Inflammation and cancer stem cells

Shigdar, Sarah; Yong, Li; Bhattacharya, Santanu; O'Connor, M. L.; Pu, Chunwen; Ji, Lin; Wang, Tao; Xiang, Dongxi; Kong, Lingxue; Wei, Ming Q.; Zhu, Y.; Zhou, Shu‐Feng; Duan, Wei

doi:10.1016/j.canlet.2013.07.031

Cited by 111 publications

(85 citation statements)

References 96 publications

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“…The exact molecular factors and cellular mechanisms governing the quiescence and activation of dormant CSCs have been intensely investigated but remain unclear, highlighting the requirement for additional research in this area. Because inflammation has been functionally related to cancer evolution and because inflammatory signals have been shown to regulate the quiescence/activation of cancer and normal SCs [8,10,47,54,55] but not much is known concerning the circuitries connecting inflammation to melanoma development, we examined the effect of TNF, which is one of the major mediators of cancerrelated inflammatory responses [9], on melanoma cell quiescence and melanoma development in 3D tumor-like sphere and in vivo-like reconstructed skin models. Using an inducible H2B-GFP system to trace the cell divisional history in vitro, we identified quiescent/slow-cycling GFP high label-retaining CSCs in melanoma cell lines and showed that transient and chronic TNF suppresses melanoma SC differentiation while enriching for a GFP high melanosphere-initiating CSC subpopulation many generations after TNF withdrawal.…”

Section: Discussionmentioning

confidence: 99%

Transient TNF regulates the self-renewing capacity of stem-like label-retaining cells in sphere and skin equivalent models of melanoma

Ostyn

Machhour

Bégard

et al. 2014

Cell Communication and Signaling

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Background: It is well established that inflammation promotes cancer, including melanoma, although the exact mechanisms involved are less known. In this study, we tested the hypothesis that inflammatory factors affect the cancer stem cell (CSC) compartment responsible for tumor development and relapse. Results: Using an inducible histone 2B-GFP fusion protein as a tracer of cell divisional history, we determined that tumor necrosis factor (TNF), which is a classical pro-inflammatory cytokine, enlarged the CSC pool of GFP-positive label-retaining cells (LRCs) in tumor-like melanospheres. Although these cells acquired melanoma stem cell markers, including ABCB5 and CD271, and self-renewal ability, they lost their capacity to differentiate, as evidenced by the diminished MelanA expression in melanosphere cells and the loss of pigmentation in a skin equivalent model of human melanoma. The undifferentiated cell phenotype could be reversed by LY294002, which is an inhibitor of the PI3K/AKT signaling pathway, and this reversal was accompanied by a significant reduction in CSC phenotypic markers and functional properties. Importantly, the changes induced by a transient exposure to TNF were long-lasting and observed for many generations after TNF withdrawal.

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Section: Discussionmentioning

confidence: 99%

Transient TNF regulates the self-renewing capacity of stem-like label-retaining cells in sphere and skin equivalent models of melanoma

Ostyn

Machhour

Bégard

et al. 2014

Cell Communication and Signaling

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“…1,2 Hence, the molecular factors that play important roles in OSCC carcinogenesis, progression, and targeted therapy need to be identified.mutation play important roles in cancer development and cancer cell origin. 3 Tumor necrosis factor receptor-associated factors (TRAFs) are adapter proteins that connect several signaling pathways and are involved in nuclear factor (NF)-κB and interferon regulatory factor (IRF) signaling activation. TRAF1 is different from six other TRAFs.…”

Section: Introductionmentioning

confidence: 99%

Expression and associations of TRAF1, BMI-1, ALDH1, and Lin28B in oral squamous cell carcinoma

et al. 2017

Tumour Biol.

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Tumor necrosis factor receptor-associated factor 1, an adaptor protein of tumor necrosis factor 2, is involved in classical nuclear factor (NF)-κB activation and lymphocyte recruitment. However, less is known about the expression and association of tumor necrosis factor receptor-associated factor 1 with cancer stem cell markers in oral squamous cell carcinoma. This study aimed to investigate the expression of tumor necrosis factor receptor-associated factor 1 and stem cell characteristic markers (lin28 homolog B, B cell-specific Moloney murine leukemia virus integration site 1, and aldehyde dehydrogenase 1) in oral squamous cell carcinoma and analyze their relations. Paraffin-embedded tissues of 78 oral squamous cell carcinomas, 39 normal oral mucosa, and 12 oral dysplasia tissues were employed in tissue microarrays, and the expression of tumor necrosis factor receptor-associated factor 1, B cell-specific Moloney murine leukemia virus integration site 1, aldehyde dehydrogenase 1, and lin28 homolog B was measured by immunohistostaining and digital pathological analysis. The expression of tumor necrosis factor receptor-associated factor 1 was higher in the oral squamous cell carcinoma group as compared with the expression in the oral mucosa (p < 0.01) and oral dysplasia (p < 0.001) groups. In addition, the expression of tumor necrosis factor receptor-associated factor 1 was associated with those of B cell-specific Moloney murine leukemia virus integration site 1, aldehyde dehydrogenase 1, and lin28 homolog B (p = 0.032, r 2 = 0.109; p < 0.0001, r 2 = 0.64; and p < 0.001, r 2 = 0.16) in oral squamous cell carcinoma. The patient survival rate was lower in the highly expressed tumor necrosis factor receptor-associated factor 1 group, although the difference was not significant. The clustering analysis showed that tumor necrosis factor receptor-associated factor 1 was most related to aldehyde dehydrogenase 1. These findings suggest that tumor necrosis factor receptor-associated factor 1 has potential direct/indirect regulations with the cancer stem cell markers in oral squamous cell carcinoma, which may help in further analysis of the cancer stem cell characteristics.

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“…There is increasing evidence that inflammation and CSCs are associated with carcinogenesis in numerous tumor types (11,(16)(17)(18)(19). Recent studies have suggested an association between inflammation within the tumor microenvironment and CSCs (17,19); however, the effect of inflammation on CSCs has yet to be fully determined.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have suggested an association between inflammation within the tumor microenvironment and CSCs (17,19); however, the effect of inflammation on CSCs has yet to be fully determined. Blaylock (19) reported that inflammation is essential to cancer induction through its mutagenic effects on stem cell DNA.…”

Section: Discussionmentioning

confidence: 99%

“…Blaylock (19) reported that inflammation is essential to cancer induction through its mutagenic effects on stem cell DNA. Shigdar et al (17) demonstrated that inflammatory response and stimuli from immune cells, including cytokines, cause cancer cells to dedifferentiate into CSCs through several signaling pathways, including the NF-κB signaling pathway. In breast cancer, several studies have reported that inflammatory signaling within the tumor microenvironment affects CSCs (20)(21)(22)(23).…”

Section: Discussionmentioning

confidence: 99%

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Association between inflammation and cancer stem cell phenotype in breast cancer

Jeong

Park

et al. 2017

Oncol Lett

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Inflammation and cancer stem cells

Cited by 111 publications

References 96 publications

Transient TNF regulates the self-renewing capacity of stem-like label-retaining cells in sphere and skin equivalent models of melanoma

Transient TNF regulates the self-renewing capacity of stem-like label-retaining cells in sphere and skin equivalent models of melanoma

Expression and associations of TRAF1, BMI-1, ALDH1, and Lin28B in oral squamous cell carcinoma

Association between inflammation and cancer stem cell phenotype in breast cancer

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