Resveratrol inhibits proliferation in human colorectal carcinoma cells by inducing G1/S-phase cell cycle arrest and apoptosis through caspase/cyclin-CDK pathways

Liu, Bin; Zhou, Ziyu; Liu, Jie; Xia, Juan; Liu, Juntao; Chen, Nianping; Li, Mingyi; Zhu, Runzhi

doi:10.3892/mmr.2014.2406

Cited by 77 publications

(41 citation statements)

References 27 publications

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“…Furthermore, the data presented herein suggest, in contrast to a study by Mahyar-Roemer et al [48], that resveratrol-induced apoptosis is dependent on p53, since a statistically significant amount of cells in the sub G 1 phase was only observed in the p53-knockout HCT-116 cells after treatment with 40 or 80 μM resveratrol. On the other hand though, results obtained by others in HCT-116 wt and Caco-2 cells [46, 49, 50] are broadly in line with the present findings.…”

Section: Discussionsupporting

confidence: 93%

Growth-Inhibiting Activity of Resveratrol Imine Analogs on Tumor Cells In Vitro

Wang¹,

Willenberg²,

Krohn

et al. 2017

PLoS ONE

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Although resveratrol exerts manifold antitumorigenic effects in vitro, its efficacy against malignancies in vivo seems limited. This has been increasingly recognized in recent years and has prompted scientists to search for structurally related compounds with more promising anticarcinogenic and/or pharmacokinetic properties. A class of structurally modified resveratrol derivatives, so-called resveratrol imine analogs (IRA’s), might meet these requirements. Therefore, the biological activity of five of these compounds was examined and compared to that of resveratrol. Firstly, the antiproliferative potency of all five IRA’s was investigated using the p53 wildtype-carrying colorectal carcinoma cell line HCT-116wt. Then, using the former and a panel of various other tumor cell lines (including the p53 knockout variant HCT-116p53-/-), the growth-inhibiting and cell cycle-disturbing effects of the most potent IRA (IRA 5, 2-[[(2-hydroxyphenyl)methylene]amino]-phenol) were studied as was its influence on cyclooxygenase-2 expression and activity. Finally, rat liver microsomes were used to determine the metabolic stability of that compound. IRA 5 was clearly the most potent compound in HCT-116wt cells, with an unusually high IC50-value of 0.6 μM. However, in the other five cell lines used, the antiproliferative activity was mostly similar to resveratrol and the effects on the cell cycle were heterogeneous. Although all cell lines were affected by treatment with IRA 5, cells expressing functional p53 seemed to react more sensitively, suggesting that this protein plays a modulating role in the induction of IRA 5-mediated biological effects. Lastly, IRA 5 led to contradictory effects on cyclooxygenase-2 expression and activity and was less glucuronidated than resveratrol. As IRA 5 is approximately 50 times more toxic towards HCT-116wt cells, exerts different effects on the cyclooxygenase-2 and is metabolized to a lesser extent, it shows certain advantages over resveratrol and could therefore serve as basis for additional chemical modifications, potentially yielding compounds with more favorable biological and pharmacokinetic features.

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Section: Discussionsupporting

confidence: 93%

Growth-Inhibiting Activity of Resveratrol Imine Analogs on Tumor Cells In Vitro

Wang¹,

Willenberg²,

Krohn

et al. 2017

PLoS ONE

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show abstract

“…The antiproliferative activity of resveratrol was related to the cell arrest at G0‐G1, S, or G2‐M phases, depending on the specific cell type used (Ahmad et al, ; Kuo et al, ; Larrosa et al, ; Lee et al, ). In the present study, 20 and 50 μM resveratrol induced an accumulation of HPA‐v cells in the S phase, which was consistent with results from SK‐Mel‐28 melanoma and HCT116 cells (Lee et al, ; Liu et al, ).…”

Section: Discussionsupporting

confidence: 92%

Resveratrol Inhibits Human Visceral Preadipocyte Proliferation and Differentiation in vitro

