Delphinidin suppresses proliferation and migration of human ovarian clear cell carcinoma cells through blocking AKT and ERK1/2 MAPK signaling pathways

Lim, Whasun; Jeong, Wooyoung; Song, Gwonhwa

doi:10.1016/j.mce.2015.12.013

Cited by 45 publications

(36 citation statements)

References 38 publications

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“…It has been reported that anthocyanins from black rice suppressed the non‐Smad MAPK pathway RAS/RAF in the breast cancer cell line MDA‐MB 453 resulting in metastasis inhibition . Also, Dp was able to block the PI3K/AKT and MAPKs signal transduction cascades of human ovarian clear cell carcinoma (ES2) . Our study therefore highlights the inhibitory effects of anthocyanidins in targeting both Smad2 and ERK signaling pathways.…”

Section: Discussionsupporting

confidence: 60%

Anthocyanidins inhibit epithelial–mesenchymal transition through a TGFβ/Smad2 signaling pathway in glioblastoma cells

Ouanouki

Lamy

Annabi

2016

Molecular Carcinogenesis

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Epidemiological studies have convincingly demonstrated that diets rich in fruits and vegetables play an important role in preventing cancer due to their polyphenol content. Among polyphenols, the anthocyanidins are known to possess anti-inflammatory, cardioprotective, anti-angiogenic, and anti-carcinogenic properties. Despite the well-known role of transforming growth factor-β (TGF-β) in high grade gliomas, the impact of anthocyanidins on TGF-β-induced epithelial-mesenchymal transition (EMT), a process that allows benign tumor cells to infiltrate surrounding tissues, remains poorly understood. The objective of this study is to investigate the impact of anthocyanidins such as cyanidin (Cy), delphinidin (Dp), malvidin (Mv), pelargonidin (Pg), and petunidin (Pt) on TGF-β-induced EMT and to determine the mechanism(s) underlying such action. Human U-87 glioblastoma (U-87 MG) cells were treated with anthocyanidins prior to, along with or following the addition of TGF-β. We found that anthocyanidins differently affected TGF-β-induced EMT, depending on the treatment conditions. Dp was the most potent EMT inhibitor through its inhibitory effect on the TGF-β Smad and non-Smad signaling pathways. These effects altered expression of the EMT mesenchymal markers fibronectin and Snail, as well as markedly reducing U-87 MG cell migration. Our study highlights a new action of anthocyanidins against EMT that supports their beneficial health and chemopreventive effects in dietary-based strategies against cancer. © 2016 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 60%

Anthocyanidins inhibit epithelial–mesenchymal transition through a TGFβ/Smad2 signaling pathway in glioblastoma cells

Ouanouki

Lamy

Annabi

2016

Molecular Carcinogenesis

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“…Accumulating evidence has demonstrated that the Akt/mTOR/MAPK pathway plays a pivotal role in multiple cellular processes, such as cell proliferation, apoptosis, and migration (27,28). It has already been mentioned that Akt/mTOR signaling pathway is activated in bladder tumor sample, emphasizing the importance of this pathway in the progression of urothelial carcinoma and making this pathway become a potential target (29).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-27 augments the inhibitory effects of sorafenib on bladder cancer cells

