Elevation of PRKCDBP, A Novel Transcriptional Target of TNF-α, and Its Downregulation by Infliximab in Patients with Ulcerative Colitis

Kim, Jung Wook; Kim, Hyo Jong; Lee, Chang Kyun; Shim, Jae‐Jun; Jang, Jae Young; Dong, Suk Ho; Kim, Byung Ho; Chang, Young Woon; Gil, Sung

doi:10.1007/s10620-014-3282-4

Cited by 6 publications

(12 citation statements)

References 33 publications

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“… 17 In this previous study, we demonstrated that, PRKCDBP expression is tightly controlled by TNF-α in patients with moderate to severe UC. 17 Along with our previous result, considering that PRKCDBP is a proapoptotic tumor suppressor and a transcriptional target of TNF-α, it seems probable that these missense SNPs could generate variant protein products, with varying levels of biological activity. Nevertheless, the association between the SNPs of PRKCDBP and susceptibility to IBD has not yet been determined.…”

Section: Discussionmentioning

confidence: 81%

“…The possible mechanism of the association between PRKCDBP and susceptibility to IBD has not been established. Based on our previous study, 17 we speculated that PRKCDBP may play a role in the inflammatory processes controlled by TNF-α in IBD.…”

Section: Discussionmentioning

confidence: 97%

“… 16 Moreover, our recent study demonstrated that colonic mucosal expression of PRKCDBP correlates strongly with TNFα expression in UC patients. 17 These observations suggest that PRKCDBP may play a role in colonic inflammation, and its dysregulation may be implicated in the pathogenesis of IBD.…”

Section: Introductionmentioning

confidence: 90%

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Polymorphisms inPRKCDBP, a Transcriptional Target of TNF-α, Are Associated With Inflammatory Bowel Disease in Korean

et al. 2015

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Background/AimsEmerging data indicate that polymorphic sequence variations in the tumor necrosis factor alpha (TNF-α) gene may affect its production, and be associated with the risk of inflammatory bowel disease (IBD). PRKCDBP is a putative tumor suppressor gene and a transcriptional target of TNF-α. The aim of this case-control study is to explore the possible association of single nucleotide polymorphisms (SNPs) in PRKCDBP with the development of IBD in Koreans.MethodsGenotyping analysis of four SNPs of PRKCDBP [rs35301211 (G210A), rs11544766 (G237C), rs12294600 (C797T), and rs1051992 (T507C)] was performed on 170 ulcerative colitis (UC),131 Crohn's disease (CD) patients, and 100 unrelated healthy controls using polymerase chain reaction and restriction fragment length polymorphism.ResultsHeterozygous configuration of three SNPs (G210A, G237C, and C797T) was very rare in both patients and healthy controls. However, allele frequencies of the T507C SNP showed a significant difference between UC patients and controls (P=0.037). The CC genotype of the T507C SNP was identified in 46.6% (61 of 131) of CD and 49.4% (84 of 170) of UC patients, but only in 33.0% (33 of 100) of healthy controls. Furthermore, CC homozygosity was more prevalent than TC heterozygosity in both CD and UC patients versus controls (P=0.016; gender-adjusted odds ratio [aOR], 2.16; 95% confidence interval [CI], 1.16-4.04 and P=0.009; aOR, 2.09; 95% CI, 1.193.64; respectively)ConclusionsOur results suggest that the T507C SNP in PRKCDBP, a TNF-α-inducible gene, might be associated with susceptibility to IBD (particularly UC) development in Koreans.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 97%

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Polymorphisms inPRKCDBP, a Transcriptional Target of TNF-α, Are Associated With Inflammatory Bowel Disease in Korean

et al. 2015

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“…In view of the loss of cavin3 in numerous cancers (Caren et al, 2011;Kim et al, 2014;Lee et al, 2008;Lee et al, 2011;Martinez et al, 2009;Tong et al, 2010;Xu et al, 2001;Zochbauer-Muller et al, 2005) and the crucial role of BRCA1 as a tumor suppressor (King et al, 2003;Miki et al, 1994;Venkitaraman et al, 2002), these studies describing a new functional partner for BRCA1 suggest that cavin3 should be considered in future diagnostic and therapeutic strategies. (Z-Leu-Leu-Leu-al, Cat no.…”

