<i>COMMD7</i> is correlated with a novel NF-κB positive feedback loop in hepatocellular carcinoma

Deng, Chang-Lin; Wang, Liang; Huang, Xiaobing; You, Nan; Tang, Yichen; Wu, Ke; Liang, Ping; Mi, Na; Li, Jing

doi:10.18632/oncotarget.9047

Cited by 12 publications

(11 citation statements)

References 20 publications

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“…Our previous research has shown that COMMD7 is correlated with a novel NF-κB-positive feedback loop in HCC cells. Moreover, NF-κB directly binds to the COMMD7 promoter and serves as an activator for COMMD7 transcription 25 . Inconsistent with our previous findings, reports indicated that COMMD7 binds to the IκB kinase alpha (IKK) complex through NEMO and induces degradation of p65 leading to the termination of NF-κB signaling 19, 26.…”

Section: Discussionsupporting

confidence: 49%

“…Among the members of the COMMD family, COMMD1 has been the most extensively characterized and operates as a terminator of NF-κB signaling; 20 COMMD1 reduction is associated with cancer progression caused by constitutive NF-κB activation 21, 22. Another member of the COMMD family, COMMD7 has been identified as a novel NF-κB essential modulator (NEMO)-interacting protein and was reported to function as molecular target in several types of cancers including pancreatic ductal adenocarcinoma 23 and HCC24, 25 in our previous studies. Moreover, we previously found that COMMD7 positively correlated with the expression of NF-κB, and that the NF-κB signaling pathway could mediate the proliferative and anti-apoptotic effects of COMMD7 in HCC cells.…”

Section: Introductionmentioning

confidence: 99%

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COMMD7 Regulates NF-κB Signaling Pathway in Hepatocellular Carcinoma Stem-like Cells

You

Huang

et al. 2019

Molecular Therapy - Oncolytics

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Previous studies showed that the COpper Metabolism gene MURR1 Domain (COMMD) family of proteins was abnormally expressed in hepatocellular carcinoma (HCC). This study aimed to explore the roles of COMMD1 and COMMD7 in regulating nuclear factor κB (NF-κB) signaling in HCC stem cells (HCSCs). In vivo, the expression of COMMD7 and COMMD1 was determined in 35 pairs of HCC cancer tissues and adjacent tissues, and the effect of COMMD7 silencing on xenograft tumor growth was evaluated. In vitro, the effects of COMMD7 silencing and COMMD1 overexpression on HCSC function were assessed. Results found that the expression levels of COMMD7 were higher, whereas COMMD1 levels were lower in HCC tissues and HCSCs. COMMD7 silencing or COMMD1 overexpression inhibited cell proliferation, migration, and invasion through suppression of NF-κB p65. Furthermore, COMMD7 positively regulated NF-κB by upregulating protein inhibitor for activated stat 4 (PIAS4). This study demonstrates that COMMD7 has a dual regulatory role in the NF-κB signaling pathway in Nanog+ HCSCs.

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Section: Discussionsupporting

confidence: 49%

Section: Introductionmentioning

confidence: 99%

COMMD7 Regulates NF-κB Signaling Pathway in Hepatocellular Carcinoma Stem-like Cells

You

Huang

et al. 2019

Molecular Therapy - Oncolytics

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“…On the other hand, COMMD7 was identified as a novel NEMO interacting protein involved in NF-κB signaling termination [ 7 ], the incorrect regulation of which is known to be associated with a variety of tumors [ 5 , 8 ]. One study demonstrated that COMMD7 played a dual regulatory role in the NF-κB signaling pathway in HCC [ 9 ]. However, to date, the expression of COMMD7 in AML and its prognostic value remain unclear.…”

Section: Introductionmentioning

confidence: 99%

High expression of COMMD7 is an adverse prognostic factor in acute myeloid leukemia

