CORM-2 prevents human gingival fibroblasts from lipoteichoic acid-induced VCAM-1 and ICAM-1 expression by inhibiting TLR2/MyD88/TRAF6/PI3K/Akt/ROS/NF-κB signaling pathway

Cheng, Ching‐Yi; Chen, Yu-Hsu; Vo, Thi Thuy Tien; Hong, Ying Chui; Wang, Ching Shuen; Vo, Quang Canh; Chou, Han-Chin; Huang, Ting-Wei; Lee, I-Te

doi:10.1016/j.bcp.2022.115099

Cited by 6 publications

(2 citation statements)

References 48 publications

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“…In our experiments, we illustrated that the IL-33/ST2L axis increases the protein level of TRAF6. As an important intracellular regulator with unique receptor binding speci city, TRAF6 can mediate signal transduction reactions such as toll-like receptor and interleukin-1 receptor (IL-1R), and ultimately activate PI3K/Akt, NF-κB, and MAPK pathways [35][36][37][38] . We found that the IL-33/ST2Lmediated up-regulation of TRAF6 protein levels further activates PI3K/Akt phosphorylation, which mediates the phosphorylation of IκBα and ultimately activates NF-κB, leading to an increase in VEGFA protein level (Fig.…”

Section: Discussionmentioning

confidence: 99%

ST2L promotes VEGFA-mediated angiogenesis in gastric cancer by activating TRAF6/PI3K/Akt/NF-κB pathway via IL-33

Zhu,

Lu,

Zhu

et al. 2024

Preprint

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Tumorigenicity 2 (ST2) is a member of the interleukin-1 receptor/ Toll-like receptor superfamily, and its specific ligand is Interleukin-33 (IL-33). IL-33/ ST2 signaling has been implicated in numerous inflammatory and allergic diseases, as well as in promoting malignant behavior of tumor cells and angiogenesis. However, the precise role of ST2 in gastric cancer angiogenesis remains incompletely elucidated. We observed a significant correlation between high expression of ST2 in gastric cancer tissues and poor prognosis, along with various clinicopathological features. In vitro experiments demonstrated that the IL-33/ ST2 axis activates the PI3K/AKT/NF-κB signaling pathway through TRAF6, thereby promoting VEGFA-mediated tumor angiogenesis; meanwhile sST2 acts as a decoy receptor to regulate the IL-33/ST2L axis. Consistent findings were also observed in subcutaneous xenograft tumor models in nude mice. Furthermore, we investigated the molecular mechanism by which IL-33 promotes ST2L expression in GC cells via upregulation of transcription factors YY1 and GATA2 through intracellular signaling pathways.

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Section: Discussionmentioning

confidence: 99%

ST2L promotes VEGFA-mediated angiogenesis in gastric cancer by activating TRAF6/PI3K/Akt/NF-κB pathway via IL-33

Zhu,

Lu,

Zhu

et al. 2024

Preprint

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“…This is also evident in Chlamydia infections which result in ROS generation, 8-oxo guanine formation, and impairment of the DNA damage response (Chumduri et al, 2013). ROS generation by MAMPs such as LPS, LTA, and flagellin is welldocumented in many immune and epithelial cells (Hsieh et al, 2012;Kim et al, 2012;Burgueño et al, 2019;Fernańdez-Rojas et al, 2020;Cheng et al, 2022), however, this is yet to be confirmed in breast tissue/mammary gland context. The proposed working model by which LPS (and possibly other MAMPs) might cause breast cancer initiation is illustrated in Figure 5.…”

Section: Microbial-associated Molecular Patternsmentioning

confidence: 99%

The microbiome: a link between obesity and breast cancer risk

Gaber,

Arnone,

Vidi

et al. 2024

Front. Microbiomes

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Globally, breast cancer is the leading cause of cancer incidence and mortality among all female cancers. Hereditary factors only account for 5-10% of breast cancers, highlighting the importance of non-hereditary factors, such as obesity. The increasing prevalence of obesity underscores the need to understand its contribution to breast cancer risk. Multiple mechanisms may mediate pro-carcinogenic effects of obesity, including altered adipokine levels, local and systemic inflammation, disruption of insulin and insulin-like growth factor signaling, increased estrogen levels, and alterations of the microbiome. In this review, we focus on the link between gut microbiome alterations and breast cancer risk in the context of obesity. First, we discuss how obesity influences the gut microbiome. Next, we describe the effect of such microbiome alterations on breast carcinogenesis, highlighting underlying molecular mechanisms. Finally, we review preclinical data on the interactions between host and bacteria, current challenges to study the obesity-microbiome connection, and future perspectives in this field.

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Carbon monoxide in cell signaling and potential therapeutics

Kashfi

2022

Biochemical Pharmacology

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CORM-2 prevents human gingival fibroblasts from lipoteichoic acid-induced VCAM-1 and ICAM-1 expression by inhibiting TLR2/MyD88/TRAF6/PI3K/Akt/ROS/NF-κB signaling pathway

Cited by 6 publications

References 48 publications

ST2L promotes VEGFA-mediated angiogenesis in gastric cancer by activating TRAF6/PI3K/Akt/NF-κB pathway via IL-33

ST2L promotes VEGFA-mediated angiogenesis in gastric cancer by activating TRAF6/PI3K/Akt/NF-κB pathway via IL-33

The microbiome: a link between obesity and breast cancer risk

Carbon monoxide in cell signaling and potential therapeutics

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