Anticancer activity of calyx of Diospyros kaki Thunb. through downregulation of cyclin D1 via inducing proteasomal degradation and transcriptional inhibition in human colorectal cancer cells

Park, Su Bin; Park, Gwang Hun; Song, Hun Min; Son, Ho-Jun; Um, Yurry; Jeong, Jin Boo

doi:10.1186/s12906-017-1954-2

Cited by 27 publications

(16 citation statements)

References 43 publications

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“…EEDK has previously been reported to inhibit Wnt/β-catenin signaling activity. Moreover, EEDK inhibition has been shown to downregulate cyclin D1 mRNA expression 19 . However, the mechanism underlying the downregulation of Wnt/β-catenin signaling by EEDK is not fully understood.…”

Section: Resultsmentioning

confidence: 99%

Anti-cancer potential of persimmon (Diospyros kaki) leaves via the PDGFR-Rac-JNK pathway

Kim

Suh

Jang

et al. 2020

Sci Rep

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Persimmon leaves are known to have some beneficial effects, including ROS elimination, lipid circulation, and neuronal protection. However, their anti-cancer properties and the underlying mechanisms remain unclear. Herein, we show that treatment with the ethanol extract of persimmon, Diospyros kaki, leaves (EEDK) induces cancer cell death and inhibits cell proliferation. Using fluorescence resonance energy transfer (FRET) technology with genetically-encoded biosensors, we first found that EEDK stimulates a PDGFR-Rac signaling cascade in live cells. Moreover, we found that downstream of the PDGFR-Rac pathway, JNKs are activated by EEDK. In contrast, JNK-downstream inhibitors, such as CoCl2, T-5224, and pepstatin A, attenuated EEDK-induced cell death. Thus, we illustrate that the PDGFR-Rac-JNK signaling axis is triggered by EEDK, leading to cancer cell death, suggesting the extract of persimmon leaves may be a promising anti-cancer agent.

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Section: Resultsmentioning

confidence: 99%

Anti-cancer potential of persimmon (Diospyros kaki) leaves via the PDGFR-Rac-JNK pathway

Kim

Suh

Jang

et al. 2020

Sci Rep

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“…Furthermore, the CCND1 gene is a proto-oncogene, which is upregulated through gene enhancement or translocation in various tumor cells. 72–74 Interestingly, cyclin D1 and Ki-67 activation were previously demonstrated to be regulated via NF-κB in cancer cells and their metastatic counterparts. 75–77 Moreover, we found that HCT116 cells express MMP-9 and CXCR4 and TNF-β induced the expression of these proteins, which is consistent with previous studies.…”

Section: Discussionmentioning

confidence: 99%

Evidence that TNF-β induces proliferation in colorectal cancer cells and resveratrol can down-modulate it

Buhrmann

Yazdi

Popper

et al. 2019

Exp Biol Med (Maywood)

