IFIT3 Is Increased in Serum from Patients with Chronic Hepatitis B Virus (HBV) Infection and Promotes the Anti-HBV Effect of Interferon Alpha via JAK-STAT2
            <i>In Vitro</i>

Xu, Siyi; Huang, Jinlan; Xun, Zhen; Li, Shiqi; Fu, Ya; Lin, Nan; Wu, Weihong; Chen, Tianbin; Liu, Can; Ou, Qishui

doi:10.1128/spectrum.01557-22

Cited by 10 publications

(7 citation statements)

References 49 publications

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“…The traditional function of NMI is binding to transcription factors and thus indirectly regulates the transcription process. STAT3 is one of the most common NMI‐binding transcription factors and the function of IFIT3 has also been reported to be related to STATs signaling 7,9 . Therefore, we proposed that whether STAT3 was the mediator between NMI and IFIT3.…”

Section: Resultsmentioning

confidence: 97%

“…STAT3 is one of the most common NMI-binding transcription factors and the function of IFIT3 has also been reported to be related to STATs signaling. 7,9 Therefore, we proposed that whether STAT3 was the mediator between NMI and IFIT3. First, we used Co-IP to confirm the binding of STAT3 and NMI in PDAC cells (Figure 6A,B).…”

Section: Nmi Regulates the Expression Of Ifit3 Via Binding To Stat3mentioning

confidence: 99%

“…Interferon‐induced protein with tetratricopeptide repeats 3 (IFIT3) is a gene associated with inflammation and is regulated through the JAK/STAT signaling pathway 7 . While previous studies have mainly focused on the antiviral role of IFIT3, emerging evidence suggests its involvement in cancer progression.…”

Section: Introductionmentioning

confidence: 99%

“…Interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) is a gene associated with inflammation and is regulated through the JAK/STAT signaling pathway. 7 While previous studies have mainly focused on the antiviral role of IFIT3, emerging evidence suggests its involvement in cancer progression. For instance, Pidugu et al reported that IFIT3 could promote metastasis in oral squamous cell carcinoma and contribute to chemotherapy resistance against cisplatin and 5-FU.…”

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confidence: 99%

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NMI promotes tumor progression and gemcitabine resistance in pancreatic cancer via STAT3‐IFIT3 axis

Hu,

Li,

Chen

et al. 2023

Molecular Carcinogenesis

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N‐myc and STAT interactor (NMI) has been reported to interact with several transcription factors, including STATs family, c‐Myc, N‐Myc, and BRCA1, to indirectly affect transcription events and participate in multiple cellular processes. However, its function in pancreatic ductal adenocarcinoma (PDAC) has seldom been studied. In this study, we investigated the regulation of NMI on PDAC progression and uncovered the underlying molecular mechanisms. We found that NMI expression was significantly upregulated in PDAC and high NMI expression was related to a worse patient survival. Cell proliferation and migration assay, including cell viability, transwell assay, wound healing, and subcutaneous mouse model were utilized to confirm the function of NMI in PDAC progression. Downregulation of NMI abrogates tumor progression of PDAC both in vitro and in vivo. RNA sequencing was utilized to identify the downstream molecules of NMI and interferon‐induced protein with tetratricopeptide repeats 3 (IFIT3) was confirmed to be regulated by NMI in both mRNA and protein level. The binding function of NMI to STAT3 was essential in regulating the IFIT3 expression. Moreover, the NMI/STAT3‐IFIT3 axis was identified to markedly facilitate the gemcitabine resistance in PDAC cells.

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Section: Resultsmentioning

confidence: 97%

Section: Nmi Regulates the Expression Of Ifit3 Via Binding To Stat3mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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NMI promotes tumor progression and gemcitabine resistance in pancreatic cancer via STAT3‐IFIT3 axis

Hu,

Li,

Chen

et al. 2023

Molecular Carcinogenesis

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“…Furthermore, high expression of STAT1, STAT2, and IRF9 in breast cells significantly increase the expression of IFIT3 after IFNβ treatment [ 75 ], are all highly expressed in cells such as esophageal squamous cell carcinoma [ 76 , 77 ] and that STAT2 could form a complex with IRF9 and bind to the IFN-stimulated gene regulatory element (ISRE) sequence on the IFIT3 promoter to promote IFIT3 transcription [ 78 ]. In another publication regarding patients with Chronic Hepatitis B Virus, STAT2 was essential for the production of IFIT3 but not STAT1 [ 79 ].…”

Section: Resultsmentioning

confidence: 99%

Tissue-specific atlas of trans-models for gene regulation elucidates complex regulation patterns

Dagostino,

Gottlieb

2024

BMC Genomics

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Background Deciphering gene regulation is essential for understanding the underlying mechanisms of healthy and disease states. While the regulatory networks formed by transcription factors (TFs) and their target genes has been mostly studied with relation to cis effects such as in TF binding sites, we focused on trans effects of TFs on the expression of their transcribed genes and their potential mechanisms. Results We provide a comprehensive tissue-specific atlas, spanning 49 tissues of TF variations affecting gene expression through computational models considering two potential mechanisms, including combinatorial regulation by the expression of the TFs, and by genetic variants within the TF. We demonstrate that similarity between tissues based on our discovered genes corresponds to other types of tissue similarity. The genes affected by complex TF regulation, and their modelled TFs, were highly enriched for pharmacogenomic functions, while the TFs themselves were also enriched in several cancer and metabolic pathways. Additionally, genes that appear in multiple clusters are enriched for regulation of immune system while tissue clusters include cluster-specific genes that are enriched for biological functions and diseases previously associated with the tissues forming the cluster. Finally, our atlas exposes multilevel regulation across multiple tissues, where TFs regulate other TFs through the two tested mechanisms. Conclusions Our tissue-specific atlas provides hierarchical tissue-specific trans genetic regulations that can be further studied for association with human phenotypes.

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Chinese medicine in the treatment of chronic hepatitis B: The mechanisms of signal pathway regulation

Zheng,

Qi,

Xue

et al. 2024

Heliyon

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IFIT3 Is Increased in Serum from Patients with Chronic Hepatitis B Virus (HBV) Infection and Promotes the Anti-HBV Effect of Interferon Alpha via JAK-STAT2 In Vitro

Cited by 10 publications

References 49 publications

NMI promotes tumor progression and gemcitabine resistance in pancreatic cancer via STAT3‐IFIT3 axis

NMI promotes tumor progression and gemcitabine resistance in pancreatic cancer via STAT3‐IFIT3 axis

Tissue-specific atlas of trans-models for gene regulation elucidates complex regulation patterns

Chinese medicine in the treatment of chronic hepatitis B: The mechanisms of signal pathway regulation

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