Peroxisome Proliferator-activated Receptor γ Agonists Induce Cell Cycle Arrest through Transcriptional Regulation of Krüppel-like Factor 4 (KLF4)

Li, Sheng; Zhou, Qibing; He, Huan; Zhao, Yahui; Liu, Zhihua

doi:10.1074/jbc.m111.317487

Cited by 37 publications

(41 citation statements)

References 30 publications

(31 reference statements)

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“…MTS Cell Proliferation Assay-MTS cell proliferation assay was performed as described previously (25). Briefly, cells were seeded in 96-well plates at a density of 1 ϫ 10 3 cells/well and then incubated in the absence or presence of 4 mM SB at 48 h intervals.…”

Section: Methodsmentioning

confidence: 99%

“…Cells were cultured in RPMI 1640 medium with 10% fetal bovine serum and antibiotics. Transfections were performed as described previously (25). Cells were transfected with siRNAs (25 nM) by HiPerFect (Qiagen) following the manufacturers' protocol.…”

Section: Methodsmentioning

confidence: 99%

“…RNA Isolation and PCR Analysis-RNA purification and RT-PCR were performed as described previously (25). The primers used are listed in Table 2.…”

Section: Methodsmentioning

confidence: 99%

“…Electrophoretic Mobility Shift Assays (EMSA)-EMSA was performed as described previously (25). Biotin-labeled and unlabeled wild-type oligonucleotide probes contained the binding motif of KLF4 (5Ј-ATAGAAAAAAGGAAGGTCGA-GGGCTAC-3Ј) and unlabeled mutant probes contained a substitution of 2 bp (underlined, 5Ј-ATAGAAAAAAGGAAT-TTCGAGGGCTAC-3Ј (designated mutant 1), 5Ј-ATAGAAA-AAAGGCCGGTCGAGGGCTAC-3Ј (designated mutant 2), and 5Ј-ATAGAAAAAAGGAAGGTTTAGGGCTAC-3Ј (designated mutant 3)).…”

Section: Methodsmentioning

confidence: 99%

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Krüppel-like Factor 4 Promotes Esophageal Squamous Cell Carcinoma Differentiation by Up-regulating Keratin 13 Expression

Yuan

et al. 2015

Journal of Biological Chemistry

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Background:The transcriptional regulation of keratin (KRT) 13 and its underlying mechanism has not been fully elucidated. Results: Up-regulation of KRT13 by Krüppel-like factor 4 (KLF4) is mediated through GKRE in the KRT13 promoter. Conclusion: KLF4 induces differentiation of ESCC by promoting KRT13 transcription. Significance: KLF4 plays a significant and previously unrecognized role in regulation of KRT13 and cell differentiation.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…RNA Isolation and PCR Analysis-RNA purification and RT-PCR were performed as described previously (25). The primers used are listed in Table 2.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Krüppel-like Factor 4 Promotes Esophageal Squamous Cell Carcinoma Differentiation by Up-regulating Keratin 13 Expression

Yuan

et al. 2015

Journal of Biological Chemistry

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“…ID1 siRNA (GS3397; Qiagen), c-Jun siRNA (GS3725; Qiagen), c-Fos siRNA (GS8061; Qiagen), and negative control siRNA (1027310; Qiagen) were purchased from Qiagen. RNA purification and qRT-PCR were performed as described previously (31). The primers used are listed in Table 1.…”

Section: Methodsmentioning

confidence: 99%

Inhibitor of Differentiation/DNA Binding 1 (ID1) Inhibits Etoposide-induced Apoptosis in a c-Jun/c-Fos-dependent Manner

Zhao

Luo

et al. 2016

Journal of Biological Chemistry

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Esophageal cancer remains one of the most virulent malignancies with ranking eighth in incidence and sixth in cancerrelated mortality worldwide (1). These malignancies are particularly prevalent in China and other countries in Asia, where esophageal squamous cell carcinoma (ESCC) 3 is most common (1). A 5-year overall survival rate has not been improved evidently despite the progressed surgical techniques and incorporation of new therapeutic approaches in the past decades (2).

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Low‐dose decitabine promotes M2 macrophage polarization in patients with primary immune thrombocytopenia via enhancing KLF4 binding to PPARγ promoter

Shao,

Xu,

et al. 2023

Clinical & Translational Med

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Background The first‐line therapy is effective for the treatment of primary immune thrombocytopenia (ITP); however, maintaining the long‐term responses remains challenging. Low‐dose decitabine (DAC) has been adopted to treat refractory ITP, while its role in macrophage polarization has not been fully understood. We aimed to investigate the mechanistic role of DAC in M2 macrophage polarization and evaluated its therapeutic effect in ITP. Methods The M2 monocytes were identified by flow cytometry from peripheral blood mononuclear cells in healthy controls (HCs) and ITP patients. The expression of PPARγ, Arg‐1, DNMT3b and NLRP3, together with IL‐10 plasma levels was measured to examine its function. Bisulfite‐sequencing PCR was used to evaluate the methylation status of PPARγ promoter, and the binding affinity of KLF4 was measured by Cut&Tag. A sh‐PPARγ THP‐1 cell line was created to verify if low‐dose DAC‐modulated M2 macrophage polarization was PPARγ‐dependent. The passive ITP models were used to investigate the therapeutic effects of low‐dose DAC and its role in modulating polarization and immunomodulatory function of macrophages. NLRP3 inflammasome and reactive oxygen species were also tested to understand the downstream of PPARγ. Results The M2 monocytes with impaired immunoregulation were observed in ITP. After high‐dose dexamethasone (HD‐DXM) treatment, M2 monocytes increased significantly with the elevated expression of PPARγ, Arg‐1 and IL‐10 in CR patients. Low‐dose DAC promoted M2 macrophage polarization in a PPARγ‐dependent way via demethylating the promoter of PPARγ, especially the KLF4 binding sites. Low‐dose DAC alleviated ITP mice by restoring the M1/M2 balance and fine‐tuning immunomodulatory function of macrophages. The downstream of the PPARγ modulation of M2 macrophage polarization might physiologically antagonize NLRP3 inflammasome. Conclusions Low‐dose DAC promoted M2 macrophage polarization due to the demethylation within the promoter of PPARγ, thus enhanced the KLF4 binding affinity in ITP.

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Peroxisome Proliferator-activated Receptor γ Agonists Induce Cell Cycle Arrest through Transcriptional Regulation of Krüppel-like Factor 4 (KLF4)

Cited by 37 publications

References 30 publications

Krüppel-like Factor 4 Promotes Esophageal Squamous Cell Carcinoma Differentiation by Up-regulating Keratin 13 Expression

Krüppel-like Factor 4 Promotes Esophageal Squamous Cell Carcinoma Differentiation by Up-regulating Keratin 13 Expression

Inhibitor of Differentiation/DNA Binding 1 (ID1) Inhibits Etoposide-induced Apoptosis in a c-Jun/c-Fos-dependent Manner

Low‐dose decitabine promotes M2 macrophage polarization in patients with primary immune thrombocytopenia via enhancing KLF4 binding to PPARγ promoter

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