Hypoxia and hyperoxia differentially control proliferation of rat neural crest stem cells via distinct regulatory pathways of the HIF1α–CXCR4 and TP53–TPM1 proteins

Chen, Chien‐Cheng; Hsia, Ching-Wu; Ho, C.L.; Liang, Chang-Min; Chen, Chieh-Min; Huang, Kunlun; Kang, Bor‐Hwang; Chen, Yihui

doi:10.1002/dvdy.24481

Cited by 11 publications

(10 citation statements)

References 158 publications

(230 reference statements)

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“…We also identified that HIF-1α can be upregulated in TNBC cells after short-term hyperoxia exposure. There is a vast body of literature demonstrating that HIF-1α increases in hypoxia while in hyperoxic regimens usually decreases [17,18]. However, in skeletal muscle cells under high oxygen concentrations (42%), the amount of HSP90-HIF-1α complex is increased and suggests that HSP90 stabilizes cytoplasmic HIF-1α under high oxygen levels [39].…”

Section: Angiogenesis Is Enhanced By 6 H O 2 Exposure In Triple Negatmentioning

confidence: 99%

“…EMT induces new cancer stem cell formation that may be responsible for cancer recurrence. However, very high levels of ROS induced by exposure to over 80% O 2 are deleterious and induce apoptosis [18]. This suggests that there is a narrow window in which certain degree of hyperoxia can promote cancer progression.We hypothesize that high concentration oxygen exposure, even of short duration, may have long term effects on cancer progression, mainly during the perioperative period when the above mentioned concurrent factors intervene.…”

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confidence: 99%

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confidence: 99%

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Long-Term Deleterious Effects of Short-term Hyperoxia on Cancer Progression—Is Brain-Derived Neurotrophic Factor an Important Mediator? An Experimental Study

Tiron

Ristescu

Postu

et al. 2020

Cancers

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Perioperative factors promoting cancer recurrence and metastasis are under scrutiny. While oxygen toxicity is documented in several acute circumstances, its implication in tumor evolution is poorly understood. We investigated hyperoxia long-term effects on cancer progression and some underlying mechanisms using both in vitro and in vivo models of triple negative breast cancer (TNBC). We hypothesized that high oxygen exposure, even of short duration, may have long-term effects on cancer growth. Considering that hyperoxic exposure results in reactive oxygen species (ROS) formation, increased oxidative stress and increased Brain-Derived Neurotrophic Factor (BDNF) expression, BDNF may mediate hyperoxia effects offering cancer cells a survival advantage by increased angiogenesis and epithelial mesenchymal transition (EMT). Human breast epithelial MCF10A, human MDA-MB-231 and murine 4T1 TNBC were investigated in 2D in vitro system. Cells were exposed to normoxia or hyperoxia (40%, 60%, 80% O 2 ) for 6 h. We evaluated ROS levels, cell viability and the expression of BDNF, HIF-1α, VEGF-R2, Vimentin and E-Cadherin by immunofluorescence. The in vivo model consisted of 4T1 inoculation in Balb/c mice and tumor resection 2 weeks after and 6 h exposure to normoxia or hyperoxia (40%, 80% O 2 ). We measured lung metastases and the same molecular markers, immediately and 4 weeks after surgery. The in vitro study showed that short-term hyperoxia exposure (80% O 2 ) of TNBC cells increases ROS, increases BDNF expression and that promotes EMT and angiogenesis. The in vivo data indicates that perioperative hyperoxia enhances metastatic disease and this effect could be BDNF mediated.Cancers 2020, 12, 688 2 of 18 but rather to local recurrence and metastasis. Cancer evolution after radical resection depends on many factors, mainly the stage of the disease, tumor biological features, initial therapy and immune function status [2]. During the perioperative period several events, such as surgical insult, systemic inflammation, anesthetic and analgesic drugs and blood transfusion, can favor cancer progression [3,4].Oxygen is the most common used drug in the perioperative period. General anesthesia invariably results in perioperative supplemental oxygen administration. Long-time considered as a definitely useful and harmless intervention, oxygen therapy is under scrutiny in recent years. The accumulation of data showing hyperoxia harmful effects during acute events (stroke, myocardial infarction, cardiac arrest) was followed by guidelines recommendation for oxygen use [5,6]. The optimal perioperative oxygen concentration is still poorly defined for specific circumstances. Clinical trials suggest that surgical oncological patients may have an increased risk of mortality and cancer progression when exposed to high oxygen concentration [7,8].The main mechanism of oxygen toxicity is mediated by free radical oxygen species (ROS). ROS production may be followed by increased expression of Brain-Derived Neurotrophic Factor (BDNF) [9][10][11]. BDNF ...

