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Ponicidin induces apoptosis via JAK2 and STAT3 signaling pathways in gastric carcinoma.

Liu YF, Lu YM, Qu GQ, Liu Y, Chen WX, Liao XH, Kong WM - Int J Mol Sci (2015)

Bottom Line: The results revealed that ponicidin could inhibit the growth of MKN28 cells significantly in both a time- and dose-dependent manner.The cell cycle was blocked and ROS generation was increased after the cells were treated with ponicidin.We therefore conclude that ponicidin exhibited significant growth inhibition of gastric carcinoma cell line MKN28 and induced apoptosis of MKN28 cells via the signaling pathway regulated by Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3).

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, China. wangyang163jed@163.com.

ABSTRACT
Ponicidin has a variety of biological effects such as immunoregulatory and anti-inflammatory functions as well as anti-viral functions especially in the upper respiratory tract infection. This study was aimed to elucidate the antitumor effect of ponicidin in gastric carcinoma MKN28 cells and the possible molecular mechanism involved. Cell viability was measured by the Cell Count Kit-8 (CCK8). Cell apoptosis was assessed by flow cytometry as well as cell cycle and reactive oxygen species (ROS) analysis. Western blot analysis was used to detect the active form of caspase-3 as well as Bax and B-cell lymphoma-2 (Bcl-2) expressions after cells were treated with different concentrations of ponicidin. The results revealed that ponicidin could inhibit the growth of MKN28 cells significantly in both a time- and dose-dependent manner. The cell cycle was blocked and ROS generation was increased after the cells were treated with ponicidin. Bcl-2 expression was down-regulated remarkably while Bax expression and the active form of caspase-3 were increased after apoptosis occurred. We therefore conclude that ponicidin exhibited significant growth inhibition of gastric carcinoma cell line MKN28 and induced apoptosis of MKN28 cells via the signaling pathway regulated by Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3). Ponicidin may serve as a potential therapeutic agent for gastric carcinoma.

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Effects of ponicidin on the activity of caspase-3 in MKN28 cells. After treatment, the activity of caspase-3 in MKN28 cells was analyzed by the caspase-3 assay kit. Ponicidin treatment time- and dose-dependently increased the activity of caspase-3 of MKN28 cells. * p < 0.05, # p < 0.01.
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ijms-16-01576-f006: Effects of ponicidin on the activity of caspase-3 in MKN28 cells. After treatment, the activity of caspase-3 in MKN28 cells was analyzed by the caspase-3 assay kit. Ponicidin treatment time- and dose-dependently increased the activity of caspase-3 of MKN28 cells. * p < 0.05, # p < 0.01.

Mentions: To clarify the effect of ponicidin on caspase-3, we also investigated the activity of caspase-3 after ponicidin treatment. As shown in Figure 6, treatment of MKN28 cells with ponicidin (10, 25 and 50 μmol/L) for different times induced caspase-3 activation respectively, from 18.80% ± 0.47% to 28.76% ± 0.38% (n = 3) in a time- and dose-dependent manner compared with control cells with that of 15.57% ± 0.47% and significantly increased in 48 h.


Ponicidin induces apoptosis via JAK2 and STAT3 signaling pathways in gastric carcinoma.

Liu YF, Lu YM, Qu GQ, Liu Y, Chen WX, Liao XH, Kong WM - Int J Mol Sci (2015)

Effects of ponicidin on the activity of caspase-3 in MKN28 cells. After treatment, the activity of caspase-3 in MKN28 cells was analyzed by the caspase-3 assay kit. Ponicidin treatment time- and dose-dependently increased the activity of caspase-3 of MKN28 cells. * p < 0.05, # p < 0.01.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4307321&req=5

ijms-16-01576-f006: Effects of ponicidin on the activity of caspase-3 in MKN28 cells. After treatment, the activity of caspase-3 in MKN28 cells was analyzed by the caspase-3 assay kit. Ponicidin treatment time- and dose-dependently increased the activity of caspase-3 of MKN28 cells. * p < 0.05, # p < 0.01.
Mentions: To clarify the effect of ponicidin on caspase-3, we also investigated the activity of caspase-3 after ponicidin treatment. As shown in Figure 6, treatment of MKN28 cells with ponicidin (10, 25 and 50 μmol/L) for different times induced caspase-3 activation respectively, from 18.80% ± 0.47% to 28.76% ± 0.38% (n = 3) in a time- and dose-dependent manner compared with control cells with that of 15.57% ± 0.47% and significantly increased in 48 h.

Bottom Line: The results revealed that ponicidin could inhibit the growth of MKN28 cells significantly in both a time- and dose-dependent manner.The cell cycle was blocked and ROS generation was increased after the cells were treated with ponicidin.We therefore conclude that ponicidin exhibited significant growth inhibition of gastric carcinoma cell line MKN28 and induced apoptosis of MKN28 cells via the signaling pathway regulated by Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3).

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, China. wangyang163jed@163.com.

ABSTRACT
Ponicidin has a variety of biological effects such as immunoregulatory and anti-inflammatory functions as well as anti-viral functions especially in the upper respiratory tract infection. This study was aimed to elucidate the antitumor effect of ponicidin in gastric carcinoma MKN28 cells and the possible molecular mechanism involved. Cell viability was measured by the Cell Count Kit-8 (CCK8). Cell apoptosis was assessed by flow cytometry as well as cell cycle and reactive oxygen species (ROS) analysis. Western blot analysis was used to detect the active form of caspase-3 as well as Bax and B-cell lymphoma-2 (Bcl-2) expressions after cells were treated with different concentrations of ponicidin. The results revealed that ponicidin could inhibit the growth of MKN28 cells significantly in both a time- and dose-dependent manner. The cell cycle was blocked and ROS generation was increased after the cells were treated with ponicidin. Bcl-2 expression was down-regulated remarkably while Bax expression and the active form of caspase-3 were increased after apoptosis occurred. We therefore conclude that ponicidin exhibited significant growth inhibition of gastric carcinoma cell line MKN28 and induced apoptosis of MKN28 cells via the signaling pathway regulated by Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3). Ponicidin may serve as a potential therapeutic agent for gastric carcinoma.

Show MeSH
Related in: MedlinePlus