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SIRT3 overexpression regulated GSTP1/JNK signaling pathway A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or <t>epirubicin</t> (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.
Epirubicin, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway"

Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

Journal: Oncotarget

doi: 10.18632/oncotarget.10319

SIRT3 overexpression regulated GSTP1/JNK signaling pathway A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.
Figure Legend Snippet: SIRT3 overexpression regulated GSTP1/JNK signaling pathway A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.

Techniques Used: Over Expression, Infection, Planar Chromatography, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Immunoprecipitation

SIRT3 overexpression sensitized HCC cells to chemotherapeutic agents A. Western blotting analysis of SIRT3 proteins in cells infected with lentivirus expressing SIRT3 or vector. GAPDH was used as a loading control. B-D. Cell viability of SIRT3-overexpressing cells exposed to chemotherapeutic agents. Forty-eight hour after lentivirus infection, SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) were treated with various concentrations of doxorubicin, cisplatin or epirubicin for 48 h. Cell viability was determined by MTS assay.
Figure Legend Snippet: SIRT3 overexpression sensitized HCC cells to chemotherapeutic agents A. Western blotting analysis of SIRT3 proteins in cells infected with lentivirus expressing SIRT3 or vector. GAPDH was used as a loading control. B-D. Cell viability of SIRT3-overexpressing cells exposed to chemotherapeutic agents. Forty-eight hour after lentivirus infection, SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) were treated with various concentrations of doxorubicin, cisplatin or epirubicin for 48 h. Cell viability was determined by MTS assay.

Techniques Used: Over Expression, Western Blot, Infection, Expressing, Plasmid Preparation, Planar Chromatography, MTS Assay

SIRT3 overexpression enhanced chemotherapeutic agents-induced apoptosis in HCC cells A-C. Apoptosis in different groups was analyzed by flow cytometry with Annexin V/PI. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h and subjected to flow cytometry analysis. *, P
Figure Legend Snippet: SIRT3 overexpression enhanced chemotherapeutic agents-induced apoptosis in HCC cells A-C. Apoptosis in different groups was analyzed by flow cytometry with Annexin V/PI. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h and subjected to flow cytometry analysis. *, P

Techniques Used: Over Expression, Flow Cytometry, Cytometry, Infection, Planar Chromatography

GSTP1 overexpression or JNK inhibitor attenuate the sensitizing effect of SIRT3 A-B. GSTP1 overexpression abolished SIRT3-induced apoptosis in HCC cells treated with chemotherapeutic agents. SMMC-7721 and Huh-7 cells stably expressing SIRT3 were transfected with plasmid expressing GSTP1 and were then exposed to doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. Apoptotic ratio in different groups was detected by flow cytometry with Annexin V/PI(A) and PARP cleavage analysis (B). *, p
Figure Legend Snippet: GSTP1 overexpression or JNK inhibitor attenuate the sensitizing effect of SIRT3 A-B. GSTP1 overexpression abolished SIRT3-induced apoptosis in HCC cells treated with chemotherapeutic agents. SMMC-7721 and Huh-7 cells stably expressing SIRT3 were transfected with plasmid expressing GSTP1 and were then exposed to doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. Apoptotic ratio in different groups was detected by flow cytometry with Annexin V/PI(A) and PARP cleavage analysis (B). *, p

Techniques Used: Over Expression, Stable Transfection, Expressing, Transfection, Plasmid Preparation, Flow Cytometry, Cytometry

