TRIB1 induces macrophages to M2 phenotype by inhibiting IKB-zeta in prostate cancer

Liu, Zezhen; Han, Zhengxue; Liang, Yingke; Chen, Junxu; Song, Wan; Zhuo, Yangjia; Cai, Zhiduan; Deng, Yulin; Lin, Zhengfang; Mo, Rujun; He, Hui‐Chan; Zhong, Weide

doi:10.1016/j.cellsig.2019.03.017

Cited by 27 publications

(30 citation statements)

References 38 publications

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“…The previous study revealed that Trib1 participates in regulating macrophage polarization. For instance, Trib1 induced differentiation of macrophages into M2 in prostate cancer immune microenvironment (Liu et al, 2019); in mice lacking Trib1, the production of proinflammatory cytokine was increased and M2-like macrophages differentiation was reduced (Akira et al, 2013). In this study, we discovered that Trib1 was negatively regulated by miR-98-5p.…”

Section: Discussionmentioning

confidence: 61%

MiR-98-5p expression inhibits polarization of macrophages to an M2 phenotype by targeting Trib1 in inflammatory bowel disease

et al. 2020

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Herein, we unfolded miR-98-5p mechanism in inflammatory bowel disease (IBD). IBD mouse model was established. The severity of colitis was assessed daily using the disease activity index (DAI). Murine peritoneal macrophages were stimulated by lipopolysaccharide (LPS). MiR-98-5p, tribbles homolog 1 (Trib1), M1 and M2 macrophage marker genes mRNA expression was analyzed. The relationship between miR-98-5p and Trib1 was explored using a luciferase reporter assay. The strategy of loss-of-function was used to explore the mechanism of miR-98-5p in macrophage polarization, inflammation and IBD. The results revealed that IBD mice had higher DAI index and miR-98-5p expression when compared to the Sham group. MiR-98-5p and Trib1 displayed a targeted regulation relationship. Knockdown of miR-98-5p transformed LPS-induced M1 macrophage polarization into M2 macrophage polarization and inhibited inflammation via up-regulating Trib1. However, shTrib1 reversed the effects. In vivo experiment, silencing of miR-98-5p, diminished the DAI and promoted M2 macrophage polarization. In conclusion, knockdown of miR-98-5p changed macrophage polarization to the M2 phenotype by increasing Trib1 expression, thereby alleviating IBD symptoms.

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Section: Discussionmentioning

confidence: 61%

MiR-98-5p expression inhibits polarization of macrophages to an M2 phenotype by targeting Trib1 in inflammatory bowel disease

et al. 2020

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“…The protein expression levels of CS in PCa and normal prostate tissues were examined by IHC based in our TMA cohort according to the protocol of our previous report. 13,14 The immunostaining was obtained using the IHC kit (UltraSensitive™ SP, MX Biotechnologies, China; Cat. No: KIT-9730) based on the manufacturer's instructions.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…CS protein expression levels in the PCa CT cells and CSsh cells were examined by Western blot assay based on our previous report. 13,14 A rabbit anti-CS primary antibody (Boster company, China; Cat. No: BM5202,) was used to detect CS expression level, and a mouse anti-β-actin primary antibody (Boster company, China; Cat.…”

Section: Western Blot Assaymentioning

confidence: 99%

<p>Aberrant Expression of Citrate Synthase is Linked to Disease Progression and Clinical Outcome in Prostate Cancer</p>

