Tumor Progression Locus 2 (Tpl2) Kinase Promotes Chemokine Receptor Expression and Macrophage Migration during Acute Inflammation

Rowley, Sean M.; Kuriakose, Teneema; Dockery, Lee M.; Tran-Nguyen, Thi; Gingerich, Aaron D.; Wei, Lai; Watford, Wendy T.

doi:10.1074/jbc.m114.559344

Cited by 25 publications

(19 citation statements)

References 64 publications

(56 reference statements)

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“…To address this possibility, mouse bone marrow macrophages were treated with JG-98 for 16 h, mRNA isolated from control and treated cells, and global gene expression analysis was assessed by microarray (GEO Series GSE82311). Among downregulated genes, we identified genes specifically implicated in the macrophage migration, including MAP3K8 (17), CXCR4 (18), and FOXM1 (19) (Fig. 2C and S2).…”

Section: Resultsmentioning

confidence: 99%

Anticancer Effects of Targeting Hsp70 in Tumor Stromal Cells

et al. 2016

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The stress-induced chaperone protein Hsp70 enables the initiation and progression of many cancers, making it an appealing therapeutic target for development. Here we show that cancer cells resistant to Hsp70 inhibitors in vitro remain sensitive to them in vivo, revealing the pathogenic significance of Hsp70 in tumor stromal cells rather than tumor cells as widely presumed. Using transgenic mouse models of cancer, we found that expression of Hsp70 in host stromal cells was essential to support tumor growth. Furthermore, genetic ablation or pharmacological inhibition of Hsp70 suppressed tumor infiltration by macrophages needed to enable tumor growth. Overall, our results illustrate how Hsp70 inhibitors mediate the anti-cancer effects by targeting both tumor cells and tumor stromal cells, with implications for the broad use of these inhibitors as tools to ablate tumor-associated macrophages that enable malignant progression.

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Section: Resultsmentioning

confidence: 99%

Anticancer Effects of Targeting Hsp70 in Tumor Stromal Cells

et al. 2016

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“…Deregulation of TPL2 expression could reflect its potential involvement in certain pathologies, such as inflammatory diseases, type 1 diabetes, and cancer . We compared hepatic TPL2 expression in normal and NAFLD‐related pathologies in a series of pilot studies.…”

Section: Resultsmentioning

confidence: 99%

Tumor Progression Locus 2 in Hepatocytes Potentiates Both Liver and Systemic Metabolic Disorders in Mice

et al. 2018

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“…Carlr suppresses mitochondrial fission and apoptosis by targeting miR-539 and PHB2 in cardiomyocytes. Interestingly, Carlr is known to be expressed in various tissues, including myeloid lineage cells and the intestine (13), and its expression is induced in macrophages and dendritic cells in response to LPS (11, 14, 15). However, unpublished studies from our group show that miR-539 levels do not change in response to LPS stimulation, and LPS-induced genes are not known to be targeted by this microRNA.…”

Section: Introductionmentioning

confidence: 99%

Cytoplasmic Form of Carlr lncRNA Facilitates Inflammatory Gene Expression upon NF-κB Activation

Castellanos–Rubio

Kratchmarov

Sebastian

et al. 2017

The Journal of Immunology

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Long non-coding RNAs (lncRNAs) have emerged as critical regulators of inflammation. To further understand the interaction between inflammatory signaling pathways and lncRNAs, we characterized the function of the lncRNA, Carlr, a lncRNA expressed in both mouse and human cells of diverse tissues. Carlr expression is increased following NF-κB signaling in macrophages, with concomitant translocation to, and enrichment of, the transcript in the cytoplasm. Knockdown of Carlr results in impaired expression of NF-κB pathway genes and influences the interaction between macrophages and intestinal cells in an inflammatory environment. In human celiac disease patient samples, increased levels of the Carlr transcript were detected in the cytoplasm, alongside elevated expression of NF-κB pathway genes. These findings suggest that increased Carlr expression and/or cytoplasmic localization, is required for efficient NF-κB signaling and is associated with the inflamed tissue state observed in human celiac disease.

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Tumor Progression Locus 2 (Tpl2) Kinase Promotes Chemokine Receptor Expression and Macrophage Migration during Acute Inflammation

Cited by 25 publications

References 64 publications

Anticancer Effects of Targeting Hsp70 in Tumor Stromal Cells

Anticancer Effects of Targeting Hsp70 in Tumor Stromal Cells

Tumor Progression Locus 2 in Hepatocytes Potentiates Both Liver and Systemic Metabolic Disorders in Mice

Cytoplasmic Form of Carlr lncRNA Facilitates Inflammatory Gene Expression upon NF-κB Activation

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