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actinomycin d  (MedChemExpress)


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    MedChemExpress actinomycin d
    RNA m 6 A methyltransferase METTL16 enhanced the mRNA stability of PDK1 and induced gefitinib resistance in lung cancer. (A) The level of total M 6 A in PC-9 and PC-9/G cells was detected by dot blotting. (B) The mRNA and protein expression levels of METTL16 were tested by quantitative reverse transcription PCR and Western blotting in PC-9 and PC-9/G cells. (C) The protein expression levels of METTL16 were tested by Western blotting in PC-9, PC-9/OR, HCC827, and HCC827/OR cell lines. (D) After silencing METTL16 in PC-9G cells, the sensitivity to gefitinib increased. (E) The apoptosis rates were determined by flow cytometry, and METTL16 knockdown in PC-9/G cells induced higher apoptosis rates. (F) 3-DAA treatment in PC-9 and PC-9/G cells reduced the expression levels of PDK1. (G) Overexpression of METTL16 in PC-9 cells showed increased expression of PDK1, and knockdown of METTL16 in PC-9/G cells showed reduced expression of PDK1. (H) PDK1 mRNA levels were determined by semi-PCR in PC-9/G cells (control and METTL16-silenced) after <t>actinomycin</t> <t>D</t> treatment (normalized to 0 h). (I) Relative wild-type (WT) or mutated (Mut) luciferase activities in METTL16-overexpressed PC-9 cells were determined by normalizing the values to those of the negative control group. (J) The RNA immunoprecipitation assay showed that total m 6 A antibody levels were enriched on PDK1 mRNA, but were significantly decreased after METTL16 silencing. Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.
    Actinomycin D, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1198 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/actinomycin+d/pmc13091346-53-2-4?v=MedChemExpress
    Average 98 stars, based on 1198 article reviews
    actinomycin d - by Bioz Stars, 2026-07
    98/100 stars

    Images

    1) Product Images from "PDK1 elevation was induced by epigenetic modifications of KDM3A and METTL16 to mediate TKI resistance and cancer development"

    Article Title: PDK1 elevation was induced by epigenetic modifications of KDM3A and METTL16 to mediate TKI resistance and cancer development

    Journal: Genes & Diseases

    doi: 10.1016/j.gendis.2025.101947

    RNA m 6 A methyltransferase METTL16 enhanced the mRNA stability of PDK1 and induced gefitinib resistance in lung cancer. (A) The level of total M 6 A in PC-9 and PC-9/G cells was detected by dot blotting. (B) The mRNA and protein expression levels of METTL16 were tested by quantitative reverse transcription PCR and Western blotting in PC-9 and PC-9/G cells. (C) The protein expression levels of METTL16 were tested by Western blotting in PC-9, PC-9/OR, HCC827, and HCC827/OR cell lines. (D) After silencing METTL16 in PC-9G cells, the sensitivity to gefitinib increased. (E) The apoptosis rates were determined by flow cytometry, and METTL16 knockdown in PC-9/G cells induced higher apoptosis rates. (F) 3-DAA treatment in PC-9 and PC-9/G cells reduced the expression levels of PDK1. (G) Overexpression of METTL16 in PC-9 cells showed increased expression of PDK1, and knockdown of METTL16 in PC-9/G cells showed reduced expression of PDK1. (H) PDK1 mRNA levels were determined by semi-PCR in PC-9/G cells (control and METTL16-silenced) after actinomycin D treatment (normalized to 0 h). (I) Relative wild-type (WT) or mutated (Mut) luciferase activities in METTL16-overexpressed PC-9 cells were determined by normalizing the values to those of the negative control group. (J) The RNA immunoprecipitation assay showed that total m 6 A antibody levels were enriched on PDK1 mRNA, but were significantly decreased after METTL16 silencing. Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.
    Figure Legend Snippet: RNA m 6 A methyltransferase METTL16 enhanced the mRNA stability of PDK1 and induced gefitinib resistance in lung cancer. (A) The level of total M 6 A in PC-9 and PC-9/G cells was detected by dot blotting. (B) The mRNA and protein expression levels of METTL16 were tested by quantitative reverse transcription PCR and Western blotting in PC-9 and PC-9/G cells. (C) The protein expression levels of METTL16 were tested by Western blotting in PC-9, PC-9/OR, HCC827, and HCC827/OR cell lines. (D) After silencing METTL16 in PC-9G cells, the sensitivity to gefitinib increased. (E) The apoptosis rates were determined by flow cytometry, and METTL16 knockdown in PC-9/G cells induced higher apoptosis rates. (F) 3-DAA treatment in PC-9 and PC-9/G cells reduced the expression levels of PDK1. (G) Overexpression of METTL16 in PC-9 cells showed increased expression of PDK1, and knockdown of METTL16 in PC-9/G cells showed reduced expression of PDK1. (H) PDK1 mRNA levels were determined by semi-PCR in PC-9/G cells (control and METTL16-silenced) after actinomycin D treatment (normalized to 0 h). (I) Relative wild-type (WT) or mutated (Mut) luciferase activities in METTL16-overexpressed PC-9 cells were determined by normalizing the values to those of the negative control group. (J) The RNA immunoprecipitation assay showed that total m 6 A antibody levels were enriched on PDK1 mRNA, but were significantly decreased after METTL16 silencing. Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Techniques Used: Expressing, Reverse Transcription, Western Blot, Flow Cytometry, Knockdown, Over Expression, Control, Luciferase, Negative Control, RNA Immunoprecipitation, Standard Deviation



