Foxp3 is a key downstream regulator of p53-mediated cellular senescence

Kim, Je; Js, Shin; Jh, Moon; Hong, Seung‐Mo; Dj, Jung; Kim, Jae‐Hun; Iy, Hwang; Shin, Young-jeon; Ey, Gong; Dh, Lee; Sm, Kim; Ey, Lee; Ys, Kim; D, Kim; D, Hur; Tw, Kim; Kim, K-P.; Dh, Jin; Lee, Won Jae

doi:10.1038/onc.2016.193

Cited by 22 publications

(15 citation statements)

References 35 publications

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“…However, it has been reported to be expressed in other types of cells such as B cells and cancer cells, and the function is still controversial . Previous studies have reported that FOXP3 is a downstream target gene of TP53, and TP53 can upregulate the expression level of FOXP3 . Our data indicated that the proliferating marker genes PCNA and Ki67 (Figure C,D) as well as TP53 and LC3B was upregulated after knockdown of FOXP3 (Figure C‐E).…”

Section: Discussionmentioning

confidence: 54%

miR‐133a‐3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

Zhang

Liu

et al. 2020

J of Cellular Biochemistry

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Although many methods and new therapeutic drugs have been developed, the overall survival rate and long-term survival rate of patients with gastric cancer (GC) are still not satisfactory. In this study, we investigated the effects of microRNA miR-133a-3p and transcription factor FOXP3 on proliferation and autophagy of GC cells and their interactions. Our results showed that knockdown of FOXP3 increased the proliferation and autophagy of GC cells.The relationship between FOXP3 and autophagy has not been reported previously. In addition, FOXP3 could directly bind the promoter region of TP53 and inhibit its expression. miR-133a-3p increased the proliferation and autophagy via decreasing the protein level of FOXP3 by targeting its 3′-UTR. Our research provides new insights into the development of GC and provides new ideas and theoretical basis for the clinical treatment of GC and the development of new drug targets. K E Y W O R D S autophagy, FOXP3, gastric cancer, miR-133a-3p, proliferation

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Section: Discussionmentioning

confidence: 54%

miR‐133a‐3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

Zhang

Liu

et al. 2020

J of Cellular Biochemistry

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“…Our functional study results showed that the ectopic expression of FOXP3 inhibited proliferation, migration and invasion of HCC cells (Hep3B and PLC/PRF/5), but increased the apoptotic population. It has been reported that FOXP3 is a key downstream regulator of p53-mediaetd cellular senescence in breast cancer cells 26 . Our data suggested that p53 may involve in the FOXP3-induced apoptosis in PLC/PRF/5 cells.…”

Section: Discussionmentioning

confidence: 99%

Nuclear FOXP3 inhibits tumor growth and induced apoptosis in hepatocellular carcinoma by targeting c-Myc

Gong

Hao

et al. 2020

Oncogenesis

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The status of FOXP3 and its isoforms in hepatocellular carcinoma (HCC) is unclear. We aimed to investigate the expression and function of FOXP3 and its isoforms in HCC. The study was performed on 84 HCC patients, HCC cell lines and a mouse tumor model. The levels of FOXP3 and its isoforms were determined by nested PCR, quantitative real-time PCR and immunohistochemistry (IHC) staining. The correlation between their levels and clinicopathologic characteristics was analyzed. The full length of FOXP3 (FOXP3) and exon 3-deleted FOXP3 (FOXP3Δ3) were found to be the major isoforms in HCC. The levels of FOXP3Δ3 mRNA and protein in HCC tumor samples were not significantly different from their adjacent normal tissues. The high expression of FOXP3 protein in HCC patients showed a good overall survival. The overexpression of FOXP3 significantly reduced tumor cell proliferation, migration and invasion. The immunofluorescence result indicated that FOXP3 needed to be translocated into the nucleus to exert its inhibitory function. The luciferase assay demonstrated that FOXP3 could be synergistic with Smad2/3/4 to inhibit the oncogene c-Myc. The co-immunoprecipitation results further revealed that FOXP3 could interact with Smad2/3/4. The chromatin immunoprecipitation (ChIP) assay showed that both FOXP3 and Smad2/3/4 bound the promoter of the c-Myc to inhibit it. The in vivo mouse tumor model study confirmed the inhibitory effect of FOXP3. Collectively, the expression of tumor FOXP3 can inhibit the growth of HCC via suppressing c-Myc directly or indirectly via interacting with Smad2/3/4. Therefore, FOXP3 is a tumor suppressor in HCC.

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“…FOXP3 protein is a number of forkhead/winged helix families and has been recovered to function as suppresser of many cancers . Mir‐198 is a 22 bases RNA which regulates many proteins expression by interfering their translation .…”

Section: Discussionmentioning

confidence: 99%

FOXP3 inhibits MYC expression via regulating miR‐198 and influences cell viability, proliferation and cell apoptosis in HepG2

et al. 2018

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ObjectiveOur study aimed to explore the effects of FOXP3 expression on liver neoplasms cells and to further investigate the relationship between FOXP3 and proto‐oncogene MYC.Methods QRT‐PCR was used for assessment of FOXP3 expression in liver neoplasms tissues and para‐carcinoma tissues. The effects of FOXP3 on cell viability were determined by CCK8 assay, clone formation experiment, and flow cytometry. For miRNA selection, chips were used to figure out the differentially expressed miRNAs in FOXP3‐overexpressing HepG2 cells. The result was followed by bioinformatics prediction to screen the possible MYC‐targeted miRNAs, and it was examined by dual luciferase assay and ChIP assay. The expression levels of MYC protein and apoptosis‐associated proteins (bcl2 and bax) were measured by Western blot assay.ResultsIt showed an under‐regulated expression of FOXP3 in liver neoplasm tissues from qRT‐PCR results. Overexpression of FOXP3 contributed to cell apoptosis as well as suppressed tumor cells’ proliferation. MiR‐198 was detected to be highly expressed in FOXP3‐overexpressing HepG2 cells. FOXP3 regulated the transcription level of miR‐198 by binding to its promoter sequence and overexpressed miR‐198 could suppress tumor cells’ proliferation and promote cell apoptosis. There existed targeted relationship between miR‐198 and MYC gene. MiR‐198 inhibited cancer by suppressing the expression of MYC in liver neoplasm.Conclusion FOXP3 up‐regulated miR‐198 expression by binding to its promoter sequence specifically, while miR‐198 inhibited proto‐oncogene MYC via targeted relationship. High level of miR‐198 contributed to the apoptosis of tumor cells and suppressed cell viability meanwhile.

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Foxp3 is a key downstream regulator of p53-mediated cellular senescence

Cited by 22 publications

References 35 publications

miR‐133a‐3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

miR‐133a‐3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

Nuclear FOXP3 inhibits tumor growth and induced apoptosis in hepatocellular carcinoma by targeting c-Myc

FOXP3 inhibits MYC expression via regulating miR‐198 and influences cell viability, proliferation and cell apoptosis in HepG2

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