<scp>TRAF</scp>6 regulates tumour metastasis through <scp>EMT</scp> and <scp>CSC</scp> phenotypes in head and neck squamous cell carcinoma

Chen, Lei; Li, Yicun; Wu, Lei; Yu, Guang‐Tao; Zhang, Wenfeng; Huang, Cong-Fa; Sun, Zhi‐Jun

doi:10.1111/jcmm.13439

Cited by 39 publications

(33 citation statements)

References 50 publications

(88 reference statements)

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“…Conditional knockout models revealed essential roles for TRAF6 in a variety of immune cellular backgrounds but also in epithelial cell types [29][30][31][32], indicating how important this factor is for normal cellular homeostasis. More recently, TRAF6 has been implicated also in cancer signalling, by regulating epithelial to mesenchymal transition (EMT) in colon cancer [33], DNA damage in breast cancer backgrounds [34], and involvement in autophagy responses [35]. Our results demonstrate the importance of TRAF6 in cell survival, following NF-B stimulation, in cancer cells.…”

Section: Discussionsupporting

confidence: 58%

HIF-1beta Positively Regulates NF-kappaB Activity via Direct Control of TRAF6

D'Ignazio¹,

Shakir²,

Batie³

et al. 2020

Preprint

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NF-B signalling is crucial for cellular responses to inflammation but has also been associated with the hypoxia response. NF-B and HIF transcription factors possess an intense molecular crosstalk. Although it is known that HIF-1beta modulates NF-kappaB transcriptional response, very little is understood regarding how HIF-1beta contributes to NF-kappaB signalling. Here, we demonstrate that HIF-1beta is required for full NF-kappaB activation in cells following canonical and non-canonical stimuli. We found that HIF-1beta specifically controls TRAF6 expression in human cells but also in Drosophila melanogaster. HIF-1beta binds to the TRAF6 gene and controls its expression independently of HIF-1alpha. Furthermore, exogenous TRAF6 expression is able to rescue all of the cellular phenotypes observed in the absence of HIF-1beta. These results indicate that HIF-1beta is an important regulator of NF-kappaB with consequences for homeostasis and human disease.

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Section: Discussionsupporting

confidence: 58%

HIF-1beta Positively Regulates NF-kappaB Activity via Direct Control of TRAF6

D'Ignazio¹,

Shakir²,

Batie³

et al. 2020

Preprint

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“…Conditional knockout models revealed essential roles for TRAF6 in a variety of immune cellular backgrounds but also in epithelial cell types [31][32][33][34], indicating how important this factor is for normal cellular homeostasis. More recently, TRAF6 was also implicated in cancer signalling, by regulating epithelial to mesenchymal transition (EMT) in colon cancer [35], DNA damage in breast cancer backgrounds [36], and involvement in autophagy responses [37]. Our results demonstrate the importance of TRAF6 in cell survival, following NF-κB stimulation, in cancer cells.…”

Section: Discussionsupporting

confidence: 58%

HIF-1β Positively Regulates NF-κB Activity via Direct Control of TRAF6

D'Ignazio

Shakir

Batie

et al. 2020

IJMS

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NF-κB signalling is crucial for cellular responses to inflammation but is also associated with the hypoxia response. NF-κB and hypoxia inducible factor (HIF) transcription factors possess an intense molecular crosstalk. Although it is known that HIF-1α modulates NF-κB transcriptional response, very little is understood regarding how HIF-1β contributes to NF-κB signalling. Here, we demonstrate that HIF-1β is required for full NF-κB activation in cells following canonical and non-canonical stimuli. We found that HIF-1β specifically controls TRAF6 expression in human cells but also in Drosophila melanogaster. HIF-1β binds to the TRAF6 gene and controls its expression independently of HIF-1α. Furthermore, exogenous TRAF6 expression is able to rescue all of the cellular phenotypes observed in the absence of HIF-1β. These results indicate that HIF-1β is an important regulator of NF-κB with consequences for homeostasis and human disease.

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“…These findings are critically important as more evidence accumulates that suggest subpopulations of CSC may be critical factors in determining the treatment strategy and overall prognosis in oral cancer patients (Ravindran et al, 2015;Mohanta et al, 2017;He et al, 2014). In fact, new evidence suggests that metastatic potential and invasiveness may be heavily dependent upon these CSC subpopulations, therefore more information regarding their properties and survival in well-characterized systems will be critical to further our understanding of these phenomenon (Rodrigues et al, 2018;Shah et al, 2018;Chen et al, 2018). As more studies evaluate the role of CSC in oral cancer, more accurate and predictive models of therapy and prognosis will be needed to more effectively treat and manage patient care (Teixeira and Corrêa, 2018;Castilho et al, 2017).…”

Section: Resultsmentioning

confidence: 99%

Isolation and Identification of Oral Cancer Stem Cells (CSC) within Commercially Available Cell Lines

Chauncey¹,

Hatch²,

Jilka³

et al. 2018

Current Research in Dentistry

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Previous studies have demonstrated some tumors develop or maintain a small sub-population of cells with stem cell-like properties. This Cancer Stem Cells (CSC) may exhibit differential properties that allow their escape from traditional radiation or chemotherapy treatments and may therefore be responsible for cancer recurrence. Few studies have explored this phenomenon among oral cancer cell lines, therefore the objective of this study was to examine multiple oral cancer cell lines to determine if any or all contained subpopulations of CSCs. Multiple commercially available Oral Squamous Carcinoma Cell (OSCC) lines were obtained for this study, including SCC15, SCC25 and CAL27. Cells were cultured for CSC screening and isolation. RNA was isolated from any potential CSC isolates for biomarker screening and verification. All OSCC lines examined developed adhesion-independent tumor spheres (AiTS), a characteristic phenotype of oral CSC. Each AiTS was manually isolated for separate, independent culture and analysis. RNA extracted from the AiTS revealed differential expression of specific CSC markers, including CD44, CD133, ABCG, CXCR6 and NANOG. These biomarkers were not observed in RNA extracted from the remaining non-CSC cell cultures. Although a previous study from this group successfully isolated AiTS from one cervical and one oral cancer cell line, this may be the first study to isolate CSC from multiple oral cancer cell lines and verify both cell-surface and intracellular CSC biomarkers. These results may suggest that many tumors and oral cancers could harbor AiTS and CSC and that screening for these sub-populations may provide guidance for treatment and therapy to improve oral cancer survival rates.

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TRAF6 regulates tumour metastasis through EMT and CSC phenotypes in head and neck squamous cell carcinoma

Cited by 39 publications

References 50 publications

HIF-1beta Positively Regulates NF-kappaB Activity via Direct Control of TRAF6

HIF-1beta Positively Regulates NF-kappaB Activity via Direct Control of TRAF6

HIF-1β Positively Regulates NF-κB Activity via Direct Control of TRAF6

Isolation and Identification of Oral Cancer Stem Cells (CSC) within Commercially Available Cell Lines

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