TNFAIP8

Last update 08 May 2025

Basic Info

Synonyms

GG2-1, Head and neck tumor and metastasis-related protein, MDC-3.13

+ [8]

Introduction

Acts as a negative mediator of apoptosis and may play a role in tumor progression. Suppresses the TNF-mediated apoptosis by inhibiting caspase-8 activity but not the processing of procaspase-8, subsequently resulting in inhibition of BID cleavage and caspase-3 activation.

100 Clinical Results associated with TNFAIP8

100 Translational Medicine associated with TNFAIP8

0 Patents (Medical) associated with TNFAIP8

197

Literatures (Medical) associated with TNFAIP8

01 Mar 2025·Journal of Physiological Investigation

MiR-455-5p Mitigates Interleukin-1 β-induced Chondrocyte Damage Linked to Osteoarthritis by Targeting TNFAIP8

Article

Author: Xu, Wensheng ; Zhang, Tao ; Xu, Zhixiong ; Li, Yuan ; Sun, Jinlei ; Wang, Wei ; Luo, Long

AbstractMicroRNAs have been extensively implicated in osteoarthritis (OA) progression. Our study aims to investigate the impact of miR-455-5p on OA progression and related molecular mechanisms. Cartilage tissues were collected from patients with OA and femoral neck fractures. An in vitro OA model was established by inducing injury in human chondrocytes (CHON-001) with interleukin (IL)-1 β. Cell viability and apoptosis were measured by cell counting kit-8 and flow cytometry assays, respectively. An enzyme-linked immunosorbent assay was performed to measure the concentrations of inflammation factors, and oxidative stress was evaluated by detecting superoxide dismutase activity and malondialdehyde levels. TargetScan was used to predict the binding sites between miR-455-5p and tumor necrosis factor (TNF)-α-induced protein 8 (TNFAIP8), which were then confirmed by dual-luciferase reporter assays. Quantitative real-time polymerase chain reaction and western blot analysis were employed to measure the related molecular markers. Our initial observations showed that the expression of miR-455-5p was downregulated in OA cartilage and IL-1 β-treated CHON-001 cells compared to normal cartilage tissues and untreated cells. Overexpression of miR-455-5p significantly protected CHON-001 cells from IL-1 β-induced injury by recovering cell viability, and inhibiting inflammation, apoptosis, and oxidative stress. TNFAIP8 was targeted by miR-455-5p and negatively regulated by miR-455-5p. TNFAIP8 knockdown imitated, while overexpression reversed the effects mediated by miR-455-5p in IL-1 β-induced chondrocyte injury, as further confirmed by the protein levels of iNOS, cleaved caspase-3, NQO1, Col2a1, and MMP13. Collectively, these results suggest that miR-455-5p may serve as a new therapeutic target for OA by targeting TNFAIP8 to alleviate IL-1 β-induced chondrocyte injury.

01 Feb 2025·International Journal of Radiation Biology

The combination of microwave hyperthermia with TIPE2 impedes the growth of orthotopic colon cancer

Article

Author: Yu, Qingqing ; Zhao, Linfang ; Zhang, Ke ; Li, Lingdi ; Mo, Weixing ; Zhang, Lidan ; Tang, Rongjun

BACKGROUNDColon cancer (CC) is the main fatal disease of humans. Microwave hyperthermia (MH) is an adjuvant therapy for diverse cancers. Tumor necrosis factor-α induced protein-8-like 2 (TIPE2) is a tumor suppressor. However, the effect of MH combined with TIPE2 on CC remains unclear.METHODSThe orthotopic CC mouse model was constructed by mouse CC CT26-Luc cells, and mice were randomized into control, model (CT26-Luc), CT26-Luc + Vector, CT26-Luc + TIPE2, CT26-Luc + MH, and CT26-Luc + MH+TIPE2 groups (n = 6). Tumor growth pretreatment and post-treatment by in vivo fluorescence image analysis was detected. TIPE2 expression and cell transfection efficiency was detected by qRT-PCR and western blot. The pathological changes by HE staining, apoptosis by TUNEL staining, serum inflammatory factors by ELISA, TIPE2 expression by immunohistochemistry, and NF-κB signaling by western blot was performed.RESULTSParacancerous tissues showed higher TIPE2 expression than in CC tissues. CT26-Luc + TIPE2, CT26-Luc + MH, and CT26-Luc + MH+TIPE2 groups reduced tumor growth, tumor cell infiltration, and increased apoptosis. CT26-Luc + TIPE2 group had lower NF-κB, TNF-α, IL-1β, IL-6, p-p65, and p-IKK expression, and elevated TIPE2 and IkB expression, which was reversed by CT26-Luc + MH group. Moreover, CT26-Luc+MH+TIPE2 group showed opposite effects on the above factor expression of CT26-Luc+MH group.CONCLUSIONSCombination of MH with TIPE2 could impede CC tumor growth, providing scientific bases for its clinical application in CC treatment.

01 Oct 2024·American Journal of Physical Medicine & Rehabilitation

Tnfaip8 and Tipe2 Gene Deletion Ameliorates Immediate Proteoglycan Loss and Inflammatory Responses in the Injured Mouse Intervertebral Disc

Article

Author: Qin, Ling ; Shofer, Frances S ; Tian, Zuozhen ; Zhang, Yejia ; Sun, Honghong ; Lu, Jiawei

ObjectiveTNFAIP8 and TIPE2 belong to TNFa-induced protein 8 (TNFAIP8/TIPE) family. They control apoptosis and direct leukocyte migration. Nucleus pulposus cell loss is a hallmark of intervertebral disc degeneration in response to injury, and inflammation may cause pain. Here, we examined the effects of TNFAIP8/TIPE2 deficiency on the intervertebral discs in mice with these genes deleted.DesignTail intervertebral discs in Tnfaip8 or Tipe2 single and double knockout mice (Tnfaip8−/− , Tipe2−/− , and Tnfaip8/Tipe2 dko), and wild-type controls were injured. The spine motion segments were stained with safranin O to reveal proteoglycans. Macrophages were identified by immunostaining, and selected inflammatory marker and collagen gene expression was examined by Real Time PCR.ResultsThe injured tail intervertebral discs of Tnfaip−/− , Tipe2−/− , and Tnfaip8/Tipe2 dko mice all displayed higher levels of proteoglycans than wild-type controls. Fewer macrophages were found in the injured intervertebral discs of Tipe2−/− and Tnfaip8/Tipe2 dko mice than wild type. Il6, Adam8, and Col1 gene expression was downregulated in the injured intervertebral discs of Tnfip8/Tipe2 dko mice.ConclusionsTNFAIP8 and TIPE2 loss of function ameliorated proteoglycan loss and inflammation in the injured intervertebral discs. They may serve as molecular targets to preserve disc structure and reduce inflammation.

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TNFAIP8

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