R-Phycoerythrin Induces SGC-7901 Apoptosis by Arresting Cell Cycle at S Phase

Tan, Huixin; Gao, Shuangquan; Zhuang, Yan; Dong, Yanhong; Guan, Weijun; Zhang, Kun; Xu, Jun; Cui, Jingru

doi:10.3390/md14090166

Cited by 28 publications

(22 citation statements)

References 38 publications

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“…When the cells begin to synthesize DNA during G1–S conversion, CDK2 will combine with its regulatory subunit cyclin E to form a Cdk2/Cyclin E complex, leading to Rb phosphorylation, and then E2F factor is released and cells are accelerated into the S phase [42]. During G0–G1 cycle arrest, the content of the CDK2/cyclin E complex decreases accordingly [43]. Our data showed that the protein expression levels of CDK2 and cyclin E in the SGC-7901 cells decreased after CBD treatment, which in turn reduced the formation of CDK2/cyclin E complexes, ultimately arresting SGC-7901 cells at the G0–G1 phase.…”

Section: Discussionmentioning

confidence: 99%

Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells

et al. 2019

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The main chemical component of cannabis, cannabidiol (CBD), has been shown to have antitumor properties. The present study examined the in vitro effects of CBD on human gastric cancer SGC-7901 cells. We found that CBD significantly inhibited the proliferation and colony formation of SGC-7901 cells. Further investigation showed that CBD significantly upregulated ataxia telangiectasia-mutated gene (ATM) and p53 protein expression and downregulated p21 protein expression in SGC-7901 cells, which subsequently inhibited the levels of CDK2 and cyclin E, thereby resulting in cell cycle arrest at the G0–G1 phase. In addition, CBD significantly increased Bax expression levels, decreased Bcl-2 expression levels and mitochondrial membrane potential, and then upregulated the levels of cleaved caspase-3 and cleaved caspase-9, thereby inducing apoptosis in SGC-7901 cells. Finally, we found that intracellular reactive oxygen species (ROS) increased after CBD treatment. These results indicated that CBD could induce G0–G1 phase cell cycle arrest and apoptosis by increasing ROS production, leading to the inhibition of SGC-7901 cell proliferation, thereby suggesting that CBD may have therapeutic effects on gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells

et al. 2019

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“…The influence of monitoring on cell cycle change is important for the development of drug delivery vectors, [37][38][39] and a few studies have reported that cell cycle arrest may lead to the induction of apoptosis. 40 Therefore, we investigated the effects of the cationic lipids on the cell cycle of NCI-H460 cells using flow cytometry after treatment with CDA14 and CDO14 for 24 h. At 15 μg mL −1 the two liposomes did not have any effects on the cell cycle phase.…”

Section: Effects On the Cell Cyclementioning

confidence: 99%

Correlation of the cytotoxic effects of cationic lipids with their headgroups

et al. 2018

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As effective non-viral vectors of gene therapy, cationic lipids still have the problem of toxicity, which has become one of the main bottlenecks for their applications. The toxicity of cationic lipids is strongly connected to the headgroup structures. In this article, we studied the cytotoxicity of two cationic lipids with a quaternary ammonium headgroup (CDA14) and a tri-peptide headgroup (CDO14), respectively, and with the same linker bond and hydrophobic domain. The IC values of CDA14 and CDO14 against NCI-H460 cells were 109.4 μg mL and 340.5 μg mL, respectively. To determine the effects of headgroup structures of cationic lipids on cytotoxicity, apoptosis related pathways were investigated. As the lipids with a quaternary ammonium headgroup could induce more apoptotic cells than the ones with a peptide headgroup, the enzymatic activity of caspase-9 and caspase-3 increased obviously, whereas the mitochondrial membrane potential (MMP) decreased. At the same time, the reactive oxygen species (ROS) levels also increased and the cell cycle was arrested at the S phase. The results showed that the toxicity of the cationic lipid had a close relationship with its headgroup structures, and the cytotoxic mechanism was mainly the caspase activation dependent signaling pathway and mitochondrial dysfunction. Through this study, we hope to provide the scientific basis for exploiting safer and more efficient cationic lipids for gene delivery.

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“…In the present study, CQ treatment induced a significant increase in the number of cells in the S phase and a decrease in the number of cells in the G 0 /G 1 phase in a concentration-dependent manner. S phase arrest accompanied with a decrease in the number of cells in G 0 /G 1 phase following treatment with antitumor drugs has also been reported in a number of other studies (31)(32)(33), and does not appear to affect the antitumor effect of these drugs. One potential explanation for this is that the inhibition of cell proliferation is associated with cell cycle arrest, but the phase at which the cells are arrested depends on the anticancer drugs and the antitumor cells involved.…”

Section: Discussionmentioning

confidence: 65%

Chloroquine exerts antitumor effects on NB4 acute promyelocytic leukemia cells and functions synergistically with arsenic trioxide

et al. 2017

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Abstract. Chloroquine (CQ) has been confirmed to exhibit antitumor effects on different types of cancer cell, but whether it exerts the same effect on acute promyelocytic leukemia (APL) cells remains to be confirmed. In the present study, the effects of various concentrations of CQ on the growth, apoptosis and cell cycle distribution ofNB4 cells, as well as the potential mechanisms underlying these effects, were examined. The combined effect of CQ and arsenic trioxide (ATO) on the growth of NB4 cells was also determined. The results of the present study demonstrated that CQ treatment inhibited cell proliferation, and induced mitochondrial pathway apoptosis and S phase arrest in a dose-dependent manner by regulating apoptosis-and cell cycle-related proteins. CQ and ATO had a synergistic effect on the growth inhibition of NB4 cells, which may have been induced through the inhibition of autophagy. In conclusion, the results of the present study indicated that CQ exhibits a cytotoxic effect on NB4 cells and has a synergistic effect when combined with ATO, which thereby improves the curative effect of ATO on APL.

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R-Phycoerythrin Induces SGC-7901 Apoptosis by Arresting Cell Cycle at S Phase

Cited by 28 publications

References 38 publications

Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells

Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells

Correlation of the cytotoxic effects of cationic lipids with their headgroups

Chloroquine exerts antitumor effects on NB4 acute promyelocytic leukemia cells and functions synergistically with arsenic trioxide

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