Chen

Zhang

et al. 2021

Aging

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Acute myeloid leukemia (AML) is a frequent malignancy in adults worldwide; identifying preferable biomarkers has become one of the current challenges. Given that COMMD7 has been reported associated with tumor progression in various human solid cancers but rarely reported in AML, herein, RNA sequencing data from TCGA and GTEx were obtained for analysis of COMMD7 expression and differentially expressed gene (DEG). Furthermore, functional enrichment analysis of COMMD7 -related DEGs was performed by GO/KEGG, GSEA, immune cell infiltration analysis, and protein-protein interaction (PPI) network. In addition, the clinical significance of COMMD7 in AML was figured out by Kaplan-Meier Cox regression and prognostic nomogram model. R package was used to analyze incorporated studies. As a result, COMMD7 was highly expressed in various malignancies, including AML, compared with normal samples. Moreover, high expression of COMMD7 was associated with poor prognosis in 151 AML samples, as well as subgroups with age >60, NPM1 mutation-positive, FLT3 mutation-negative, and DNMT3A mutation-negative, et al. ( P < 0.05). High COMMD7 was an independent prognostic factor in Cox regression analysis; Age and cytogenetics risk were included in the nomogram prognostic model. Furthermore, a total of 529 DEGs were identified between the high- and the low- expression group, of which 92 genes were up-regulated and 437 genes were down-regulated. Collectively, high expression of COMMD7 is a potential biomarker for adverse outcomes in AML. The DEGs and pathways recognized in the study provide a preliminary grasp of the underlying molecular mechanisms of AML carcinogenesis and progression.

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“…The human hepatocellular carcinoma cell lines Hepg2, MHCC97H, HuH7, and Bel-7402, and the live cell line L-02, and human embryonic kidney 293 (HEK-293) cells were purchased from Cell Bank of Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences. As previous described (22), cells were cultured in RPMI-1640 medium (Hyclone, Logan, uT, uSA) and supplemented with 10% fetal bovine serum (gibco, Carlsbad, CA, uSA), 1% penicillin/streptomycin at 37˚C in 5% Co 2 .…”

Section: Methodsmentioning

confidence: 99%

miR-30e acts as a tumor suppressor in hepatocellular carcinoma partly via JAK1/STAT3 pathway

Mao

Pang

et al. 2017

Oncology Reports

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Hepatocellular carcinoma (HCC) is the leading cause of cancer-associated mortalities. The effective diagnostic and therapeutic targets for HCC are still unclear. miR-30e was differentially expressed in the majority of HCC tissues and cell lines. The aim of this study was to investigate the functional roles of miR-30e and their modulation of cancer networks in HCC cells. We determined the expression of miR-30e by quantitative real-time polymerase chain reaction, and found downregulation of miR-30e in HepG2 and HuH7 cells. miR-30e mimics significantly inhibited the proliferation, migration, and invasion of HepG2 and HuH7 cells, and promoted cell apoptosis, but did not influence the cell cycle. Dual-luciferase reporter assays were applied to identify JAK1 as target of miR-30e. miR-30e mimics downregulated the expression levels of JAK1 and vimentin in mRNA and protein in HepG2 and HuH7 cells. Silence of JAK1 by small interfering RNAs inhibited cell proliferation, migration and invasion of HCC cells. Furthermore, we verified that, IL-6, an agonist of JAK1/STAT3 pathway partly recovered the inhibition of miR-30e mimics on cell migration. Taken together, these findings confirmed our speculation that the functional effect of miR-30e on HCC cells, in part, is dependent on the JAK1/STAT3 signaling pathway. It was suggested that miR-30e has a critical role in the suppression of HCC and presents a novel mechanism of miRNA-mediated JAK1 expression in cancer cells that might be a good prognostic marker for survival of HCC patients.

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COMMD7 is correlated with a novel NF-κB positive feedback loop in hepatocellular carcinoma

Cited by 12 publications

References 20 publications

COMMD7 Regulates NF-κB Signaling Pathway in Hepatocellular Carcinoma Stem-like Cells

COMMD7 Regulates NF-κB Signaling Pathway in Hepatocellular Carcinoma Stem-like Cells

High expression of COMMD7 is an adverse prognostic factor in acute myeloid leukemia

miR-30e acts as a tumor suppressor in hepatocellular carcinoma partly via JAK1/STAT3 pathway

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