Chemotherapeutic agents inhibited SIRT3 expression in HCC cells A. SIRT3 expression in three HCC cell lines (SMMC-7721, Huh-7 and PLC/PRF/5) and one immortalized liver cell line (MIHA) by using qPCR and western blotting analysis. β-actin mRNA expression was used as an internal control for qPCR. GAPDH was used as a loading control in western blotting analysis. B-D. Chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) inhibited SIRT3 expression. SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h before subjected to qPCR and western blotting analysis. E-F. The expression of SIRT3 was examined in SMMC-7721 and Huh-7 cells treated with various concentrations of chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) by using western blotting analysis. GAPDH was used as a loading control.
Figure Legend Snippet: Chemotherapeutic agents inhibited SIRT3 expression in HCC cells A. SIRT3 expression in three HCC cell lines (SMMC-7721, Huh-7 and PLC/PRF/5) and one immortalized liver cell line (MIHA) by using qPCR and western blotting analysis. β-actin mRNA expression was used as an internal control for qPCR. GAPDH was used as a loading control in western blotting analysis. B-D. Chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) inhibited SIRT3 expression. SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h before subjected to qPCR and western blotting analysis. E-F. The expression of SIRT3 was examined in SMMC-7721 and Huh-7 cells treated with various concentrations of chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) by using western blotting analysis. GAPDH was used as a loading control.

Techniques Used: Expressing, Planar Chromatography, Real-time Polymerase Chain Reaction, Western Blot

Related Articles

Clone Assay:

Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway
Article Snippet: Plasmids, antibodies and chemotherapeutic agents The plenti6-SIRT3 expression vector was cloned as previously reported [ ]. .. Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

Expressing:

Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway
Article Snippet: The pCMV6-XL5-GSTP1 expression vector (SC119655) was obtained from Origene (USA). .. Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

Spectrophotometry:

Article Title: A small-molecule competitive inhibitor of phosphatidic acid binding by the AAA+ protein NSF/Sec18 blocks the SNARE-priming stage of vacuole fusion
Article Snippet: Epirubicin was from Cayman Chemical. .. NMR data were recorded on a Bruker spectrophotometer equipped with a CryoProbe (500 MHz, 1 H) using deuterated DMSO as a solvent and internal reference (δ = 2.50 ppm).

Indirect Immunoperoxidase Assay:

Article Title: A small-molecule competitive inhibitor of phosphatidic acid binding by the AAA+ protein NSF/Sec18 blocks the SNARE-priming stage of vacuole fusion
Article Snippet: Epirubicin was from Cayman Chemical. .. IPA purity was assessed using NMR and LC/MS.

Nuclear Magnetic Resonance:

Article Title: A small-molecule competitive inhibitor of phosphatidic acid binding by the AAA+ protein NSF/Sec18 blocks the SNARE-priming stage of vacuole fusion
Article Snippet: Epirubicin was from Cayman Chemical. .. IPA purity was assessed using NMR and LC/MS.

Liquid Chromatography with Mass Spectroscopy:

Article Title: A small-molecule competitive inhibitor of phosphatidic acid binding by the AAA+ protein NSF/Sec18 blocks the SNARE-priming stage of vacuole fusion
Article Snippet: Epirubicin was from Cayman Chemical. .. IPA purity was assessed using NMR and LC/MS.

Plasmid Preparation:

Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway
Article Snippet: The pCMV6-XL5-GSTP1 expression vector (SC119655) was obtained from Origene (USA). .. Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

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    Cayman Chemical epirubicin
    SIRT3 overexpression regulated GSTP1/JNK signaling pathway A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or <t>epirubicin</t> (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.
    Epirubicin, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/epirubicin/product/Cayman Chemical
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    epirubicin - by Bioz Stars, 2020-04
    94/100 stars
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    SIRT3 overexpression regulated GSTP1/JNK signaling pathway A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: SIRT3 overexpression regulated GSTP1/JNK signaling pathway A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Over Expression, Infection, Planar Chromatography, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Immunoprecipitation

    SIRT3 overexpression sensitized HCC cells to chemotherapeutic agents A. Western blotting analysis of SIRT3 proteins in cells infected with lentivirus expressing SIRT3 or vector. GAPDH was used as a loading control. B-D. Cell viability of SIRT3-overexpressing cells exposed to chemotherapeutic agents. Forty-eight hour after lentivirus infection, SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) were treated with various concentrations of doxorubicin, cisplatin or epirubicin for 48 h. Cell viability was determined by MTS assay.

