Polydatin-induced cell apoptosis and cell cycle arrest are potentiated by Janus kinase 2 inhibition in leukemia cells

Cao, Wenhui; Wu, Ke; Wang, Chong; Wan, Dingming

doi:10.3892/mmr.2016.4909

Cited by 22 publications

(20 citation statements)

References 40 publications

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“… 17 PD also induced cell cycle arrest and apoptosis in leukemia, lung cancer and colorectal cancer cells. 10 , 18 , 19 However, little is known about the effects of PD on RCC cells.…”

Section: Discussionmentioning

confidence: 99%

Polydatin exerts anti-tumor effects against renal cell carcinoma cells via induction of caspase-dependent apoptosis and inhibition of the PI3K/Akt pathway

Jin¹,

Xin²,

Zhou³

et al. 2018

OTT

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PurposePolydatin, a stilbenoid glucoside of a resveratrol derivative, has many biological functions, including antitumor effects. However, the antitumor effects of polydatin in renal cell carcinoma (RCC) have not been investigated.Materials and methodsIn the current study, MTT assays, transwell invasion assays and wound healing assays were performed to examine cell proliferation, invasion and migration. An apoptosis nucleosome ELISA was used to measure apoptosis. Caspase activity assays were applied to measure the activities of caspase-3/9. A Western blot assay was used to measure the change in protein levels.ResultsOur data demonstrated that polydatin inhibited the proliferation of RCC cells but not normal renal epithelial cells in a time- and dose-dependent manner. Polydatin also triggered apoptosis in a caspase-dependent manner. Moreover, polydatin treatment also led to the downregulation of Bcl-2 and Mcl-1 and to activation of Bax. Ectopic expression of Bcl-2 and Mcl-1 or silencing of Bax could repress the apoptosis that was induced by polydatin. Moreover, incubation with polydatin also suppressed the PI3K/Akt signaling pathway in RCC cells.ConclusionTaken together, our data indicated that polydatin may be applied as a potent agent against RCC.

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“… 17 PD also induced cell cycle arrest and apoptosis in leukemia, lung cancer and colorectal cancer cells. 10 , 18 , 19 However, little is known about the effects of PD on RCC cells.…”

Section: Discussionmentioning

confidence: 99%

Polydatin exerts anti-tumor effects against renal cell carcinoma cells via induction of caspase-dependent apoptosis and inhibition of the PI3K/Akt pathway

Jin¹,

Xin²,

Zhou³

et al. 2018

OTT

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“…A significant reduction in motility was observed in both cell lines (34.67% for U-2OS, 40.00% for MG-63; P < 0.05) in response to treatment with polydatin (100 μM, U-2OS; or 200 μM, MG-63) compared with the control group ( Figure 1C). Moreover, the apoptotic rate was significantly increased (36.00% for U-2OS, 19.29% for MG-63; P < 0.05) in both cell lines compared with that observed in the control group ( Figure 1D). In the result of Western blot analysis, we found that in both cell lines polydatin significantly increased the expression of p21, caspase 3, and PAPR, whereas it significantly decreased the expression of Ki67, cyclin A, cyclin E, cyclin-dependent kinase 2 (CDK2), matrix metalloproteinase-2 (MMP-2), MMP-9, and poly(ADP-ribose) polymerase 1 (PARP1) (P < 0.05) ( Figure 1E and 1F).…”

