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Inhibitory effect of dihydromyricetin on the proliferation of JAR cells and its mechanism of action.

ABSTRACT: Dihydromyricetin (DMY) is a novel natural drug with antitumor activity against some cancer cells without obvious toxicity. Previously, its apoptotic effect on human choriocarcinoma was detected. The present study further investigated the therapeutic potential of DMY as a new drug for the treatment of choriocarcinoma, as well as its anti-proliferative effect and mechanism of action. The short-term proliferation of JAR cells was determined by MTT assay, whereas the effect of DMY on long-term cell proliferation was determined by colony forming assay. Flow cytometry was used to detect changes in the cell cycle. Furthermore, western blotting was used to detect the expression levels of proliferation-associated proteins such as cyclin A1, cyclin D1, SMAD3 and SMAD4. Reverse transcription-quantitative PCR (RT-qPCR) was used to quantify mRNA expression levels. The results indicated that DMY inhibited short and long-term proliferation of JAR cells in a concentration-dependent manner. Flow cytometry demonstrated S/G2/M cell cycle arrest, and western blotting revealed the downregulation of SMAD3, SMAD4, cyclin A1 and cyclin D1 expression levels. The results of RT-qPCR and western blotting were consistent. Overall, the findings of the present study suggest that DMY inhibits the proliferation of human choriocarcinoma JAR cells, potentially through cell cycle arrest via the downregulation of cyclin A1, cyclin D1, SMAD3 and SMAD4 expression levels.

SUBMITTER: Zuo Y

PROVIDER: S-EPMC7286138 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Inhibitory effect of dihydromyricetin on the proliferation of JAR cells and its mechanism of action.

Zuo Yanzhen Y Lu Yanjie Y Xu Qian Q Sun Dayong D Liang Xiujun X Li Xiaoru X Li Yuhong Y

Oncology letters 20200416 1

Dihydromyricetin (DMY) is a novel natural drug with antitumor activity against some cancer cells without obvious toxicity. Previously, its apoptotic effect on human choriocarcinoma was detected. The present study further investigated the therapeutic potential of DMY as a new drug for the treatment of choriocarcinoma, as well as its anti-proliferative effect and mechanism of action. The short-term proliferation of JAR cells was determined by MTT assay, whereas the effect of DMY on long-term cell ...[more]

PMID: 32565961

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Project description:BackgroundThe bark of Uncaria rhynchophylla has been traditionally used to treat convulsion, bleeding, hypertension, auto-immune conditions, cancer, and other diseases. The main focus of this research is done for the purpose of exploring the antitumor activity and mechanism of action (MOA) for hirsutine isolated from U. rhynchophylla.MethodsJurkat clone E6-1 cells were treated using 10, 25 and 50 μM for 48 h. Inhibition of cell proliferation due to hirsutine treatment was evaluated by CCK8 assay. Flow cytometry was applied to ascertain Jurkat cell cycle progression and apoptosis after treatment with 10, 25 and 50 μM hirsutine for 48 h. The expression and level of the apoptosis-related genes and proteins was analyzed by Real-time Quantitative polymerase chain reaction (qPCR) and Western blotting method, respectively.ResultsCCK8 analyses revealed that hirsutine could significantly inhibit the proliferation of Jurkat clone E6-1 cells, in a concentration and time-dependent fashion. Flow cytometry assays revealed that hirsutine could drive apoptotic death and G0/G1 phase arrest in Jurkat cells. Apoptotic cells frequencies were 4.99 ± 0.51%, 13.69 ± 2.00% and 40.21 ± 15.19%, and respective cell cycle arrest in G0/G1 accounted for 34.85 ± 1.81%, 42.83 ± 0.70% and 49.12 ± 4.07%. Simultaneously, compared with the control group, Western blot assays indicated that the up-regulation of pro-apoptotic Bax, cleaved-caspase3, cleaved-caspase9 and Cyto c proteins, as well as the down-regulation of Bcl-2 protein which guards against cell death, might be correlated with cell death induction and inhibition of cell proliferation. QPCR analyses indicated that hirsutine could diminish BCL2 expression and, at the same time, improve Bax, caspase-3 and caspase-9 mRNA levels, thus reiterating a putative correlation of hirsutine treatment in vitro with apoptosis induction and inhibition of cell proliferation (p-value < 0.05). Excessive hirsutine damages the ultrastructure in mitochondria, leading to the release of Cyt c from the mitochondria to cytoplasm in Jurkat clone E6-1 cells, thereby inducing the activated caspase cascade apoptosis process through a mitochondria-mediated pathway.ConclusionAn important bioactive constituent-hirsutine-appears to have antitumor effects in human T-cell leukemia, thus enlightening the use of phytomedicines as a novel source for tumor therapy. It is speculated that hirsutine may induce apoptosis of Jurkat Clone E6-1 cells through the mitochondrial apoptotic pathway.

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Inhibitory effect of dihydromyricetin on the proliferation of JAR cells and its mechanism of action.

Publications

Inhibitory effect of dihydromyricetin on the proliferation of JAR cells and its mechanism of action.

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