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: SIRT3 overexpression sensitized HCC cells to chemotherapeutic agents A. Western blotting analysis of SIRT3 proteins in cells infected with lentivirus expressing SIRT3 or vector. GAPDH was used as a loading control. B-D. Cell viability of SIRT3-overexpressing cells exposed to chemotherapeutic agents. Forty-eight hour after lentivirus infection, SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) were treated with various concentrations of doxorubicin, cisplatin or epirubicin for 48 h. Cell viability was determined by MTS assay.

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Over Expression, Western Blot, Infection, Expressing, Plasmid Preparation, Planar Chromatography, MTS Assay

    SIRT3 overexpression enhanced chemotherapeutic agents-induced apoptosis in HCC cells A-C. Apoptosis in different groups was analyzed by flow cytometry with Annexin V/PI. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h and subjected to flow cytometry analysis. *, P

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: SIRT3 overexpression enhanced chemotherapeutic agents-induced apoptosis in HCC cells A-C. Apoptosis in different groups was analyzed by flow cytometry with Annexin V/PI. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h and subjected to flow cytometry analysis. *, P

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Over Expression, Flow Cytometry, Cytometry, Infection, Planar Chromatography

    GSTP1 overexpression or JNK inhibitor attenuate the sensitizing effect of SIRT3 A-B. GSTP1 overexpression abolished SIRT3-induced apoptosis in HCC cells treated with chemotherapeutic agents. SMMC-7721 and Huh-7 cells stably expressing SIRT3 were transfected with plasmid expressing GSTP1 and were then exposed to doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. Apoptotic ratio in different groups was detected by flow cytometry with Annexin V/PI(A) and PARP cleavage analysis (B). *, p

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: GSTP1 overexpression or JNK inhibitor attenuate the sensitizing effect of SIRT3 A-B. GSTP1 overexpression abolished SIRT3-induced apoptosis in HCC cells treated with chemotherapeutic agents. SMMC-7721 and Huh-7 cells stably expressing SIRT3 were transfected with plasmid expressing GSTP1 and were then exposed to doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. Apoptotic ratio in different groups was detected by flow cytometry with Annexin V/PI(A) and PARP cleavage analysis (B). *, p

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Over Expression, Stable Transfection, Expressing, Transfection, Plasmid Preparation, Flow Cytometry, Cytometry

    Chemotherapeutic agents inhibited SIRT3 expression in HCC cells A. SIRT3 expression in three HCC cell lines (SMMC-7721, Huh-7 and PLC/PRF/5) and one immortalized liver cell line (MIHA) by using qPCR and western blotting analysis. β-actin mRNA expression was used as an internal control for qPCR. GAPDH was used as a loading control in western blotting analysis. B-D. Chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) inhibited SIRT3 expression. SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h before subjected to qPCR and western blotting analysis. E-F. The expression of SIRT3 was examined in SMMC-7721 and Huh-7 cells treated with various concentrations of chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) by using western blotting analysis. GAPDH was used as a loading control.

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: Chemotherapeutic agents inhibited SIRT3 expression in HCC cells A. SIRT3 expression in three HCC cell lines (SMMC-7721, Huh-7 and PLC/PRF/5) and one immortalized liver cell line (MIHA) by using qPCR and western blotting analysis. β-actin mRNA expression was used as an internal control for qPCR. GAPDH was used as a loading control in western blotting analysis. B-D. Chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) inhibited SIRT3 expression. SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h before subjected to qPCR and western blotting analysis. E-F. The expression of SIRT3 was examined in SMMC-7721 and Huh-7 cells treated with various concentrations of chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) by using western blotting analysis. GAPDH was used as a loading control.

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Expressing, Planar Chromatography, Real-time Polymerase Chain Reaction, Western Blot