TNFAIP8: Inflammation, Immunity and Human Diseases

Niture, Suryakant K.; Moore, John T.; Kumar, Deepak

doi:10.33696/immunology.1.007

Cited by 7 publications

(1 citation statement)

References 46 publications

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“…1a and 1b). All TIPEs have a conserved C-terminus and a variable-terminus (Niture et al, 2019). The C-terminus of TIPEs contained a TIPE homology (TH) domain characterized by six/seven α-helix structures (Zhang et al, 2009).…”

Section: Tipe Family Structuresmentioning

confidence: 99%

Structure, function, and mechanism of the TNFAIP8 (TIPE) family of proteins in cancer and inflammation

LIN,

TANG,

KANG

et al. 2023

BIOCELL

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The multiple roles of the tumor necrosis factor (TNF)-α-inducible protein 8 (TNFAIP8), also named TIPE family of proteins have been shown in tumor and inflammation progression and regulation of cellular autophagy and apoptosis. In this review, we found that the TIPE family showed highly homologous sequences and conserved functional domains, such as the death effector domain (DED)-like domain but displayed different roles and mechanisms in different biological activities. For example, while TIPE is primarily associated with tumor progression and antitumor drug resistance, TIPE1 suppresses tumor progression in most instances. TIPE2 has multiple roles in tumor progression regulation, and antitumor drug resistance. Moreover, TIPE2 was also involved in inflammatory response regulation, tumor typing, and staging. A few studies reported that TIPE3 was engaged in tumor development by activating the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. The structure, function, and mechanism of the TIPE family in cancer and inflammation have been summarized in this review. This might serve as a reference for further research on the TIPE family and shed new light on the crosstalk among antitumor responses, inflammation, and immunology.

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Section: Tipe Family Structuresmentioning

confidence: 99%

Structure, function, and mechanism of the TNFAIP8 (TIPE) family of proteins in cancer and inflammation

LIN,

TANG,

KANG

et al. 2023

BIOCELL

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TNFAIP8 regulates autophagy, cell steatosis, and promotes hepatocellular carcinoma cell proliferation

et al. 2020

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Tumor necrosis factor-α-induced protein 8 (TNFAIP8) expression has been linked to tumor progression in various cancer types, but the detailed mechanisms of TNFAIP8 are not fully elucidated. Here we define the role of TNFAIP8 in early events associated with development of hepatocellular carcinoma (HCC). Increased TNFAIP8 levels in HCC cells enhanced cell survival by blocking apoptosis, rendering HCC cells more resistant to the anticancer drugs, sorafenib and regorafenib. TNFAIP8 also induced autophagy and steatosis in liver cancer cells. Consistent with these observations, TNFAIP8 blocked AKT/mTOR signaling and showed direct interaction with ATG3-ATG7 proteins. TNFAIP8 also exhibited binding with fatty acids and modulated expression of lipid/fatty-acid metabolizing enzymes. Chronic feeding of mice with alcohol increased hepatic levels of TNFAIP8, autophagy, and steatosis but not in high-fat-fed obese mice. Similarly, higher TNFAIP8 expression was associated with steatotic livers of human patients with a history of alcohol use but not in steatotic patients with no history of alcohol use. Our data indicate a novel role of TNFAIP8 in modulation of drug resistance, autophagy, and hepatic steatosis, all key early events in HCC progression.

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RETRACTED ARTICLE: MicroRNA-205-5p inhibits skin cancer cell proliferation and increase drug sensitivity by targeting TNFAIP8

Niture

Lin

et al. 2021

Sci Rep

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Tumor necrosis factor-α-induced protein 8 (TNFAIP8) is a member of the TIPE/TNFAIP8 family which regulates tumor growth and survival. Our goal is to delineate the detailed oncogenic role of TNFAIP8 in skin cancer development and progression. Here we demonstrated that higher expression of TNFAIP8 is associated with basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and melanoma development in patient tissues. Induction of TNFAIP8 expression by TNFα or by ectopic expression of TNFAIP8 in SCC or melanoma cell lines resulted in increased cell growth/proliferation. Conversely, silencing of TNFAIP8 decreased cell survival/cell migration in skin cancer cells. We also showed that miR-205-5p targets the 3′UTR of TNFAIP8 and inhibits TNFAIP8 expression. Moreover, miR-205-5p downregulates TNFAIP8 mediated cellular autophagy, increased sensitivity towards the B-RAFV600E mutant kinase inhibitor vemurafenib, and induced cell apoptosis in melanoma cells. Collectively our data indicate that miR-205-5p acts as a tumor suppressor in skin cancer by targeting TNFAIP8.

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TNFAIP8: Inflammation, Immunity and Human Diseases

Cited by 7 publications

References 46 publications

Structure, function, and mechanism of the TNFAIP8 (TIPE) family of proteins in cancer and inflammation

Structure, function, and mechanism of the TNFAIP8 (TIPE) family of proteins in cancer and inflammation

TNFAIP8 regulates autophagy, cell steatosis, and promotes hepatocellular carcinoma cell proliferation

RETRACTED ARTICLE: MicroRNA-205-5p inhibits skin cancer cell proliferation and increase drug sensitivity by targeting TNFAIP8

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