EMT: A new vision of hypoxia promoting cancer progression

Jiang, Jian; Tang, Yaling; Liang, Xin‐hua

doi:10.4161/cbt.11.8.15274

Cited by 230 publications

(229 citation statements)

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“…However, certain cancer cells in the hypoxic environment undergo adaptive changes and produce energy via anaerobic glycolysis, enabling their survival and proliferation (28,29). Ki-67, a proliferation-related nuclear protein, is expressed in proliferating cells during all active phase of the cell cycle (30,31).…”

Section: Discussionmentioning

confidence: 99%

Expression and clinical significance of glucose transporter-1 in pancreatic cancer

Lǚ

Yang

et al. 2016

Oncology Letters

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Abstract.Increasing evidence has demonstrated that malignant cells exhibit increased glucose uptake, which facilitates survival and growth in a hypoxic environment. The glucose transporter-1 (GLUT-1) is overexpressed in a variety of malignant tumors. However, the association between GLUT-1 expression and clinicopathological factors, 18 F-fluorodeoxyglucose uptake and tumor proliferation in pancreatic cancer has not been investigated to date. In the present study, the expression of GLUT-1 in 53 pancreatic cancer tissues was analyzed, which revealed that GLUT-1 was overexpressed in pancreatic tissue and correlated with poor prognosis and clinicopathological characteristics, including increased tumor size, clinical stage and lymph node metastasis, maximum standardized uptake value (SUV max ) and Ki-67 expression. The receiver operating characteristic curve analysis indicated that a cut-off SUV max value of 4.830 was associated with optimal sensitivity (88%) and specificity (71.4%) for the detection of strong positive GLUT-1 expression. In addition, as the expression of GLUT-1 was found to correlate with Ki-67 expression, GLUT-1 may exhibit a significant effect on cell proliferation in pancreatic cancer. Overall, these findings indicate that GLUT-1 may represent a prognostic indicator, and a potential therapeutic target for pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

Expression and clinical significance of glucose transporter-1 in pancreatic cancer

Lǚ

Yang

et al. 2016

Oncology Letters

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“…5 The burgeoning interest in hypoxia was further fuelled by the critical finding that hypoxia selects for stress-resistant, more malignant tumour cells. [6][7][8] This implied that tumour cells that survive hypoxic stress were likely to be a significant source of viable clonogens that can repopulate tumours with more malignant/metastatic cells. Unfortunately, most treatment protocols are less effective against hypoxic cells, which are resistant not only to RT but also to standard cytotoxic chemotherapy (CCT); 9,10 although it has been reported recently that, in a few situations, hypoxia may enhance the effects of CCT.…”

mentioning

confidence: 99%

Defining normoxia, physoxia and hypoxia in tumours—implications for treatment response

McKeown

2014

BJR

803

712

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Tumour hypoxia is increasingly recognized as a major deleterious factor in cancer therapies, as it compromises treatment and drives malignant progression. This review seeks to clarify the oxygen levels that are pertinent to this issue. It is argued that normoxia (20% oxygen) is an extremely poor comparator for "physoxia", i.e. the much lower levels of oxygen universally found in normal tissues, which averages about 5% oxygen, and ranges from about 3% to 7.4%. Importantly, it should be recognized that the median oxygenation in untreated tumours is significantly much lower, falling between approximately 0.3% and 4.2% oxygen, with most tumours exhibiting median oxygen levels ,2%. This is partially dependent on the tissue of origin, and it is notable that many prostate and pancreatic tumours are profoundly hypoxic. In addition, therapy can induce even further, often unrecognized, changes in tumour oxygenation that may vary longitudinally, increasing or decreasing during treatment in ways that are not always predictable. Studies that fail to take cognizance of the actual physiological levels of oxygen in tissues (approximately 5%) and tumours (approximately 1%) may fail to identify the real circumstances driving tumour response to treatment and/or malignant progression. This can be of particular importance in genetic studies in vitro when comparison to human tumours is required.

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“…The hypoxic environment within the core of the solid tumor has been established as one of the crucial cellular factors driving EMT [15][16][17][18][19]. Uncontrolled cell proliferation of tumor cells leads to larger tumor mass.…”

Section: Signaling Factors Involved In Epithelial-to-mesenchymal Tranmentioning

confidence: 99%

Epithelial To Mesenchymal Transition in Breast Cancer Metastasis: Mitochondria Take the Center Stage

Guha¹

2016

CBCM

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Epithelial to Mesenchymal Transition (EMT), a process involved in organogenesis and wound healing is now at the center stage of cancer metastasis. While most of the current research is focused on defects arising in the nuclear genome, the contribution of defects in mitochondria has remained under investigated. In the past decade, the association between mitochondrial genomic (mtDNA) and functional defects resulting in altered metabolism with tumor progression and poor outcome has become more evident. Here we review the contribution of mitochondria in epithelial-to-mesenchymal transition, particularly focusing on breast cancer. Our goal is to highlight the critical role that mitochondrial genome defects induced retrograde signaling play in driving cellular plasticity. We will further discuss the molecular intermediates of the retrograde signaling pathway, which can potentially be novel therapeutic targets in mitochondrial stress induced EMT.

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EMT: A new vision of hypoxia promoting cancer progression

Cited by 230 publications

References 0 publications

Expression and clinical significance of glucose transporter-1 in pancreatic cancer

Expression and clinical significance of glucose transporter-1 in pancreatic cancer

Defining normoxia, physoxia and hypoxia in tumours—implications for treatment response

Epithelial To Mesenchymal Transition in Breast Cancer Metastasis: Mitochondria Take the Center Stage

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