Cao

Yin

et al. 2017

Braz J Med Biol Res

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Both sorafenib and interleukin-27 (IL-27) are antineoplastic drugs. This study aimed to investigate the synergistic effect of these two drugs on bladder cancer cells. HTB-9 and T24 cells were stimulated with IL-27 (50 ng/mL), sorafenib (2 μM) or the synergistic action of these two drugs. The cells without treatment acted as control. Cell proliferation, apoptosis and invasion were measured by bromodeoxyuridine assay, flow cytometry and modified Boyden chamber, respectively. Simultaneously, both modified Boyden chamber and scratch assay were used to assess cell migration. Finally, the phosphorylation levels of key kinases in the Akt/mechanistic target of rapamycin (mTOR)/mitogen-activated protein kinase (MAPK) pathway, and expression levels of matrix metalloproteinase (MMP)-2 and MMP-9 were detected by western blot analysis. Stimulation with IL-27 or sorafenib repressed proliferation, migration and invasion but promoted apoptosis, and the effects were all enhanced by the combination of these two drugs in HTB-9 cells. The effect of the combined treatment on bladder cancer cells was verified in T24 cells. Additionally, the phosphorylation levels of AKT, mTOR and MAPK as well as the expression levels of MMP-2 and MMP-9 were all decreased by a single treatment of IL-27 or sorafenib, and further decreased by the combined treatment of these two drugs. The combination of IL-27 and sorafenib inhibited proliferation, migration and invasion and promoted apoptosis of bladder cancer cells compared with mono-drug treatment. Additionally, the AKT/mTOR/MAPK pathway might be implicated in the functional effects by down-regulations of MMP-2 and MMP-9.

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“…Extensive studies have shown that the consumption of dietary flavonoids affords significant anti-tumor effects [7-10]. Moreover, there have been multiple studies performed at the cellular level to investigate the effects of flavonoids on tumor proliferation, migration, and invasion [11-13]. This study focused on cyanidin, which belongs to a branch of the flavone compounds.…”

Section: Introductionmentioning

confidence: 99%

Cyanidin Curtails Renal Cell Carcinoma Tumorigenesis

Liu

Zhang

Hao

et al. 2018

Cell Physiol Biochem

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Background/Aims: Cyanidin is an anthocyanin found in many foods. Although its variable antioxidant levels are well-documented, little is known about its effects on renal cell carcinoma (RCC) tumorigenesis. This study, therefore, investigated the effects of cyanidin on the proliferation, migration, and invasion of renal cell carcinoma lines and demonstrated, for the first time, significant inhibitory effects of cyanidin on RCC tumorigenesis. Methods: RCC cells were treated with different doses of cyanidin and the effects were tested by Cell Counting Kit-8 reagent, clone formation assay, transwell assay, and flow cytometry. Moreover, the cyanidin-mediated mechanism that curtailed tumorigenesis was analyzed by RNA sequencing (RNA-seq). Sequencing data from The Cancer Genome Atlas (TCGA) were used to compare the expression of both early growth response protein 1 (EGR1) and selenoprotein W (SEPW1) in RCC and tumor-free adjacent normal tissue samples. Real-time PCR (RT-PCR) and/or western blot were used to assess the expression of E-cadherin, cleaved-caspase3, Bcl2, p62, and ATG4. Results: We found significantly greater induction of cell-cycle arrest, apoptosis, and suppression of RCC cell invasion and migration at concentrations of 25 µM and 100 µM than at a concentration of 50 µM. It was also discovered, first through RNA-seq then confirmed by RT-PCR, that cyanidin (100 µM) inhibited RCC carcinogenesis through EGR1 and SEPW1. TCGA data indicated that the expression level of EGR1 was lower and that of SEPW1 was higher in RCC tumor tissue than in normal tissues. Moreover, western blot and/or RT-PCR indicated that cleaved-caspase3 was enhanced and E-cadherin was inhibited by cyanidin treatment. Furthermore, western blot and RT-PCR also showed regulation of p62 and ATG4, which are associated with autophagy. Cyanidin in vivo significantly inhibited the growth of xenografts in nude mice. Conclusions: The results of this study showed the therapeutic potential of cyanidin for the treatment of RCC and the prevention of recurrence and metastasis.

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Delphinidin suppresses proliferation and migration of human ovarian clear cell carcinoma cells through blocking AKT and ERK1/2 MAPK signaling pathways

Cited by 45 publications

References 38 publications

Anthocyanidins inhibit epithelial–mesenchymal transition through a TGFβ/Smad2 signaling pathway in glioblastoma cells

Anthocyanidins inhibit epithelial–mesenchymal transition through a TGFβ/Smad2 signaling pathway in glioblastoma cells

Interleukin-27 augments the inhibitory effects of sorafenib on bladder cancer cells

Cyanidin Curtails Renal Cell Carcinoma Tumorigenesis

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