Sun

Han

et al. 2019

Lipids

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Visceral obesity is a high‐risk factor for diabetes and metabolic syndrome. Resveratrol, a natural polyphenolic compound, has been reported to inhibit preadipocyte differentiation. However, the effect of resveratrol on human visceral preadipocyte (HPA‐v) differentiation remains largely unknown. LIM domain only 3 (LMO3) promotes human preadipocyte differentiation by enhancing peroxisome proliferator‐activated receptor γ (PPARγ) transcriptional activity, which is the master regulator of adipogenesis. The purpose of our study was to determine the effect of resveratrol (0–50 μM) on HPA‐v proliferation and differentiation, and the role of LMO3 in resveratrol‐mediated regulation of HPA‐v differentiation. Resveratrol inhibited HPA‐v proliferation and differentiation in a dose‐dependent manner, and significantly decreased the mRNA expression levels of PPARG, CCAAT/enhancer‐binding protein α (CEBPA), fatty acid‐binding protein 4 (FABP4), acetyl‐CoA carboxylase (ACC), and fatty acid synthase (FAS) (p < 0.05) at 10, 20, and 50 μM. The mRNA and protein levels of LMO3 were significantly reduced by ≥20 μM resveratrol (p < 0.05), and overexpression of LMO3 partially attenuated resveratrol‐induced reduction of HPA‐v differentiation by enhancing the PPARG transcriptional activity. Together, our study suggested that resveratrol reduced HPA‐v proliferation and differentiation, as well as LMO3, which was partially responsible for the reduction of resveratrol‐mediated adipocyte differentiation.

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“…K562 cells were treated with various concentrations (0, 10, 20, 30, and 40 µg/ml) of Jellyfish-HE for 24 h and cell extracts were subjected to immunoblotting and densitometry analysis. Cyclin D1 and CDK4 are known to be expressed in the initial stages of the G1 and S1 phase transitions (Liu et al, 2014). Therefore, downregulation of Cyclin D1 and CDK4 is regarded as an indicator of G0/G1 cell cycle arrest.…”

Section: Resultsmentioning

confidence: 99%

Jellyfish extract induces apoptotic cell death through the p38 pathway and cell cycle arrest in chronic myelogenous leukemia K562 cells

Jin

Kwak

et al. 2017

PeerJ

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Jellyfish species are widely distributed in the world’s oceans, and their population is rapidly increasing. Jellyfish extracts have several biological functions, such as cytotoxic, anti-microbial, and antioxidant activities in cells and organisms. However, the anti-cancer effect of Jellyfish extract has not yet been examined. We used chronic myelogenous leukemia K562 cells to evaluate the mechanisms of anti-cancer activity of hexane extracts from Nomura’s jellyfish in vitro. In this study, jellyfish are subjected to hexane extraction, and the extract is shown to have an anticancer effect on chronic myelogenous leukemia K562 cells. Interestingly, the present results show that jellyfish hexane extract (Jellyfish-HE) induces apoptosis in a dose- and time-dependent manner. To identify the mechanism(s) underlying Jellyfish-HE-induced apoptosis in K562 cells, we examined the effects of Jellyfish-HE on activation of caspase and mitogen-activated protein kinases (MAPKs), which are responsible for cell cycle progression. Induction of apoptosis by Jellyfish-HE occurred through the activation of caspases-3,-8 and -9 and phosphorylation of p38. Jellyfish-HE-induced apoptosis was blocked by a caspase inhibitor, Z-VAD. Moreover, during apoptosis in K562 cells, p38 MAPK was inhibited by pretreatment with SB203580, an inhibitor of p38. SB203580 blocked jellyfish-HE-induced apoptosis. Additionally, Jellyfish-HE markedly arrests the cell cycle in the G0/G1 phase. Therefore, taken together, the results imply that the anti-cancer activity of Jellyfish-HE may be mediated apoptosis by induction of caspases and activation of MAPK, especially phosphorylation of p38, and cell cycle arrest at the Go/G1 phase in K562 cells.

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Resveratrol inhibits proliferation in human colorectal carcinoma cells by inducing G1/S-phase cell cycle arrest and apoptosis through caspase/cyclin-CDK pathways

Cited by 77 publications

References 27 publications

Growth-Inhibiting Activity of Resveratrol Imine Analogs on Tumor Cells In Vitro

Growth-Inhibiting Activity of Resveratrol Imine Analogs on Tumor Cells In Vitro

Resveratrol Inhibits Human Visceral Preadipocyte Proliferation and Differentiation in vitro

Jellyfish extract induces apoptotic cell death through the p38 pathway and cell cycle arrest in chronic myelogenous leukemia K562 cells

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