucleotide synthesis and ATP production [8,9,127,128]. However, in other cell types such as neuroblastoma and H1299 lung cancer cells, acidosis stimulates the expression of oncogenes such as c-Myc and high mobility group box 1 ( HMGB-1 ) [124,129]. Acidosis may also stimulate epigenetic rearrangements to increase the expression of a novel metabolic proto-oncogene fatty acid synthase ( FAS ) in breast cancer cells [130].…”

Section: Molecular Connections Between Acidosis and Cancer Cell Mementioning

confidence: 99%

Molecular Connections between Cancer Cell Metabolism and the Tumor Microenvironment

Justus

Sanderlin

Yang

2015

IJMS

127

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Cancer cells preferentially utilize glycolysis, instead of oxidative phosphorylation, for metabolism even in the presence of oxygen. This phenomenon of aerobic glycolysis, referred to as the “Warburg effect”, commonly exists in a variety of tumors. Recent studies further demonstrate that both genetic factors such as oncogenes and tumor suppressors and microenvironmental factors such as spatial hypoxia and acidosis can regulate the glycolytic metabolism of cancer cells. Reciprocally, altered cancer cell metabolism can modulate the tumor microenvironment which plays important roles in cancer cell somatic evolution, metastasis, and therapeutic response. In this article, we review the progression of current understandings on the molecular interaction between cancer cell metabolism and the tumor microenvironment. In addition, we discuss the implications of these interactions in cancer therapy and chemoprevention.

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Section: Molecular Connections Between Acidosis and Cancer Cell Mementioning

confidence: 99%

Molecular Connections between Cancer Cell Metabolism and the Tumor Microenvironment

Justus

Sanderlin

Yang

2015

IJMS

127

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“…It is established that CO 2 pneumoperitoneum alters the chemical environment through hypoxia, pH fluctuations, and increased IAP that influence diverse cell functions . Our results provide evidence that CO 2 insufflation pressures of 10 mmHg may be ideal in reducing the viability of carcinoma cells in an in vitro setting and that the effects on cancer cell growth may take longer than 7 days to show effect.…”

Section: Discussionmentioning

confidence: 91%

“…The impact of pressure on cell growth and proliferation in a CO 2 ‐rich environment has been studied in vitro in human colon, gastric and cervical cancer, and neuroblastoma cell lines. Cell line‐dependent and dose‐response effects have been observed with pressures higher than 10 mmHg and longer duration and have a more apparent effect on influencing cancer cell growth …”

Section: Introductionmentioning

confidence: 99%

In vitro evaluation of a simulated pneumoperitoneum environment using carbon dioxide on canine transitional cell carcinoma

et al. 2018

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The pH in the media significantly decreased immediately after CO exposure but returned to normal within 1 hour. The viability of the cell lines was variably affected at the evaluated pressures. Insufflation pressure of 10 mmHg resulted in significantly decreased cell viability compared with control. The impact of 15 mmHg CO was comparable to 0 mmHg and control. CO insufflation pressure had no significant effects on proliferation up to 7 days postexposure. Conclusion/Clinical significance: A positive pressure CO environment significantly decreased the viability of TCC and MDCK cells under specific conditions without influencing their proliferation up to 7 days postexposure. Investigating these effects in clinical patients undergoing CO laparoscopy is essential to assess for port site metastasis or peritoneal carcinomatosis in order to translate these in vitro results to clinical recommendations.

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“…2 The CO 2 influence on NB cell growth and biology continues to be an enigma for researchers. 3,4 CO 2 insufflation induces metabolic acidosis and hypoxia influencing cell functions. 4 Hypoxia plays an important role in regulating key aspects of tumor biology contributing to tumor cell survival/death and progression.…”

Section: Introductionmentioning

confidence: 99%

“…3,4 CO 2 insufflation induces metabolic acidosis and hypoxia influencing cell functions. 4 Hypoxia plays an important role in regulating key aspects of tumor biology contributing to tumor cell survival/death and progression. The response to hypoxia is mainly mediated through the activation of the oxygen-sensitive transcription factors, hypoxia-inducible factors (HIFs), which transcriptionally regulate the expression of several genes involved in apoptosis, proliferation, angiogenesis, metabolism, and invasion/metastasis.…”

Section: Introductionmentioning

confidence: 99%

CO2 Pneumoperitoneum Effects on Molecular Markers of Tumor Invasiveness in SH-SY5Y Neuroblastoma Cells

et al. 2019

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Introduction CO2 pneumoperitoneum can influence the biological behavior of neuroblastoma (NB). Angiogenesis and genetic features are responsible for malignant phenotype of this tumor. We examined the CO2 effects on N-Myc, vascular endothelial growth factor (VEGF), and matrix metalloproteinase-2 (MMP-2) expression as critical biomarkers of tumor invasiveness, in NB cells without N-Myc amplification. Materials and Methods SH-SY5Y cells were exposed to CO2 (100%) at 15 mm Hg pressure for 4 hours and then moved to normal condition for 24 hours. Control cells were incubated with 5% CO2 for the same time. In control and CO2-exposed cells, the messenger ribonucleic acid (mRNA) levels of hypoxia-inducible factor (HIF)-1α, HIF-2α, VEGF-A, and MMP-2 were quantified by real-time polymerase chain reaction. N-Myc expression was evaluated by Western blot analysis. Results The exposure to 15 mm Hg CO2 (100%) for 4 hours induced an increase in HIF-1α, but not in HIF-2α, mRNA levels. No differences were observed in N-Myc expression between exposed and control cells at each incubation time. Similarly, no significant differences were found for VEGF-A and MMP-2 transcript levels. In CO2 exposed cells, we observed only a slight increase in both VEGF-A and MMP-2 mRNA levels after 4 and 24 hours in comparison to controls. Conclusion In our study, the hypoxic environment induced by CO2 exposure does not affect the expression of critical biomarkers of NB aggressiveness, such as N-Myc, VEGF, and MMP-2, in human SH-SY5Y NB cells without N-Myc amplification. These data suggest that CO2 pneumoperitoneum might not adversely impact NB cell invasiveness; however, it is necessary to evaluate these effects in others in vitro and in vivo models.

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Carbon dioxide, Hypoxia and Low pH Lead to Overexpression ofc-mycandHMGB-1Oncogenes in Neuroblastoma Cells

Abstract: Exposures mimicking conditions of CO (2) pneumoperitoneum lead to significant overexpression of C-MYC and HMGB-1 in neuroblastoma cells with decreased apoptosis. These results point to a negative influence and potentially increased malignancy of tumor cells.

Cited by 26 publications

References 24 publications

Molecular Connections between Cancer Cell Metabolism and the Tumor Microenvironment

Molecular Connections between Cancer Cell Metabolism and the Tumor Microenvironment

In vitro evaluation of a simulated pneumoperitoneum environment using carbon dioxide on canine transitional cell carcinoma

CO2 Pneumoperitoneum Effects on Molecular Markers of Tumor Invasiveness in SH-SY5Y Neuroblastoma Cells

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