Reciprocal activation of cancer-associated fibroblasts and oral squamous carcinoma cells through CXCL1

Wei, Ling-Ying; Lee, Jang‐Jaer; Yeh, Chiou-Yueh; Yang, Chia‐Ju; Kok, Sang‐Heng; Ko, Jenq‐Yuh; Tsai, Feng-Chiao; Chia, Jean-San

doi:10.1016/j.oraloncology.2018.11.002

Cited by 49 publications

(40 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This allows the activation of the NLRP3 inflammasome, the production of IL-1β, leading to tumor progression and lung metastasis [ 214 ]. Another study showed that IL-1β expressed in OSCC cells leads to CXCL1 production by CAFs, which in turn promotes cancer cell migration [ 215 ]. Further studies are required to evaluate whether these two pathways can co-exist.…”

Section: Pro-and Anti-tumor Effects Of Il-1βmentioning

confidence: 99%

Interleukin-1β and Cancer

Rébé

Ghiringhelli

2020

Cancers

201

110

View full text Add to dashboard Cite

Within a tumor, IL-1β is produced and secreted by various cell types, such as immune cells, fibroblasts, or cancer cells. The IL1B gene is induced after “priming” of the cells and a second signal is required to allow IL-1β maturation by inflammasome-activated caspase-1. IL-1β is then released and leads to transcription of target genes through its ligation with IL-1R1 on target cells. IL-1β expression and maturation are guided by gene polymorphisms and by the cellular context. In cancer, IL-1β has pleiotropic effects on immune cells, angiogenesis, cancer cell proliferation, migration, and metastasis. Moreover, anti-cancer treatments are able to promote IL-1β production by cancer or immune cells, with opposite effects on cancer progression. This raises the question of whether or not to use IL-1β inhibitors in cancer treatment.

show abstract

Section: Pro-and Anti-tumor Effects Of Il-1βmentioning

confidence: 99%

Interleukin-1β and Cancer

Rébé

Ghiringhelli

2020

Cancers

201

110

View full text Add to dashboard Cite

show abstract

“…animals. 33 In addition to immunity, ROS produced by NOX2 play an irreplaceable role in physiological processes and promoting cancer. 34 In order to fully prove the upstream and downstream relationship of this pathway, we choose these three inhibitors.…”

Section: Discussionmentioning

confidence: 99%

“…IL‐1β, IL‐6 and TNF‐α are important proinflammatory cytokines that participate not only in the inflammatory response but also in vascular injury and the formation of new blood vessels; these cytokines are associated with the occurrence and development of various inflammation‐related diseases and can lead to the worsening of cancer 30‐32 . Moreover, mPGES‐1 induces the expression of the proangiogenic chemokine CXCL1 in cancer cells, thereby promoting tumour tissue angiogenesis in a variety of cancer cell lines and model animals 33 . In addition to immunity, ROS produced by NOX2 play an irreplaceable role in physiological processes and promoting cancer 34 .…”

Section: Discussionmentioning

confidence: 99%

Targeting IRS‐1/mPGES‐1/NOX2 to inhibit the inflammatory response caused by insulin‐like growth factor‐I‐induced activation of NF‐κB and NLRP3 in cancer cells

Wang

et al. 2020

Vet Comparative Oncology

View full text Add to dashboard Cite

The levels of insulin-like growth factor-l (IGF-1) and reactive oxygen species (ROS) are abnormally elevated in various tumour tissues, and IGF-1 has been reported to be associated with the development and progression of inflammation in cancers. In this study, we found that IGF-1 activated nuclear factor-κB (NF-κB) and NLRP3 inflammatory signalling via IRS-1/mPGES-1/NOX2-regulated ROS. Additionally, in the B16-F10 tumour-bearing mouse model, the number of tumours, tumour growth, invasion of tissues and expression of proinflammatory factors in peripheral blood were significantly decreased by treatment with an inhibitor combination compared with those of the IGF-1 group. Taken together, targeting IRS-1/mPGES-1/NOX2 to inhibit inflammation related to NF-κB and NLRP3 is a potential strategy for controlling the development and progression of cancer.

show abstract

“…The transformation of normal fibroblasts into CAFs is also mediated by molecules that are released from OSCC cells. For instance, IL1β expression becomes progressively increased in OSCC cells and is released, activating the NFκB pathway in fibroblasts that induces release of the chemokine (C-X-C motif) ligand 1, CXCL1 ( 38 ). CXCL1 generates an autocrine mechanism that transforms fibroblasts into high-α-SMA expressing CAFs ( 39 ), suggesting that early carcinogenesis events provoke slight inflammatory alterations in the epithelial cells that then lead to the generation of CAFs.…”

Section: The Microenvironment Of the Osccmentioning

confidence: 99%

Role of Autophagy in the Microenvironment of Oral Squamous Cell Carcinoma

et al. 2020

View full text Add to dashboard Cite

Oral squamous cell carcinoma, the most common type of oral cancer, affects more than 275,000 people per year worldwide. Oral squamous cell carcinoma is very aggressive, as most patients die after 3 to 5 years post-diagnosis. The initiation and progression of oral squamous cell carcinoma are multifactorial: smoking, alcohol consumption, and human papilloma virus infection are among the causes that promote its development. Although oral squamous cell carcinoma involves abnormal growth and migration of oral epithelial cells, other cell types such as fibroblasts and immune cells form the carcinoma niche. An underlying inflammatory state within the oral tissue promotes differential stress-related responses that favor oral squamous cell carcinoma. Autophagy is an intracellular degradation process that allows cancer cells to survive under stress conditions. Autophagy degrades cellular components by sequestering them in vesicles called autophagosomes, which ultimately fuse with lysosomes. Although several autophagy markers have been associated with oral squamous cell carcinoma, it remains unclear whether up- or down-regulation of autophagy favors its progression. Autophagy levels during oral squamous cell carcinoma are both timing- and cell-specific. Here we discuss how autophagy is required to establish a new cellular microenvironment in oral squamous cell carcinoma and how autophagy drives the phenotypic change of oral squamous cell carcinoma cells by promoting crosstalk between carcinoma cells, fibroblasts, and immune cells.

show abstract

Reciprocal activation of cancer-associated fibroblasts and oral squamous carcinoma cells through CXCL1

Cited by 49 publications

References 44 publications

Interleukin-1β and Cancer

Interleukin-1β and Cancer

Targeting IRS‐1/mPGES‐1/NOX2 to inhibit the inflammatory response caused by insulin‐like growth factor‐I‐induced activation of NF‐κB and NLRP3 in cancer cells

Role of Autophagy in the Microenvironment of Oral Squamous Cell Carcinoma

Contact Info

Product

Resources

About