Section: Polydatin Inhibited Progression and Induced Apoptosis In Umentioning

confidence: 77%

Polydatin enhances the chemosensitivity of osteosarcoma cells to paclitaxel

Zhao

Chen

Guan

2019

J of Cellular Biochemistry

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Despite improvements in the prognosis of osteosarcoma patients, chemotherapy fails in a considerable number of cases due to drug resistance. The development of novel agents may enhance chemosensitivity. This study explored the anticancer function of polydatin and its ability—in combination with paclitaxel—to overcome drug resistance in human osteosarcoma U‐2OS and MG‐63 cell lines. A cell proliferation assay (celll counting kit‐8), a cell‐cycle assay, an apoptosis assay (annexin V‐fluorescein isothiocyanate/propidium iodide), and a cell migration assay (Transwell) were used to analyze cell activity. Western blot analysis and quantitative reverse‐transcription polymerase chain reaction were performed to examine function‐related mRNA and protein levels. Treatment with polydatin suppressed cell growth and migration in both cell lines. Moreover, polydatin induced cell apoptosis in both parental and paclitaxel‐resistant cells, and cell‐cycle arrest in the S phase. Furthermore, it altered the expression of various proteins associated with cell growth (Ki67, p21, cyclin A, cyclin E, and cyclin‐dependent kinase 2), migration (matrix metalloproteinase‐2 [MMP‐2], MMP‐9, and tissue inhibitor of metalloproteinase‐1), apoptosis (poly[ADP‐ribose] polymerase 1 and caspase 3), and drug resistance (p‐glycoprotein 1, lung resistance‐related protein 1, growth arrest and DNA damage‐45α, glutathione S‐transferase π, and heat shock protein 27) in paclitaxel‐resistant osteosarcoma cells. Cells transfected with myr‐Akt caused obvious upregulation and activation of Akt, which were significantly attenuated via polydatin treatment. In conclusion, polydatin may enhance the chemosensitivity of osteosarcoma cells to paclitaxel.

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“…A previous study also proved that polydatin inhibited radiation-induced apoptosis in lung epithelial cells [14], and another study found that PD also inhibited methylglyoxal-induced apoptosis through reducing ROS and improving mitochondrial function in HUVEC cells [15]. However, in many cancer cells, polydatin exhibits apoptosis-promoting effects, including lung cancer cells, cervical cancer cells, and leukemia cells [16–19]. The diverse role of polydatin in cancer cells and normal cells provide a novel possibility in application in cancer radiotherapy.…”

Section: Discussionmentioning

confidence: 99%

Polydatin Alleviates Radiation-Induced Testes Injury by Scavenging ROS and Inhibiting Apoptosis Pathways

Jia

2018

Med Sci Monit

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BackgroundExposure to ionizing radiation (IR) induces severe damage in multiple human tissues. The testes are extremely sensitive to IR, and testes irradiation can result in infertility and abnormality. A novel and safe radioprotector for testes injury from IR is needed. Polydatin (PD) has been proved to have anti-oxidant and anti-inflammatory effects, indicating its potential application in radiation protection.Material/MethodsMale wild-type C57BL/6 mice (8 weeks old) were exposed to ionizing radiation. At different times after irradiation, testes were isolated and subjected to hematoxylin-eosin (HE) staining and TUNEL staining, as well as related quantification. ELISA assay was used to measure the level of inflammatory cytokines, and apoptosis proteins were detected by Western blot assay. Intracellular ROS was measured by DCFH-DA flow cytometry method.ResultsIn the present study, we demonstrated that polydatin effectively alleviated testes injury and retained sperm viability. PD pretreatment also inhibited cell apoptosis caused by irradiation. Radiation-induced decrease of FSH and testosterone was also inhibited by PD treatment. Finally, we showed that PD obviously reduced the ROS level, using DCFH-DA method. We also found that PD reduced the concentration of the oxidative products MDA and 8-OHdG. PD also inhibited apoptosis-related proteins such as Bax and caspase 3.ConclusionsOur data proved that polydatin effectively alleviated testes injury after irradiation, mainly through reducing ROS and oxidative stress. Our findings suggest polydatin as a potential radioprotector for testes radiation damage.

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Polydatin-induced cell apoptosis and cell cycle arrest are potentiated by Janus kinase 2 inhibition in leukemia cells

Cited by 22 publications

References 40 publications

Polydatin exerts anti-tumor effects against renal cell carcinoma cells via induction of caspase-dependent apoptosis and inhibition of the PI3K/Akt pathway

Polydatin exerts anti-tumor effects against renal cell carcinoma cells via induction of caspase-dependent apoptosis and inhibition of the PI3K/Akt pathway

Polydatin enhances the chemosensitivity of osteosarcoma cells to paclitaxel

Polydatin Alleviates Radiation-Induced Testes Injury by Scavenging ROS and Inhibiting Apoptosis Pathways

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