Targeting cancer-promoting inflammation — have anti-inflammatory therapies come of age?

Hou, Jiajie; Karin, Michael; Sun, Beicheng

doi:10.1038/s41571-020-00459-9

Cited by 223 publications

(150 citation statements)

References 262 publications

Supporting

Mentioning

149

Contrasting

Order By: Relevance

“…454 Growing evidence suggests that TME is one of the major obstacles for cancer immunotherapy, where chronic inflammation plays a predominant role in tumor cell proliferation, angiogenesis, and immunosuppression. 6,455 Furthermore, the side-effects of immune checkpoint blockade (ICB) and CAR-T therapies, such as coagulopathy and "cytokine storm" have limited their full application in cancer therapy, 29,30,456 suggesting that reduction of these harmful immunotherapy-associated inflammation would be beneficial for the outcome of cancer patients. However, acute inflammation induced by other therapies can improve the effectiveness of immunotherapy.…”

Section: Therapy-elicited Inflammationmentioning

confidence: 99%

Inflammation and tumor progression: signaling pathways and targeted intervention

Zhao

Yan

et al. 2021

Sig Transduct Target Ther

1,265

682

View full text Add to dashboard Cite

Cancer development and its response to therapy are regulated by inflammation, which either promotes or suppresses tumor progression, potentially displaying opposing effects on therapeutic outcomes. Chronic inflammation facilitates tumor progression and treatment resistance, whereas induction of acute inflammatory reactions often stimulates the maturation of dendritic cells (DCs) and antigen presentation, leading to anti-tumor immune responses. In addition, multiple signaling pathways, such as nuclear factor kappa B (NF-kB), Janus kinase/signal transducers and activators of transcription (JAK-STAT), toll-like receptor (TLR) pathways, cGAS/STING, and mitogen-activated protein kinase (MAPK); inflammatory factors, including cytokines (e.g., interleukin (IL), interferon (IFN), and tumor necrosis factor (TNF)-α), chemokines (e.g., C-C motif chemokine ligands (CCLs) and C-X-C motif chemokine ligands (CXCLs)), growth factors (e.g., vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β), and inflammasome; as well as inflammatory metabolites including prostaglandins, leukotrienes, thromboxane, and specialized proresolving mediators (SPM), have been identified as pivotal regulators of the initiation and resolution of inflammation. Nowadays, local irradiation, recombinant cytokines, neutralizing antibodies, small-molecule inhibitors, DC vaccines, oncolytic viruses, TLR agonists, and SPM have been developed to specifically modulate inflammation in cancer therapy, with some of these factors already undergoing clinical trials. Herein, we discuss the initiation and resolution of inflammation, the crosstalk between tumor development and inflammatory processes. We also highlight potential targets for harnessing inflammation in the treatment of cancer.

show abstract

Section: Therapy-elicited Inflammationmentioning

confidence: 99%

Inflammation and tumor progression: signaling pathways and targeted intervention

Zhao

Yan

et al. 2021

Sig Transduct Target Ther

1,265

682

View full text Add to dashboard Cite

show abstract

“…On the contrary, another group has reported that high IL-1β expression in breast cancer is associated with better overall survival and distant metastasis-free survival, preventing metastasis-initiating cells from generating highly proliferative E-cadherin-positive cells [ 304 ]. In summary, extensive investigation is required for the development and future clinical application of inflammation-targeted breast cancer therapies [ 305 ].…”

Section: Role Of Inflammation In Cancer Typesmentioning

confidence: 99%

Inflammation-Induced Tumorigenesis and Metastasis

Hibino

Kawazoe

Kasahara

et al. 2021

IJMS

143

View full text Add to dashboard Cite

Inflammation, especially chronic inflammation, plays a pivotal role in tumorigenesis and metastasis through various mechanisms and is now recognized as a hallmark of cancer and an attractive therapeutic target in cancer. In this review, we discuss recent advances in molecular mechanisms of how inflammation promotes tumorigenesis and metastasis and suppresses anti-tumor immunity in various types of solid tumors, including esophageal, gastric, colorectal, liver, and pancreatic cancer as well as hematopoietic malignancies.

show abstract

“…Many mechanisms for castration resistance have been proposed [5,[7][8][9][10]: the continuous role of androgen receptor (AR) signaling in CRPC due to the amplification/mutation of ARs or the increased expression of AR splice variants or androgen synthesis enzymes in PCa cells [5,6,11]; the activation of other signaling transduction pathways that lead to either the enhanced activity of ARs and its coactivators or the bypassing of ARs in the presence of low levels or even in the absence of androgen [5,6,12]; and the existence of PCa stem cells that do not depend on ARs to survive [5,6]. We and many others have reported that immune/inflammatory signaling in both cancer cells and the tumor microenvironment (TME) plays important roles in CRPC growth and development [13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

“…Inflammatory signaling activation has been found in almost all cancers and is associated with cell transformation, tumorigenesis, tumor progression, and therapy resistance [14][15][16]. NF-κB transcription factors play crucial roles in the regulation of inflammation, immune responses, and survival of both normal and malignant cells.…”

Section: Introductionmentioning

confidence: 99%

Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance

Zhong

Huang

Chen

et al. 2021

JCM

View full text Add to dashboard Cite

Although castration-resistant prostate cancer (CRPC) as a whole, by its name, refers to the tumors that relapse and/or regrow independently of androgen after androgen deprivation therapy (ADT), untreated tumor, even in early-stage primary prostate cancer (PCa), contains androgen-independent (AI) PCa cells. The transformation of androgen-dependent (AD) PCa to AI PCa under ADT is a forced evolutionary process, in which the small group of AI PCa cells that exist in primary tumors has the unique opportunity to proliferate and expand selectively and dominantly, while some AD PCa cells that have escaped from ADT-induced death acquire the capability to survive in an androgen-depleted environment. The adaptation and reprogramming of both PCa cells and the tumor microenvironment (TME) under ADT make PCa much stronger than primary tumors so that, currently, there are no effective therapeutic methods available for the treatment of CRPC. Many mechanisms have been found to be related to the emergence and maintenance of PCa castration resistance; in this review, we focus on the role of inflammatory signaling in both PCa cells and the TME for the emergence and maintenance of CRPC and summarize the recent advances of therapeutic strategies that target inflammatory signaling for the treatment of CRPC.

show abstract

Targeting cancer-promoting inflammation — have anti-inflammatory therapies come of age?

Cited by 223 publications

References 262 publications

Inflammation and tumor progression: signaling pathways and targeted intervention

Inflammation and tumor progression: signaling pathways and targeted intervention

Inflammation-Induced Tumorigenesis and Metastasis

Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance

Contact Info

Product

Resources

About