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Cucurbitacin B inhibits proliferation and induces apoptosis via STAT3 pathway inhibition in A549 lung cancer cells.

Zhang M, Bian ZG, Zhang Y, Wang JH, Kan L, Wang X, Niu HY, He P - Mol Med Rep (2014)

Bottom Line: Natural products are a great source of cancer chemotherapeutic agents.Apoptosis induced by CuB was shown to be associated with cytochrome c release, B-cell lymphoma 2 downregulation and signal transducer and activator of transcription 3 pathway inhibition.CuB may prove to be a useful approach for the chemotherapy of lung cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.

ABSTRACT
Natural products are a great source of cancer chemotherapeutic agents. The present study was conducted to investigate whether cucurbitacin B (CuB), one of the most potent and widely used cucurbitacins, inhibits proliferation and induces apoptosis in the A549 lung cancer cell line. Furthermore, CuB induced apoptosis of A549 cells in a -concentration-dependent manner, as determined by fluorescence microscopy, flow cytometry and transmission electron microscopy. The present study also demonstrated that CuB dose-dependently inhibited lung cancer cell proliferation, with cell cycle inhibition and cyclin B1 downregulation. Apoptosis induced by CuB was shown to be associated with cytochrome c release, B-cell lymphoma 2 downregulation and signal transducer and activator of transcription 3 pathway inhibition. CuB may prove to be a useful approach for the chemotherapy of lung cancer.

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CuB induces disruption of ΔΨm. (A) A549 cells were treated with CuB (0, 0.1 and 1.0 μmol/l) for 24 h. The cells were then harvested, stained with rhodamine 123 and flow cytometric analysis was performed to analyze ΔΨm. (B) Quantification of the depolarization data from the histograms in A. *P<0.05 vs. the control group; **P<0.01 vs. the control group. CuB, cucurbitacin B; ΔΨm, mitochondrial membrane potential.
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f8-mmr-10-06-2905: CuB induces disruption of ΔΨm. (A) A549 cells were treated with CuB (0, 0.1 and 1.0 μmol/l) for 24 h. The cells were then harvested, stained with rhodamine 123 and flow cytometric analysis was performed to analyze ΔΨm. (B) Quantification of the depolarization data from the histograms in A. *P<0.05 vs. the control group; **P<0.01 vs. the control group. CuB, cucurbitacin B; ΔΨm, mitochondrial membrane potential.

Mentions: The effect of CuB on Δψm following CuB treatment was examined by rhodamine 123 staining and flow cytometric analysis. The integral under the Δψm curve decreased and shifted toward the left; therefore, the proportion of depolarized cells increased in a dose-dependent manner following CuB treatment (Fig. 8). The results indicated that cucurbitacin B treatment induced significant disruption of the Δψm. As cytochrome c release may be a limiting factor in caspase-9 activation and represents a control coordinating step in apoptosis, the ability of CuB to trigger cytochrome c release was examined in A549 cells. As demonstrated in Fig. 9, CuB treatment induced the release of mitochondrial cytochrome c into the cytosol.


Cucurbitacin B inhibits proliferation and induces apoptosis via STAT3 pathway inhibition in A549 lung cancer cells.

Zhang M, Bian ZG, Zhang Y, Wang JH, Kan L, Wang X, Niu HY, He P - Mol Med Rep (2014)

CuB induces disruption of ΔΨm. (A) A549 cells were treated with CuB (0, 0.1 and 1.0 μmol/l) for 24 h. The cells were then harvested, stained with rhodamine 123 and flow cytometric analysis was performed to analyze ΔΨm. (B) Quantification of the depolarization data from the histograms in A. *P<0.05 vs. the control group; **P<0.01 vs. the control group. CuB, cucurbitacin B; ΔΨm, mitochondrial membrane potential.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4227420&req=5

f8-mmr-10-06-2905: CuB induces disruption of ΔΨm. (A) A549 cells were treated with CuB (0, 0.1 and 1.0 μmol/l) for 24 h. The cells were then harvested, stained with rhodamine 123 and flow cytometric analysis was performed to analyze ΔΨm. (B) Quantification of the depolarization data from the histograms in A. *P<0.05 vs. the control group; **P<0.01 vs. the control group. CuB, cucurbitacin B; ΔΨm, mitochondrial membrane potential.
Mentions: The effect of CuB on Δψm following CuB treatment was examined by rhodamine 123 staining and flow cytometric analysis. The integral under the Δψm curve decreased and shifted toward the left; therefore, the proportion of depolarized cells increased in a dose-dependent manner following CuB treatment (Fig. 8). The results indicated that cucurbitacin B treatment induced significant disruption of the Δψm. As cytochrome c release may be a limiting factor in caspase-9 activation and represents a control coordinating step in apoptosis, the ability of CuB to trigger cytochrome c release was examined in A549 cells. As demonstrated in Fig. 9, CuB treatment induced the release of mitochondrial cytochrome c into the cytosol.

Bottom Line: Natural products are a great source of cancer chemotherapeutic agents.Apoptosis induced by CuB was shown to be associated with cytochrome c release, B-cell lymphoma 2 downregulation and signal transducer and activator of transcription 3 pathway inhibition.CuB may prove to be a useful approach for the chemotherapy of lung cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.

ABSTRACT
Natural products are a great source of cancer chemotherapeutic agents. The present study was conducted to investigate whether cucurbitacin B (CuB), one of the most potent and widely used cucurbitacins, inhibits proliferation and induces apoptosis in the A549 lung cancer cell line. Furthermore, CuB induced apoptosis of A549 cells in a -concentration-dependent manner, as determined by fluorescence microscopy, flow cytometry and transmission electron microscopy. The present study also demonstrated that CuB dose-dependently inhibited lung cancer cell proliferation, with cell cycle inhibition and cyclin B1 downregulation. Apoptosis induced by CuB was shown to be associated with cytochrome c release, B-cell lymphoma 2 downregulation and signal transducer and activator of transcription 3 pathway inhibition. CuB may prove to be a useful approach for the chemotherapy of lung cancer.

Show MeSH
Related in: MedlinePlus