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Proteomic analysis of bladder cancer indicates Prx-I as a key molecule in BI-TK/GCV treatment system.

Jiang L, Xiao X, Ren J, Tang Y, Weng H, Yang Q, Wu M, Tang W - PLoS ONE (2014)

Bottom Line: In order to understand the molecular mechanisms of Bifidobacterium infantis thymidine kinase/nucleoside analogue ganciclovir (BI-TK/GCV) treatment system which was proven to exhibit sustainable anti-tumor growth activity and induce apoptosis in bladder cancer, a proteomic approach of isobaric tags for relative and absolute quantification (iTRAQ), followed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used. 192 down-regulated and 210 up-regulated proteins were identified after treatment with BI-TK/GCV system in Sprague-Dawley (SD) rats.Western blot analysis and immunohistochemistry analysis confirmed that Peroxiredoxin-I (Prx-I) was significantly down-regulated in bladder cancer after treatment.Prx-I silencing by transfection of Prx-I shRNA significantly suppressed growth, promoted apoptosis and regulated the cell cycle in T24 cells and reduced the phospho-NF-κB p50 and p65 protein expression which revealed the links between Prx-I and NF-κB pathway implied by Ingenuity pathway analysis (IPA).

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

ABSTRACT
In order to understand the molecular mechanisms of Bifidobacterium infantis thymidine kinase/nucleoside analogue ganciclovir (BI-TK/GCV) treatment system which was proven to exhibit sustainable anti-tumor growth activity and induce apoptosis in bladder cancer, a proteomic approach of isobaric tags for relative and absolute quantification (iTRAQ), followed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used. 192 down-regulated and 210 up-regulated proteins were identified after treatment with BI-TK/GCV system in Sprague-Dawley (SD) rats. Western blot analysis and immunohistochemistry analysis confirmed that Peroxiredoxin-I (Prx-I) was significantly down-regulated in bladder cancer after treatment. Prx-I silencing by transfection of Prx-I shRNA significantly suppressed growth, promoted apoptosis and regulated the cell cycle in T24 cells and reduced the phospho-NF-κB p50 and p65 protein expression which revealed the links between Prx-I and NF-κB pathway implied by Ingenuity pathway analysis (IPA). These findings yield new insights into the therapy of bladder cancer, revealing Prx-I as a new therapeutic target and indicating BI-TK/GCV system as a prospective therapy by down-regulation of Prx-I through NF-κB signaling pathway.

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Effect of Prx-I-shRNA transfection on the apoptosis and cell cycle of T24 cells.A: Prx-I knockdown induced apoptosis in T24 cells. B: Representative pictures of FACS analysis showing Prx-I knockdown induced G0/G1 cell cycle arrest in T24 cells with a corresponding decrease in S-phase cells (P<0.05).
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pone-0098764-g006: Effect of Prx-I-shRNA transfection on the apoptosis and cell cycle of T24 cells.A: Prx-I knockdown induced apoptosis in T24 cells. B: Representative pictures of FACS analysis showing Prx-I knockdown induced G0/G1 cell cycle arrest in T24 cells with a corresponding decrease in S-phase cells (P<0.05).

Mentions: The effects of Prx-I knockdown on apoptosis and cell cycle of T24 cell were investigated. After 48 h of transfection, the apoptosis rate in the sh-1 group (21.99±1.10%) was significantly higher compared with the con shRNA group (4.51±0.73%) and parental group (4.96±0.46%) (P<0.05) (Figure 6A). Cell cycle analysis showed that G0/G1 phase ratio in the sh-1 group (61.13±.50%) was significantly higher compared with the con sh group (49.62±0.84%) and parental group (48.03±1.17%) (P<0.05) (Figure 6B).


Proteomic analysis of bladder cancer indicates Prx-I as a key molecule in BI-TK/GCV treatment system.

Jiang L, Xiao X, Ren J, Tang Y, Weng H, Yang Q, Wu M, Tang W - PLoS ONE (2014)

Effect of Prx-I-shRNA transfection on the apoptosis and cell cycle of T24 cells.A: Prx-I knockdown induced apoptosis in T24 cells. B: Representative pictures of FACS analysis showing Prx-I knockdown induced G0/G1 cell cycle arrest in T24 cells with a corresponding decrease in S-phase cells (P<0.05).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4048271&req=5

pone-0098764-g006: Effect of Prx-I-shRNA transfection on the apoptosis and cell cycle of T24 cells.A: Prx-I knockdown induced apoptosis in T24 cells. B: Representative pictures of FACS analysis showing Prx-I knockdown induced G0/G1 cell cycle arrest in T24 cells with a corresponding decrease in S-phase cells (P<0.05).
Mentions: The effects of Prx-I knockdown on apoptosis and cell cycle of T24 cell were investigated. After 48 h of transfection, the apoptosis rate in the sh-1 group (21.99±1.10%) was significantly higher compared with the con shRNA group (4.51±0.73%) and parental group (4.96±0.46%) (P<0.05) (Figure 6A). Cell cycle analysis showed that G0/G1 phase ratio in the sh-1 group (61.13±.50%) was significantly higher compared with the con sh group (49.62±0.84%) and parental group (48.03±1.17%) (P<0.05) (Figure 6B).

Bottom Line: In order to understand the molecular mechanisms of Bifidobacterium infantis thymidine kinase/nucleoside analogue ganciclovir (BI-TK/GCV) treatment system which was proven to exhibit sustainable anti-tumor growth activity and induce apoptosis in bladder cancer, a proteomic approach of isobaric tags for relative and absolute quantification (iTRAQ), followed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used. 192 down-regulated and 210 up-regulated proteins were identified after treatment with BI-TK/GCV system in Sprague-Dawley (SD) rats.Western blot analysis and immunohistochemistry analysis confirmed that Peroxiredoxin-I (Prx-I) was significantly down-regulated in bladder cancer after treatment.Prx-I silencing by transfection of Prx-I shRNA significantly suppressed growth, promoted apoptosis and regulated the cell cycle in T24 cells and reduced the phospho-NF-κB p50 and p65 protein expression which revealed the links between Prx-I and NF-κB pathway implied by Ingenuity pathway analysis (IPA).

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

ABSTRACT
In order to understand the molecular mechanisms of Bifidobacterium infantis thymidine kinase/nucleoside analogue ganciclovir (BI-TK/GCV) treatment system which was proven to exhibit sustainable anti-tumor growth activity and induce apoptosis in bladder cancer, a proteomic approach of isobaric tags for relative and absolute quantification (iTRAQ), followed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used. 192 down-regulated and 210 up-regulated proteins were identified after treatment with BI-TK/GCV system in Sprague-Dawley (SD) rats. Western blot analysis and immunohistochemistry analysis confirmed that Peroxiredoxin-I (Prx-I) was significantly down-regulated in bladder cancer after treatment. Prx-I silencing by transfection of Prx-I shRNA significantly suppressed growth, promoted apoptosis and regulated the cell cycle in T24 cells and reduced the phospho-NF-κB p50 and p65 protein expression which revealed the links between Prx-I and NF-κB pathway implied by Ingenuity pathway analysis (IPA). These findings yield new insights into the therapy of bladder cancer, revealing Prx-I as a new therapeutic target and indicating BI-TK/GCV system as a prospective therapy by down-regulation of Prx-I through NF-κB signaling pathway.

Show MeSH
Related in: MedlinePlus