Section: /07/20mentioning

confidence: 99%

“…Cavin3 belongs to a family of proteins that includes caveolaeassociated protein 1 (cavin1), caveolae-associated protein 2 (cavin2), and the muscle-specific member caveolae-associated protein 4 (cavin4) (Ariotti and Parton, 2013;Bastiani et al, 2009;Hansen et al, 2009Lo et al, 2015;McMahon et al, 2009). Cavin3 is a putative tumor suppressor gene that is epigenetically silenced in a range of human malignancies (Xu et al, 2001), principally due to hypermethylation of its promoter region (Caren et al, 2011;Kim et al, 2014;Lee et al, 2008;Lee et al, 2011;Martinez et al, 2009;Tong et al, 2010;Zochbauer-Muller et al, 2005). Furthermore, cavin3 has previously suggested to interact with BRCA1, although no data has been formally published to support this interaction (Xu et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Cavin3 released from caveolae interacts with BRCA1 to regulate the cellular stress response

McMahon

Stroud

Gambin

et al. 2020

Preprint

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Caveolae-associated protein 3 (cavin3), a putative tumor suppressor protein, is inactivated in most cancers. We characterized how cavin3 affects the cellular proteome using genome-edited cells together with label-free quantitative proteomics. These studies revealed a prominent role for cavin3 in DNA repair with BRCA1 and BRCA1 A-complex components being downregulated on cavin3 deletion. Cellular and cell-free expression assays, we show a direct interaction between BRCA1 and cavin3. Association of BRCA1 and cavin3 occurs when cavin3 is released from caveolae that are disassembled in response to UV and mechanical stress. Supporting a role in DNA repair, cavin3-deficient cells were sensitized to the effects of PARP inhibition, which compromises DNA repair, and showed reduced recruitment of the BRCA1 A-complex to UV DNA damage foci. Overexpression and RNAi-depletion revealed that cavin3 sensitized various cancer cells to UV-induced apoptosis. We conclude that cavin3 functions together with BRCA1 in multiple pathways that contribute to tumorigenesis.

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The sodium new houttuyfonate suppresses NSCLC via activating pyroptosis through TCONS‐14036/miR‐1228‐5p/PRKCDBP pathway

Jiang

Feng

et al. 2023

Cell Proliferation

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Several studies have suggested the potential value of Houttuynia cordata as a therapeutic agent in lung cancer, but direct evidence is still lacking. The study aimed to determine the regulatory impact of a major H. cordata constituent derivative (sodium new houttuyfonate [SNH]) on lncRNA networks in non-small cell lung cancer (NSCLC) to identify new potential therapeutic targets. After exposing NSCLC cells to SNH, we analysed the following: cell death (via flow cytometry, TUNEL and ASC speck formation assays), immune factors (via ELISA), gene transcription (via RT-qPCR), subcellular localisation (via FISH), gene-gene and gene-protein interactions (via dual-luciferase reporter and RNA immunoprecipitation assays, respectively) and protein expression and distribution (via western blotting and immunocytochemistry or immunohistochemistry). In addition, statistical analysis (via one-way ANOVA or unpaired t-tests) was performed. Exposure to SNH promoted NSCLC cell pyroptosis, concomitant with significant up-regulation of TCONS-14036, a novel lncRNA. Mechanistic research demonstrated that TCONS-14036 functions as a competing endogenous (ce)RNA by sequestering microRNA (miR)-1228-5p, thereby up-regulating PRKCDBP-encoding transcript levels. Indeed, PRKCDBP promoted pyroptosis by activating the NLRP3 inflammasome, resulting in CASP1, IL-1β and GSDMD cleavage. Rilei Jiang, Bing Lu and Fanchao Feng contributed equally to this work.

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Elevation of PRKCDBP, A Novel Transcriptional Target of TNF-α, and Its Downregulation by Infliximab in Patients with Ulcerative Colitis

Cited by 6 publications

References 33 publications

Polymorphisms inPRKCDBP, a Transcriptional Target of TNF-α, Are Associated With Inflammatory Bowel Disease in Korean

Polymorphisms inPRKCDBP, a Transcriptional Target of TNF-α, Are Associated With Inflammatory Bowel Disease in Korean

Cavin3 released from caveolae interacts with BRCA1 to regulate the cellular stress response

The sodium new houttuyfonate suppresses NSCLC via activating pyroptosis through TCONS‐14036/miR‐1228‐5p/PRKCDBP pathway

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