Cai¹,

Deng²,

Ye³

et al. 2020

CMAR

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Citrate synthase (CS) is a rate-limiting enzyme in the citrate cycle and is capable of catalyzing oxaloacetate and acetyl-CoA to citrate. CS has been uncovered to be upregulated in a variety of cancers, and its expression and clinical significance in prostate cancer (PCa) remain unknown. Methods: In this study, we examined the association between CS expression level and clinicopathological features of prostate cancer patients in a TMA cohort and the public cancer database (The Cancer Genome Atlas-Prostate Adenocarcinoma, TCGA-PRAD). The CS knockdown cell lines were constructed to study the effects of CS downregulation on proliferation, colony formation, migration, invasion, and cell cycle of prostate cancer cells in vitro. And the effect of CS downregulation on tumor growth in mice was studied in vivo. In addition, the metabolomics and mitochondrial function were detected in the CS knockdown cell lines. Results: CS expression level in PCa tissues was higher than that in normal tissues (P < 0.05). CS upregulation was significantly associated with high Gleason score (P < 0.05), advanced pathological stage (P < 0.001), and biochemical recurrence (P < 0.001). Functionally, decreased expression of CS inhibited PCa cell proliferation, colony formation, migration, invasion and cell cycle in vitro, and inhibited tumor growth in vivo. In addition, CS downregulation exerted potential inhibitory effects on the lipid metabolism and mitochondrial function of PCa cells. Conclusion: In conclusion, these findings suggested that CS upregulation may contribute to the aggressive progression and poor prognosis of PCa patients, which might be partially associated with its influences on the cell lipid metabolism and mitochondrial function.

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“…Tribbles homolog 1 (Trib1), as a member of the mammalian Tribbles homolog pseudokinase family, has been shown to be critical for the differentiation of tissue residence of M2-like macrophages (19). Trib1 induced macrophages to express M2 phenotype markers in prostate cancer (20), whereas Trib1 deficiency attenuated the expression of M2-marker genes upon IL-4 stimulation (21). M2 macrophages exhibited a selective depletion after myocardial infarction in Trib1 −/− mice compared with wild-type (WT) mice (22).…”

Section: Introductionmentioning

confidence: 99%

SHIP-1 Regulates Phagocytosis and M2 Polarization Through the PI3K/Akt–STAT5–Trib1 Circuit in Pseudomonas aeruginosa Infection

Qin

Zhou

et al. 2020

Front. Immunol.

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SHIP-1 is an inositol phosphatase that hydrolyzes phosphatidylinositol 3-kinase (PI3K) products and negatively regulates protein kinase B (Akt) activity, thereby modulating a variety of cellular processes in mammals. However, the role of SHIP-1 in bacterial-induced sepsis is largely unknown. Here, we show that SHIP-1 regulates inflammatory responses during Gram-negative bacterium Pseudomonas aeruginosa infection. We found that infected-SHIP-1 −/− mice exhibited decreased survival rates, increased inflammatory responses, and susceptibility owing to elevated expression of PI3K than wild-type (WT) mice. Inhibiting SHIP-1 via siRNA silencing resulted in lipid raft aggregates, aggravated oxidative damage, and bacterial burden in macrophages after PAO1 infection. Mechanistically, SHIP-1 deficiency augmented phosphorylation of PI3K and nuclear transcription of signal transducer and activator of transcription 5 (STAT5) to induce the expression of Trib1, which is critical for differentiation of M2 but not M1 macrophages. These findings reveal a previously unrecognized role of SHIP-1 in inflammatory responses and macrophage homeostasis during P. aeruginosa infection through a PI3K/Akt-STAT5-Trib1 axis.

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TRIB1 induces macrophages to M2 phenotype by inhibiting IKB-zeta in prostate cancer

Cited by 27 publications

References 38 publications

MiR-98-5p expression inhibits polarization of macrophages to an M2 phenotype by targeting Trib1 in inflammatory bowel disease

MiR-98-5p expression inhibits polarization of macrophages to an M2 phenotype by targeting Trib1 in inflammatory bowel disease

<p>Aberrant Expression of Citrate Synthase is Linked to Disease Progression and Clinical Outcome in Prostate Cancer</p>

SHIP-1 Regulates Phagocytosis and M2 Polarization Through the PI3K/Akt–STAT5–Trib1 Circuit in Pseudomonas aeruginosa Infection

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