Vitamin D3 Upregulated Protein 1 Suppresses TNF-α–Induced NF-κB Activation in Hepatocarcinogenesis

Kwon, Hyojung; Won, Young‐Suk; Suh, Hyun‐Woo; Jeon, Jun-Ho; Shao, Yan; Yoon, Suk-Ran; Chung, Jin-Woong; Kim, Tae-Don; Kim, Hwan‐Mook; Nam, Ki-Hoan; Yoon, Won-Kee; Kim, Dae‐Ghon; Kim, Jeong‐Hwan; Kim, Young-Sung; Kim, Dae-Yong; Kim, Hyoung-Chin; Choi, Inpyo

doi:10.4049/jimmunol.1000990

Cited by 100 publications

(90 citation statements)

References 45 publications

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“…diabetes, carcinogenesis, and inflammation) (23)(24)(25). In the context of inflammation, Txnip has previously been shown to suppress cytokine-induced NF-B activation (26), findings that are corroborated in the present study. However, we found the mechanism by which Txnip levels acutely decrease to be primarily through heightened ubiquitination and proteasomal degradation, with attenuated transcription playing a lesser role.…”

Section: Discussionsupporting

confidence: 89%

Thioredoxin-mediated Denitrosylation Regulates Cytokine-induced Nuclear Factor κB (NF-κB) Activation

Kelleher

Sha

Foster

et al. 2014

Journal of Biological Chemistry

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Background: S-nitrosylation inhibits mediators of the immune response including the transcription factor NF-B (p50/p65). Results: Exogenous and endogenous inhibitors of thioredoxin prevent p65 denitrosylation and downstream activation of NF-B. Conclusion: Thioredoxin activates inflammatory signaling through targeted denitrosylation of NF-B. Significance: Mechanisms that augment protein S-nitrosylation can be utilized to suppress the immune response.

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Section: Discussionsupporting

confidence: 89%

Thioredoxin-mediated Denitrosylation Regulates Cytokine-induced Nuclear Factor κB (NF-κB) Activation

Kelleher

Sha

Foster

et al. 2014

Journal of Biological Chemistry

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“…Sheth et al have shown that spontaneous mutation of VDUP1 in a mouse model is associated with a higher incidence of HCC [15]. We also found that loss of VDUP1 increased susceptibility to chemically-induced hepatocarcinogenesis in association with increased compensatory proliferation [33]. Importantly, activation of the ERK1/2 and Akt pathways correlates with increased tumor cell proliferation and tumor aggressiveness [34,35].…”

Section: Discussionsupporting

confidence: 65%

Vitamin D3 up-regulated protein 1 deficiency accelerates liver regeneration after partial hepatectomy in mice

Kwon

Won

Yoon³

et al. 2011

Journal of Hepatology

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“…via suppression of the anti-apoptotic gene B-cell lymphoma 2 (Bcl-2) in prostate cancer cells [12]. The vitamin D target vitamin D 3 -upregulated protein-1 (VDUP-1) is a candidate tumor suppressor that negatively regulates hepatocarcinogenesis by suppressing TNF-α-induced NF-κB activation [13]. Thus, the vitamin D pathway might also regulate apoptosis in HCC.…”

Section: Introductionmentioning

confidence: 99%

Expression of Apoptosis- and Vitamin D Pathway-Related Genes in Hepatocellular Carcinoma

Fingas

Altınbaş²,

Schlattjan³

et al. 2013

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Background/Aims: Hepatocellular carcinoma (HCC) is the sixth most common malignancy worldwide and therapeutic options are scarce. As they might represent future targets for cancer therapy, the expression of apoptosis-related genes in HCC is of particular interest. In this pilot study, we further examined apoptosis-related genes in human HCC and also focused on vitamin D signaling as this might be a regulator of HCC cell apoptosis. Methods: We employed tumor tissue and serum samples from 62 HCC patients as well as 62 healthy controls for these studies. Tissue and serum specimens were analyzed by quantitative RT-PCR, immunohistochemistry and ELISA. Results: In HCC patients the apoptosis marker M30 was found to be elevated and several pro-apoptotic (TRAIL, FasL and FasR) as well as anti-apoptotic genes (Mcl-1 and Bcl-2) were simultaneously upregulated in tumor tissue and especially tumor-surrounding tissue as compared to healthy control livers. Moreover, vitamin D serum levels were decreased in HCC patients whereas vitamin D receptor mRNA expression was increased in tumor tissue and tumor-surrounding tissue as compared to healthy livers. Conclusions: In human HCC, M30 serum levels are elevated indicating an increased cell turnover. Modulation of the vitamin D pathway might be a supportive, pro-apoptotic HCC therapy.

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Vitamin D3 Upregulated Protein 1 Suppresses TNF-α–Induced NF-κB Activation in Hepatocarcinogenesis

Cited by 100 publications

References 45 publications

Thioredoxin-mediated Denitrosylation Regulates Cytokine-induced Nuclear Factor κB (NF-κB) Activation

Thioredoxin-mediated Denitrosylation Regulates Cytokine-induced Nuclear Factor κB (NF-κB) Activation

Vitamin D3 up-regulated protein 1 deficiency accelerates liver regeneration after partial hepatectomy in mice

Expression of Apoptosis- and Vitamin D Pathway-Related Genes in Hepatocellular Carcinoma

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