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Although much is understood about the proinflammatory cytokine TNF-α, very limited data are available about TNF-β (lymphotoxin). Whether TNF-β can induce the proliferation of tumor cells, how TNF-β-induced proliferation of tumor cells is affected by natural products such as resveratrol and the role of NF-κB in this process, is not understood. In the present study, we used clonogenic and cytotoxic methods to show the effect of TNF-β on cell proliferation. We also examined the impact of resveratrol on TNF-β-promoted proliferation and on NF-κB activation in HCT116 colorectal cancer (CRC). Our findings showed that TNF-β induced the proliferation and invasion in CRC cells and this was comparable with that of TNF-α. TNF-β-stimulated proliferation of CRC cells was blocked via anti-TNF-β-receptor. We found that resveratrol reversed the TNF-β-induced proliferation and invasion of CRC cells, and this correlated with the suppression of TNF-β-stimulated NF-κB signaling. Like resveratrol, IκB-kinase (IKK) inhibitor (BMS-345541), also reversed TNF-β-stimulated proliferation, NF-κB activation and these were mediated through inhibition of IκB-kinase, phosphorylation of IκBα, suppression of phosphorylation, and nuclear translocation of the p65 subunit of NF-κB. Furthermore, resveratrol similar to BMS-345541 suppressed TNF-β-promoted NF-κB-mediated gene biomarkers linked with proliferation, apoptosis, and invasion. Overall, our findings indicate for the first time that TNF-β/TNF-β-receptor signaling is involved in proliferation of CRC cells in parallel to TNF-α, and that resveratrol down-modulates TNF-β/TNF-β-receptor-mediated inflammatory response, at least in part through down modulating NF-κB activation, thereby regulating tumor cell growth. Impact statement The mechanism by which natural products such as resveratrol suppresses TNF-β-promoted tumor cell proliferation, invasion, and colony formation is unknown. In this study, we explored for the first time the effect of resveratrol on the proinflammatory cytokine TNF-β-, compared to TNF-α-stimulated proliferative and pro-inflammatory signaling in HCT116 cells. Our findings suggest that expression of TNF-β and TNF-β-receptor, like TNF-α, can lead to activation of inflammatory transcription factor (NF-κB) and NF-κB-regulated gene biomarkers, which are involved in the promotion of cancer proliferation, invasion, metastasis, and cell survival of tumor. Resveratrol can block TNF-β/TNF-β-receptor-induced activation of NF-κB, NF-κB-modulated gene products, and inhibition of caspase-3 cleavage. These results highlight the therapeutic effect of resveratrol-mediated anti-tumor activity by multitargeting cellular signaling pathways.

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“…it has been reported that mir-365 inhibited cell cycle progression and promoted apoptosis of colon cancer cells by targeting cyclin d1 and Bcl-2 (29). diospyros kaki Thunb (persimmon) may downregulate cyclin d1 as one of the potential anticancer targets via inducing proteasomal degradation and transcriptional inhibition in human colorectal cancer cells (30). a study reported that mir-519d reduces the 5-fluorouracil resistance in colorectal cancer cells by downregulating the expression of ccnd1 (31).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Guo

Xue

2020

Mol Med Report

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Microrna (mir)-628-5p serves as an antitumor gene in a variety of cancers; however, the role of mir-628-5p in colorectal cancer remains largely unclear. The purpose of this study was to investigate the role and mechanism of mir-628-5p in colorectal cancer. reverse transcription-quantitative Pcr (RT-qPCR), colony formation assays and flow cytometric analysis were used to determine the expression levels of mir-628-5p in colorectal cancer tissues and cell lines, and the proliferative ability of colorectal cancer cells. TargetScan version 7.2 and dual-luciferase reporter assay were performed to predict and confirm mir-628-5p target genes. The expression levels of cyclin d1 (ccnd1) and related genes were determined using rT-qPcr or/and western blotting analysis. mir-628-5p mimics and ccnd1 plasmids were used to overexpress mir-628-5p and ccnd1; it was demonstrated that the expression levels of miR-628-5p were significantly downregulated in colorectal cancer tissues and cell lines. mir-628-5p mimic-transfected cells inhibited the proliferation and induced apoptosis of HT-29 cells. ccnd1, a downstream effector of mir-628-5p, promoted the proliferation and suppressed apoptosis of HT-29 cells, and the effects were reversed by mir-628-5p mimics. in conclusion, the present study suggested that colorectal cancer progression may be regulated through the mir-628-5p/ccnd1 axis, and mir-628-5p could be used as a potential diagnostic and prognostic biomarker for colorectal cancer.

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Anticancer activity of calyx of Diospyros kaki Thunb. through downregulation of cyclin D1 via inducing proteasomal degradation and transcriptional inhibition in human colorectal cancer cells

Cited by 27 publications

References 43 publications

Anti-cancer potential of persimmon (Diospyros kaki) leaves via the PDGFR-Rac-JNK pathway

Anti-cancer potential of persimmon (Diospyros kaki) leaves via the PDGFR-Rac-JNK pathway

Evidence that TNF-β induces proliferation in colorectal cancer cells and resveratrol can down-modulate it

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

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