<scp>CCK</scp>8 negatively regulates the <scp>TLR</scp>9‐induced activation of human peripheral blood p<scp>DC</scp>s by targeting <scp>TRAF</scp>6 signaling

Jia, Xianxian; Cong, Bin; Zhang, Jingge; Li, Hui; Liu, Wenxuan; He-ping, Chang; Dong, Ming; Ma, Chunling

doi:10.1002/eji.201343725

Cited by 22 publications

(17 citation statements)

References 39 publications

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“…The Human Genome Variation Society (HGVS) name of rs187084 is NM_017442.3:c.-1486 T > C [ 19 , 20 ]. Three case-control studies (987cases and 405 controls) addressed the relationship between rs187084 polymorphism and the risk of TB.…”

Section: Resultsmentioning

confidence: 99%

Association between toll-like receptors 9 (TLR9) gene polymorphism and risk of pulmonary tuberculosis: meta-analysis

et al. 2015

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BackgroundPrevious studies indicated that the single nucleotide polymorphisms (SNPs) in TLR9 gene might be associated with Tuberculosis (TB) risk. However, the results are inconsistent and inconclusive.Methods1745 articles from four databases were involved in our study. A meta-analysis on the associations between the seven polymorphisms and TB risk was carried out by comparison using different genetic models.ResultsIn this systematic review 8 studies from seven English articles were analyzed. Our results showed that rs352139 is significantly associated with TB risk (AA vs. AG, OR 0.77, 95% CI 0.65-0.92, P = 0.004). In the ethnic subgroup analysis, Indonesians with AA genotype had a decreased susceptibility while Mexicans with GG allele had an increased risk.ConclusionsThe meta-analysis indicated that rs352139 polymorphism might be associated with decreased TB risk in Indonesians whereas increased risk in Mexicans. Whether the observed association was due to causal effect needs to be further studied.

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Section: Resultsmentioning

confidence: 99%

Association between toll-like receptors 9 (TLR9) gene polymorphism and risk of pulmonary tuberculosis: meta-analysis

et al. 2015

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“…We employed an established (D’Apolito et al 2015, Jia et al 2014) non radioactive ELISA-based PKC enzymatic assay (Enzo Life Science, Farmingdale, NY, USA) with HepG2 cells (0.5 µg total protein) in a 30 µL reaction volume following the manufacturer’s recommendations.…”

Section: Methodsmentioning

confidence: 99%

Increased IGFBP-1 phosphorylation in response to leucine deprivation is mediated by CK2 and PKC

Malkani

Biggar

Shehab

et al. 2016

Molecular and Cellular Endocrinology

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Insulin-like growth factor binding protein-1 (IGFBP-1), secreted by fetal liver, is a key regulator of IGF-I bioavailability and fetal growth. IGFBP-1 phosphorylation decreases IGF-I bioavailability and diminishes its growth-promoting effects. Growth-restricted fetuses have decreased levels of circulating essential amino acids. We recently showed that IGFBP-1 hyperphosphorylation (pSer101/119/169) in response to leucine deprivation is regulated via activation of the amino acid response (AAR) in HepG2 cells. Here we investigated nutrient-sensitive protein kinases CK2/PKC/PKA in mediating IGFBP-1 phosphorylation in leucine deprivation. We demonstrated that leucine deprivation stimulated CK2 activity (enzymatic assay) and induced IGFBP-1 phosphorylation (immunoblotting/MRM-MS). Inhibition (pharmacological/siRNA) of CK2/PKC, but not PKA, prevented IGFBP-1 hyperphosphorylation in leucine deprivation. PKC inhibition also prevented leucine deprivation-stimulated CK2 activity. Functionally, leucine deprivation decreased IGF-I-induced-IGF-1R autophosphorylation when CK2/PKC were not inhibited. Our data strongly support that PKC promotes leucine deprivation-induced IGFBP-1 hyperphosphorylation via CK2 activation, mechanistically linking decreased amino acid availability and reduced fetal growth.

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“…CD133 + cells were isolated by magnetic-activated cell sorting (MACS) with a CD133 MicroBead Tumor Tissue Kit (Miltenyi Biotec, 130-100-857) using methods described previously (18). The cells were cultured in serum-free media for sphere formation assays.…”

Section: Cell Isolation and Culturementioning

confidence: 99%

CD2+ T-helper 17-like cells differentiated from a CD133+ subpopulation of non-small cell lung carcinoma cells promote the growth of lung carcinoma

Jia¹,

Jia²,

Zhang³

et al. 2021

Ann Transl Med

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Background: Cancer stem cells (CSCs) give rise to a diverse variety of differentiated cells, which comprise the bulk of the tumor microenvironment (TME). However, the exact multi-directional differentiation potential of CSCs has not been fully clarified. This study was designed to explore whether CSCs differentiate into cellular components of the TME to promote the growth of lung carcinoma. Methods:The present of CD133 + , CD2 + , and CD133 + CD2 + cells in both clinical lung adenocarcinoma tissue and non-small cell lung carcinoma (NSCLC) cell lines were monitored using polymerase chain reaction (PCR) Array, flow cytometry (FCM), quantitative real-time PCR (qRT-PCR) and immunohistofluorescence (IF). Stem-like properties of CD133 + cells and CD2 + cells were detected by sphere formation assay, IF, and western blot. Colony formation and xenograft tumors experiments were performed to assess the malignant behaviors of CD2 + cells. The differentiation of CD133 + cells to CD2 + Th17-like cells was observed by FCM. The interleukin (IL)-2/phosphorylated signal transducer and activator of transcription protein 5 (pSTAT5)/ retinoic acid receptor-related orphan receptor gamma t (RORγt) signaling pathway was evaluated by western blot and FCM. Results: We found that CD133 + cells within both clinical lung adenocarcinoma tissue and NSCLC cell lines included a subset of CD2-expressing cells, which were correlated with the grade of malignancy (r=0.7835, P<0.01) and exhibited stem-like properties. Then, we determined the tumorigenic effects of CD2 on the growth of transplanted Lewis lung carcinoma cells (LLC1) in C57/BL6 mice. The results indicated that CD2 + cells were effective in promoting tumor growth in vivo (P<0.01). Furthermore, we obtained direct evidence of an ability of CD133 + cells to transform to T-helper 17-like cells via an intermediate CD133 + CD2 + progenitor cell that is able to secrete IL-17A and IL-23. Furthermore, we found that IL-2 can inhibit the production of T-helper 17-like cells (P<0.001) by modulating the activation of STAT5 signaling pathways to downregulate the expression of RORγt (P<0.001).Conclusions: Our data demonstrates that Th17-like cells generated from CSCs support cancer progression. These findings enrich the definition of multidirectional differentiation potential of CSCs and improve the understanding of the role of CSCs in cancer progression, which aids the improvement and creation of therapies.

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CCK8 negatively regulates the TLR9‐induced activation of human peripheral blood pDCs by targeting TRAF6 signaling

Cited by 22 publications

References 39 publications

Association between toll-like receptors 9 (TLR9) gene polymorphism and risk of pulmonary tuberculosis: meta-analysis

Association between toll-like receptors 9 (TLR9) gene polymorphism and risk of pulmonary tuberculosis: meta-analysis

Increased IGFBP-1 phosphorylation in response to leucine deprivation is mediated by CK2 and PKC

CD2+ T-helper 17-like cells differentiated from a CD133+ subpopulation of non-small cell lung carcinoma cells promote the growth of lung carcinoma

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