PPAR&amp;#947; against Tumors by Different Signaling Pathways

Zhang, Zhi; Xü, Ying; Qi, Xu; Hou, Yongzhong

doi:10.1159/000355328

Cited by 34 publications

(37 citation statements)

References 39 publications

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“…PPARg is a member of the nuclear receptor superfamily of ligand-activated transcription factors (16). It exhibits multiple biologic functions, including direct or indirect inhibition of development of inflammation, involving in the regulatory network of adipogenesis and suppressing tumor progression (10,17). Previous studies have demonstrated that PPARg expression is regulated by various miRNAs.…”

Section: Discussionmentioning

confidence: 99%

rSjP40 protein promotes PPARγ expression in LX‐2 cells through microRNA‐27b

et al. 2018

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miR-27b is reported to participate in the proliferation and differentiation of hepatic stellate cells (HSCs) and to regulate fat metabolism of rat HSCs by targeting retinoid X receptor α. Our previous study also indicated that the recombinant P40 protein from Schistosoma japonicum (rSjP40) inhibited the activation of HSCs. In this study, we observed the expression of miR-27b in rSjP40-treated LX-2 cells and explored its potential mechanisms. Quantitative real-time PCR showed that rSjP40 inhibits the expression of miR-27b in LX-2 cells. Further results obtained by Western blot and dual-luciferase reporter assay confirmed that miR-27b regulates peroxisome proliferator-activated receptor γ (PPARγ) expression in rSjP40-treated LX-2 cells by targeting the 3'-UTR of PPARγ. 5-AZA-2'-deoxycytidine (5-AZA-dC), which inhibits methylation of HSCs, partially reversed rSjP40-induced down-regulation expression of miR-27b in LX-2 cells. 5-AZA-dC also partially reversed rSjP40-induced up-regulation expression of PPARγ in LX-2 cells. The increased expression of PPARγ in rSjP40-treated LX-2 cells may be partially due to miR-27b methylation. Therefore, our study provides further insight into the mechanism by which rSjP40 inhibits HSC activation and provides a basis for future study of the blocking effect of rSjP40 in liver fibrosis.-Zhu, D., Lyu, L., Shen, P., Wang, J., Chen, J., Sun, X., Chen, L., Zhang, L., Zhou, Q., Duan, Y. rSjP40 protein promotes PPARγ expression in LX-2 cells through microRNA-27b.

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Section: Discussionmentioning

confidence: 99%

rSjP40 protein promotes PPARγ expression in LX‐2 cells through microRNA‐27b

et al. 2018

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“…c-fos and c-jun constitute the AP-1 transcription factor, and activate several genes involved in cell growth and division, leading to cell transformation and tumorigenesis [50][51][52][53][54]. c-MYC contributes to the genesis of many human cancers, and there are several reviews on the pathways leading to cancers [55][56][57]. Elevated intracellular Ca 2+ due to a low level cadmium can cause activation of the small guanine nucleotide-binding protein Ras [58], a protein which is related to some human cancers.…”

Section: Ca 2+ Homeostasis Disorder-mediated Cancers Induced By Cadmiummentioning

confidence: 99%

Calcium Homeostasis Disruption - a Bridge Connecting Cadmium-Induced Apoptosis, Autophagy and Tumorigenesis

et al. 2015

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Calcium and cadmium are divalent metals and have similar chemical properties. Both can enter cells through, albeit different, channels, or through protein-dependent permeation. However, cadmium disturbs the calcium homeostasis by inhibiting calcium channels and/or related proteins. Cadmium can also alter membrane phospholipid concentrations, and so induce a calcium homeostasis disorder. The altered calcium homeostasis induced by cadmium results in cell apoptosis, autophagy or tumorigenesis. In this review, calcium homeostasis disruption is summarized as a bridge connecting cadmium-induced apoptosis, autophagy, and tumorigenesis.

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“…Peroxisome proliferator‐activated receptor‐γ (PPARγ) is a critical regulator of inflammation, adipocyte differentiation, glucose homeostasis, and tumorigenesis . PPARγ ligands have entered the clinical arena as therapeutic agents for epithelial and hematopoietic malignancies .…”

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confidence: 99%

Angiotensin II type 1 receptor blocker telmisartan induces apoptosis and autophagy in adult T‐cell leukemia cells

et al. 2016

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Adult T‐cell leukemia/lymphoma ( ATL ), an aggressive T‐cell malignancy that develops after long‐term infection with human T‐cell leukemia virus ( HTLV ‐1), requires new treatments. Drug repositioning, reuse of a drug previously approved for the treatment of another condition to treat ATL , offers the possibility of reduced time and risk. Among clinically available angiotensin II receptor blockers, telmisartan is well known for its unique ability to activate peroxisome proliferator‐activated receptor‐γ, which plays various roles in lipid metabolism, cellular differentiation, and apoptosis. Here, telmisartan reduced cell viability and enhanced apoptotic cells via caspase activation in ex vivo peripheral blood monocytes from asymptomatic HTLV ‐1 carriers ( AC s) or via caspase‐independent cell death in acute‐type ATL , which has a poor prognosis. Telmisartan also induced significant growth inhibition and apoptosis in leukemia cell lines via caspase activation, whereas other angiotensin II receptor blockers did not induce cell death. Interestingly, telmisartan increased the LC 3‐ II ‐enriched protein fraction, indicating autophagosome accumulation and autophagy. Thus, telmisartan simultaneously caused caspase activation and autophagy. A hypertension medication with antiproliferation effects on primary and leukemia cells is intriguing. Patients with an early diagnosis of ATL are generally monitored until the disease progresses; thus, suppression of progression from AC and indolent ATL to acute ATL is important. Our results suggest that telmisartan is highly effective against primary cells and leukemia cell lines in caspase‐dependent and ‐independent manners, and its clinical use may suppress acute transformation and improve prognosis of patients with this mortal disease. This is the first report demonstrating a cell growth‐inhibitory effect of telmisartan in fresh peripheral blood mononuclear cells from leukemia patients.

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PPARγ against Tumors by Different Signaling Pathways

Cited by 34 publications

References 39 publications

rSjP40 protein promotes PPARγ expression in LX‐2 cells through microRNA‐27b

rSjP40 protein promotes PPARγ expression in LX‐2 cells through microRNA‐27b

Calcium Homeostasis Disruption - a Bridge Connecting Cadmium-Induced Apoptosis, Autophagy and Tumorigenesis

Angiotensin II type 1 receptor blocker telmisartan induces apoptosis and autophagy in adult T‐cell leukemia cells

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