14-3-3ζ Regulates Immune Response through Stat3 Signaling in Oral Squamous Cell Carcinoma

Han, Xinguang; Han, Yongfu; Jiao, Huifeng; Jie, Yaqiong

doi:10.14348/molcells.2015.02101

Cited by 21 publications

(11 citation statements)

References 44 publications

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“…Previous studies have suggested the oncogenic roles of 14-3-3ζ in diverse cancer types including HCC 17 , 18 . For example, 14-3-3ζ was upregulated in HCC and can promote HCC invasion and metastasis through binding to AXL (activity of the receptor tyrosine kinase Axl) 9 or through interacting with αB-crystallin mediated by TGF-β and ERK signaling pathways 8 .…”

Section: Discussionmentioning

confidence: 99%

14-3-3ζ delivered by hepatocellular carcinoma-derived exosomes impaired anti-tumor function of tumor-infiltrating T lymphocytes

et al. 2018

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Increasing evidence shows that the anti-tumor functions of tumor-infiltrating T lymphocytes (TILs) were inhibited significantly, but the underlying mechanisms remain not fully understood. In this study, we found that 14-3-3ζ expression was up-regulated in hepatocellular carcinoma (HCC) cells and in TILs. TILs with 14-3-3ζ high-expression (14-3-3ζhigh) exhibited impaired activation (CD69), proliferation (Ki67) and anti-tumor functions compared to 14-3-3ζ low expression (14-3-3ζlow) TILs. Flow cytometry assay showed that compared with 14-3-3ζlow CD8+T cells, 14-3-3ζhigh ones exhibited higher frequency of exhausted phenotypes as measured by inhibitory receptors such as PD-1, TIM-3, LAG3, and CTLA-4. 14-3-3ζ overexpression inhibited the activity and proliferation of peripheral blood CD3+ T cells, deviated the differentiation of naive T cells from effector T cells to regulatory T cells. Moreover, we found that 14-3-3ζ expression levels in TILs correlated positively with those in HCC cells. Naive T cells co-cultured with HCC cells or the visible components of culture medium of HCC cells exhibited increased 14-3-3ζ expression. Stochastic optical reconstruction microscopy (STORM) and confocal assay showed that 14-3-3ζ-containing exosomes derived from HCC cells could be swallowed by T cells, suggesting that 14-3-3ζ might be transmitted from HCC cells to TILs at least partially through exosomes. In conclusion, our study for the first time demonstrated that 14-3-3ζ is up-regulated in and inhibited the anti-tumor functions of tumor-infiltrating T cells in HCC microenvironment and that 14-3-3ζ might be transmitted from HCC cells to T cells at least partially through exosomes.

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Section: Discussionmentioning

confidence: 99%

14-3-3ζ delivered by hepatocellular carcinoma-derived exosomes impaired anti-tumor function of tumor-infiltrating T lymphocytes

et al. 2018

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“…Inhibition of YWHAZ could mimic all the functions of miR-451 overexpression. YWHAZ plays a critical role in signaling transduction through interaction with target proteins via phosphorylation motif [43] or directly regulating phosphorylation [44, 45]. We identify that forced expression of miR-451 or knockdown of YWHAZ or c-Myc result in decreased p-AKT levels in AML.…”

Section: Discussionmentioning

confidence: 99%

c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia

Gong

Chen

et al. 2016

Oncotarget

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Aberrant activation of c-Myc plays an important oncogenic role via regulating a series of coding and non-coding genes in acute myeloid leukemia (AML). Histone deacetylases (HDACs) can remove acetyl group from histone and regulate gene expression via changing chromatin structure. Here, we found miR-451 is abnormally down-regulated in AML patient samples; c-Myc recruits HDAC3 to form a transcriptional suppressor complex, co-localizes on the miR-451 promoter, epigenetically inhibits its transcription and finally induces its downregulation in AML. Furthermore, our in vitro and in vivo results suggest that miR-451 functions as a tumor suppressor via promoting apoptosis and suppressing malignant cell proliferation. The mechanistic study demonstrated that miR-451 directly targets YWHAZ mRNA and suppresses YWHAZ/AKT signaling in AML. Knockdown of c-Myc results in restoration of miR-451 and inhibition of YWHAZ/AKT signaling. In AML patients, low level of miR-451 is negatively correlated with high levels of c-Myc and YWHAZ, while c-Myc level is positively related to YWHAZ expression. These results suggested that c-Myc⊣miR-451⊣YWHAZ/AKT cascade might play a crucial role during leukemogenesis, and reintroduction of miR-451 could be as a potential strategy for AML therapy.

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“…59 ), HNRNPA2B1 (ref. 60 ) and YWHAZ 61 . In conclusion, our proteome analysis verifies the induction of an appropriate host response in SARS-CoV-2-infected Huh7 cells and further supports an important role for IFN and MAPK signalling in SARS-CoV-2 infection.…”

Section: Biological Functions Of Sars-cov-2 Rna-binding Proteinsmentioning

confidence: 99%

The SARS-CoV-2 RNA–protein interactome in infected human cells

et al. 2020

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Characterizing the interactions that SARS-CoV-2 viral RNAs make with host cell proteins during infection can improve our understanding of viral RNA functions and the host innate immune response. Using RNA antisense purification and mass spectrometry, we identified up to 104 human proteins that directly and specifically bind to SARS-CoV-2 RNAs in infected human cells. We integrated the SARS-CoV-2 RNA interactome with changes in proteome abundance induced by viral infection and linked interactome proteins to cellular pathways relevant to SARS-CoV-2 infections. We demonstrated by genetic perturbation that cellular nucleic acid-binding protein (CNBP) and La-related protein 1 (LARP1), two of the most strongly enriched viral RNA binders, restrict SARS-CoV-2 replication in infected cells and provide a global map of their direct RNA contact sites. Pharmacological inhibition of three other RNA interactome members, PPIA, ATP1A1, and the ARP2/3 complex, reduced viral replication in two human cell lines. The identification of host dependency factors and defence strategies as presented in this work will improve the design of targeted therapeutics against SARS-CoV-2.

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14-3-3ζ Regulates Immune Response through Stat3 Signaling in Oral Squamous Cell Carcinoma

Cited by 21 publications

References 44 publications

14-3-3ζ delivered by hepatocellular carcinoma-derived exosomes impaired anti-tumor function of tumor-infiltrating T lymphocytes

14-3-3ζ delivered by hepatocellular carcinoma-derived exosomes impaired anti-tumor function of tumor-infiltrating T lymphocytes

c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia

The SARS-CoV-2 RNA–protein interactome in infected human cells

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