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MiR-181a contributes to bufalin-induced apoptosis in PC-3 prostate cancer cells.

Zhai XF, Fang FF, Liu Q, Meng YB, Guo YY, Chen Z - BMC Complement Altern Med (2013)

Bottom Line: However, effects and mechanism of bufalin on prostate cancer cells remain unknown.Bufalin was found to induce the expression of miR-181a, a small non-coding RNA believed to induce apoptosis by repressing its target gene, BCL-2.In prostate cancer PC-3cell line, bufalin-induced apoptosis can be largely attenuated by a miR-181a inhibitor, which blocked bufalin-induced Bcl-2 reduction and caspase-3 activation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Integrative Oncology, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, Shanghai 200433, China. chenzhech@163.com.

ABSTRACT

Background: Bufalin is a major active compound of cinobufacini, which comes from dried toad venom and has been used for treatments of various cancers in China for many years. A number of studies have demonstrated that bufalin can induce apoptosis in some cancers. However, effects and mechanism of bufalin on prostate cancer cells remain unknown.

Methods: Apoptosis assay was measured by the annexin-V/PI flow cytometric assay. Western blot was used to measure Caspase-3 and Bcl-2. qRT-PCR was used to measure the relative expression of miR-181a.

Results: Bufalin was found to induce the expression of miR-181a, a small non-coding RNA believed to induce apoptosis by repressing its target gene, BCL-2. In prostate cancer PC-3cell line, bufalin-induced apoptosis can be largely attenuated by a miR-181a inhibitor, which blocked bufalin-induced Bcl-2 reduction and caspase-3 activation.

Conclusions: Our dataindicatedthat miR-181a mediates bufalin-induced apoptosis in PC-3 cells. Thus, we presented here a new pharmacological mechanism for bufalin in anti-tumor therapy.

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Related in: MedlinePlus

MiR-181a inhibitor attenuatedbufalin-induced apoptosis in PC-3 cell. A. Apoptotic cells were stained by Annexin-V-FITC/PI and assayed by flow cytometer. Bufalin induced significant apoptosis that was effectively attenuated by miR-181a inhibitor. B. Statistical histogram from A was shown. P values were calculated byStudent’s t-test, based on three replications.
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Figure 2: MiR-181a inhibitor attenuatedbufalin-induced apoptosis in PC-3 cell. A. Apoptotic cells were stained by Annexin-V-FITC/PI and assayed by flow cytometer. Bufalin induced significant apoptosis that was effectively attenuated by miR-181a inhibitor. B. Statistical histogram from A was shown. P values were calculated byStudent’s t-test, based on three replications.

Mentions: Both bufalin and miR-181a could induce apoptosis in various cancer cells [4-7,14-21,23-26]. As bufalin can induce miR-181a expression, we speculated that bufalin-induced apoptosis may be mediated, at least partly, by miR-181a. To address this point, we tried to use miR-181a inhibitor to block bufalin-induced apoptosis. Bufalin treatment resulted in a 22.8% apoptosis rate in PC-3 cells, whereas the apoptosis rate decreased to 5.5% in cells transfected with miR-181a inhibitor (Figure 2). These data indicated that inhibition of miR-181a activity could attenuate bufalin-induced apoptosis in PC-3 cells.


MiR-181a contributes to bufalin-induced apoptosis in PC-3 prostate cancer cells.

Zhai XF, Fang FF, Liu Q, Meng YB, Guo YY, Chen Z - BMC Complement Altern Med (2013)

MiR-181a inhibitor attenuatedbufalin-induced apoptosis in PC-3 cell. A. Apoptotic cells were stained by Annexin-V-FITC/PI and assayed by flow cytometer. Bufalin induced significant apoptosis that was effectively attenuated by miR-181a inhibitor. B. Statistical histogram from A was shown. P values were calculated byStudent’s t-test, based on three replications.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4222721&req=5

Figure 2: MiR-181a inhibitor attenuatedbufalin-induced apoptosis in PC-3 cell. A. Apoptotic cells were stained by Annexin-V-FITC/PI and assayed by flow cytometer. Bufalin induced significant apoptosis that was effectively attenuated by miR-181a inhibitor. B. Statistical histogram from A was shown. P values were calculated byStudent’s t-test, based on three replications.
Mentions: Both bufalin and miR-181a could induce apoptosis in various cancer cells [4-7,14-21,23-26]. As bufalin can induce miR-181a expression, we speculated that bufalin-induced apoptosis may be mediated, at least partly, by miR-181a. To address this point, we tried to use miR-181a inhibitor to block bufalin-induced apoptosis. Bufalin treatment resulted in a 22.8% apoptosis rate in PC-3 cells, whereas the apoptosis rate decreased to 5.5% in cells transfected with miR-181a inhibitor (Figure 2). These data indicated that inhibition of miR-181a activity could attenuate bufalin-induced apoptosis in PC-3 cells.

Bottom Line: However, effects and mechanism of bufalin on prostate cancer cells remain unknown.Bufalin was found to induce the expression of miR-181a, a small non-coding RNA believed to induce apoptosis by repressing its target gene, BCL-2.In prostate cancer PC-3cell line, bufalin-induced apoptosis can be largely attenuated by a miR-181a inhibitor, which blocked bufalin-induced Bcl-2 reduction and caspase-3 activation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Integrative Oncology, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, Shanghai 200433, China. chenzhech@163.com.

ABSTRACT

Background: Bufalin is a major active compound of cinobufacini, which comes from dried toad venom and has been used for treatments of various cancers in China for many years. A number of studies have demonstrated that bufalin can induce apoptosis in some cancers. However, effects and mechanism of bufalin on prostate cancer cells remain unknown.

Methods: Apoptosis assay was measured by the annexin-V/PI flow cytometric assay. Western blot was used to measure Caspase-3 and Bcl-2. qRT-PCR was used to measure the relative expression of miR-181a.

Results: Bufalin was found to induce the expression of miR-181a, a small non-coding RNA believed to induce apoptosis by repressing its target gene, BCL-2. In prostate cancer PC-3cell line, bufalin-induced apoptosis can be largely attenuated by a miR-181a inhibitor, which blocked bufalin-induced Bcl-2 reduction and caspase-3 activation.

Conclusions: Our dataindicatedthat miR-181a mediates bufalin-induced apoptosis in PC-3 cells. Thus, we presented here a new pharmacological mechanism for bufalin in anti-tumor therapy.

Show MeSH
Related in: MedlinePlus