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Section: Angiogenesis Is Enhanced By 6 H O 2 Exposure In Triple Negatmentioning

confidence: 99%

mentioning

confidence: 99%

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Long-Term Deleterious Effects of Short-term Hyperoxia on Cancer Progression—Is Brain-Derived Neurotrophic Factor an Important Mediator? An Experimental Study

Tiron

Ristescu

Postu

et al. 2020

Cancers

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“…The expression in NC migrating cells of genes involved in NCC delamination, such as SNAIL2, SOX10 or C-X-C chemokine receptor type 4 (CXCR4), was higher under hypoxic conditions, stimulating the migration of NCC. Hypoxia seems to induce proliferation in rat neural crest stem cells [21]. Both phenomena were dependent on hypoxia inducible factor 1 alpha (HIF-1α), a transcription factor typically stabilised and activated under hypoxic conditions.…”

Section: Hypoxia and The Origin Of Neuroblastomamentioning

confidence: 99%

“…Hypoxia-mediated gene-expression regulation in neuroblastoma. HIF-1α, HIF-2α, SNAIL-2, SOX10, CXCR4, PDGF1-α, FZD-6, TRKAIII[21][22][23]25,26,31] …”

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confidence: 99%

Hypoxia in the Initiation and Progression of Neuroblastoma Tumours

Castaño

Gómez-Muñoz

Pardal

et al. 2019

IJMS

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Neuroblastoma is the most frequent extracranial solid tumour in children, causing 10% of all paediatric oncology deaths. It arises in the embryonic neural crest due to an uncontrolled behaviour of sympathetic nervous system progenitors, giving rise to heterogeneous tumours. Low local or systemic tissue oxygen concentration has emerged as a cellular stimulus with important consequences for tumour initiation, evolution and progression. In neuroblastoma, several evidences point towards a role of hypoxia in tumour initiation during development, tumour cell differentiation, survival and metastatic spreading. However, the heterogeneous nature of the disease, its developmental origin and the lack of suitable experimental models have complicated a clear understanding of the effect of hypoxia in neuroblastoma tumour progression and the molecular mechanisms implicated. In this review, we have compiled available evidences to try to shed light onto this important field. In particular, we explore the effect of hypoxia in neuroblastoma cell transformation and differentiation. We also discuss the experimental models available and the emerging alternatives to study this problem, and we present hypoxia-related therapeutic avenues being explored in the field.

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The role of oxygen tension in cell fate and regenerative medicine: implications of hypoxia/hyperoxia and free radicals

et al. 2023

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Hypoxia and hyperoxia differentially control proliferation of rat neural crest stem cells via distinct regulatory pathways of the HIF1α–CXCR4 and TP53–TPM1 proteins

Cited by 11 publications

References 158 publications

Long-Term Deleterious Effects of Short-term Hyperoxia on Cancer Progression—Is Brain-Derived Neurotrophic Factor an Important Mediator? An Experimental Study

Long-Term Deleterious Effects of Short-term Hyperoxia on Cancer Progression—Is Brain-Derived Neurotrophic Factor an Important Mediator? An Experimental Study

Hypoxia in the Initiation and Progression of Neuroblastoma Tumours

The role of oxygen tension in cell fate and regenerative medicine: implications of hypoxia/hyperoxia and free radicals

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