Interleukin‐1β/nuclear factor‐κB signaling promotes osteosarcoma cell growth through the microRNA‐181b/phosphatase and tensin homolog axis

Wang, Weiguo; Wang, Zhengguang; Chen, Shijie; Zang, Xiaofang

doi:10.1002/jcb.27477

Cited by 19 publications

(6 citation statements)

References 40 publications

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“…IL-1β induces the expression of miR-425, miR-181a, and miR-181b through NF-κB, in gastric cancer, colon cancer, and osteosarcoma cells, respectively. These miRNA repress PTEN expression, leading to apoptosis inhibition and proliferation-associated cancer cell growth [ 74 , 116 , 117 ]. PTEN expression in myeloid cells dictates NLRP3 inflammasome activation and IL-1β expression.…”

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

confidence: 99%

Interleukin-1β and Cancer

Rébé

Ghiringhelli

2020

Cancers

217

110

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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.

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

confidence: 99%

Interleukin-1β and Cancer

Rébé

Ghiringhelli

2020

Cancers

217

110

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“…Although miR‐181a and miR‐181b expressions were detected in PAH animal models, further studies with clinical samples could better elucidate the correlation of miR‐181a/b expression with PAH. It is broadly reported that miR‐181a and miR‐181b can also target multiple genes, like PTEN, to mediate the regulation of various pathological processes (W. Wang et al, ; X. F. Wu, Zhou, & Zou, ). In the meanwhile, previous studies have indicated the implications of PTEN in pulmonary vascular remodeling (Nemenoff et al, ; Ravi et al, ).…”

Section: Discussionmentioning

confidence: 99%

miR‐181a/b‐5p ameliorates inflammatory response in monocrotaline‐induced pulmonary arterial hypertension by targeting endocan

Zhao

Guo

Sun

et al. 2019

Journal Cellular Physiology

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Pulmonary arterial hypertension (PAH) is a progressive disorder characterized by vascular remodeling, endothelial cell (EC) dysfunction, and inflammation. The roles of microRNAs have received much critical attention. Thus, this study was attempted to show the biological function of miR-181a/b-5p (miR-181a/b) in monocrotaline (MCT)induced PAH. Here, rats injected with MCT were used as PAH models. The expression of miR-181a/b and its effect on PAH pathologies were examined using miR-181a/b overexpression lentivirus. A luciferase reporter analysis was performed to measure the relationships between miR-181a/b and endocan. Additionally, primary rat pulmonary arterial endothelial cells (rPAECs) treated with tumor necrosis factor-α (TNF-α) were employed to further validate the regulatory mechanism of miR-181a/b in vitro. Our results showed that miR-181a/b expression was reduced in PAH, and its upregulation significantly attenuated the short survival period, right ventricular systolic pressure and mean pulmonary artery pressure increments, right ventricular remodeling, and lung injury. Furthermore, the increase of intercellular cell adhesion molecule-1 (ICAM1) and vascular cell adhesion molecule-1 (VCAM1) in PAH rats was inhibited by miR-181a/b overexpression. Similarly, our in vitro results showed that inducing miR-181a/b suppressed TNF-α-stimulated increase of ICAM1 and VCAM1 in rPAECs. Importantly, the increased expression of endocan in PAH model or TNF-αtreated rPAECs was restored by miR-181a/b upregulation. Further analysis validated the direct targeting relationships between miR-181a/b and endocan. Collectively, this study suggests that miR-181a/b targets endocan to ameliorate PAH symptoms by inhibiting inflammatory states, shedding new lights on the prevention and treatment of PAH. K E Y W O R D Sendocan, inflammation, miR-181a-5p, miR-181b-5p, pulmonary arterial hypertension

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“…The role of IL-1β and Wnt signaling has also been implicated in the bone metastatic growth of breast cancer [21], which will be discussed in the section dedicated to the IL-1 family in bone metastasis. In OS cell lines, IL-1β, through the induction of NF-κB, also upregulates miR-181b expression, which, by repressing phosphatase and tensin homolog (PTEN) expression, promotes OS cell proliferation [42]. Additionally, IL-1β has been implicated in OS drug resistance.…”

Section: Il-1 Family In Osteosarcomamentioning

confidence: 99%

IL-1 Family Members in Bone Sarcomas

Landuzzi,

Ruzzi,

Pellegrini

et al. 2024

Cells

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IL-1 family members have multiple pleiotropic functions affecting various tissues and cells, including the regulation of the immune response, hematopoietic homeostasis, bone remodeling, neuronal physiology, and synaptic plasticity. Many of these activities are involved in various pathological processes and immunological disorders, including tumor initiation and progression. Indeed, IL-1 family members have been described to contribute to shaping the tumor microenvironment (TME), determining immune evasion and drug resistance, and to sustain tumor aggressiveness and metastasis. This review addresses the role of IL-1 family members in bone sarcomas, particularly the highly metastatic osteosarcoma (OS) and Ewing sarcoma (EWS), and discusses the IL-1-family-related mechanisms that play a role in bone metastasis development. We also consider the therapeutic implications of targeting IL-1 family members, which have been proposed as (i) relevant targets for anti-tumor and anti-metastatic drugs; (ii) immune checkpoints for immune suppression; and (iii) potential antigens for immunotherapy.

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Interleukin‐1β/nuclear factor‐κB signaling promotes osteosarcoma cell growth through the microRNA‐181b/phosphatase and tensin homolog axis

Cited by 19 publications

References 40 publications

Interleukin-1β and Cancer

Interleukin-1β and Cancer

miR‐181a/b‐5p ameliorates inflammatory response in monocrotaline‐induced pulmonary arterial hypertension by targeting endocan

IL-1 Family Members in Bone Sarcomas

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