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    RNA m 6 A methyltransferase METTL16 enhanced the mRNA stability of PDK1 and induced gefitinib resistance in lung cancer. (A) The level of total M 6 A in PC-9 and PC-9/G cells was detected by dot blotting. (B) The mRNA and protein expression levels of METTL16 were tested by quantitative reverse transcription PCR and Western blotting in PC-9 and PC-9/G cells. (C) The protein expression levels of METTL16 were tested by Western blotting in PC-9, PC-9/OR, HCC827, and HCC827/OR cell lines. (D) After silencing METTL16 in PC-9G cells, the sensitivity to gefitinib increased. (E) The apoptosis rates were determined by flow cytometry, and METTL16 knockdown in PC-9/G cells induced higher apoptosis rates. (F) 3-DAA treatment in PC-9 and PC-9/G cells reduced the expression levels of PDK1. (G) Overexpression of METTL16 in PC-9 cells showed increased expression of PDK1, and knockdown of METTL16 in PC-9/G cells showed reduced expression of PDK1. (H) PDK1 mRNA levels were determined by semi-PCR in PC-9/G cells (control and METTL16-silenced) after <t>actinomycin</t> <t>D</t> treatment (normalized to 0 h). (I) Relative wild-type (WT) or mutated (Mut) luciferase activities in METTL16-overexpressed PC-9 cells were determined by normalizing the values to those of the negative control group. (J) The RNA immunoprecipitation assay showed that total m 6 A antibody levels were enriched on PDK1 mRNA, but were significantly decreased after METTL16 silencing. Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.
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    RNA m 6 A methyltransferase METTL16 enhanced the mRNA stability of PDK1 and induced gefitinib resistance in lung cancer. (A) The level of total M 6 A in PC-9 and PC-9/G cells was detected by dot blotting. (B) The mRNA and protein expression levels of METTL16 were tested by quantitative reverse transcription PCR and Western blotting in PC-9 and PC-9/G cells. (C) The protein expression levels of METTL16 were tested by Western blotting in PC-9, PC-9/OR, HCC827, and HCC827/OR cell lines. (D) After silencing METTL16 in PC-9G cells, the sensitivity to gefitinib increased. (E) The apoptosis rates were determined by flow cytometry, and METTL16 knockdown in PC-9/G cells induced higher apoptosis rates. (F) 3-DAA treatment in PC-9 and PC-9/G cells reduced the expression levels of PDK1. (G) Overexpression of METTL16 in PC-9 cells showed increased expression of PDK1, and knockdown of METTL16 in PC-9/G cells showed reduced expression of PDK1. (H) PDK1 mRNA levels were determined by semi-PCR in PC-9/G cells (control and METTL16-silenced) after <t>actinomycin</t> <t>D</t> treatment (normalized to 0 h). (I) Relative wild-type (WT) or mutated (Mut) luciferase activities in METTL16-overexpressed PC-9 cells were determined by normalizing the values to those of the negative control group. (J) The RNA immunoprecipitation assay showed that total m 6 A antibody levels were enriched on PDK1 mRNA, but were significantly decreased after METTL16 silencing. Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.
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    RNA m 6 A methyltransferase METTL16 enhanced the mRNA stability of PDK1 and induced gefitinib resistance in lung cancer. (A) The level of total M 6 A in PC-9 and PC-9/G cells was detected by dot blotting. (B) The mRNA and protein expression levels of METTL16 were tested by quantitative reverse transcription PCR and Western blotting in PC-9 and PC-9/G cells. (C) The protein expression levels of METTL16 were tested by Western blotting in PC-9, PC-9/OR, HCC827, and HCC827/OR cell lines. (D) After silencing METTL16 in PC-9G cells, the sensitivity to gefitinib increased. (E) The apoptosis rates were determined by flow cytometry, and METTL16 knockdown in PC-9/G cells induced higher apoptosis rates. (F) 3-DAA treatment in PC-9 and PC-9/G cells reduced the expression levels of PDK1. (G) Overexpression of METTL16 in PC-9 cells showed increased expression of PDK1, and knockdown of METTL16 in PC-9/G cells showed reduced expression of PDK1. (H) PDK1 mRNA levels were determined by semi-PCR in PC-9/G cells (control and METTL16-silenced) after actinomycin D treatment (normalized to 0 h). (I) Relative wild-type (WT) or mutated (Mut) luciferase activities in METTL16-overexpressed PC-9 cells were determined by normalizing the values to those of the negative control group. (J) The RNA immunoprecipitation assay showed that total m 6 A antibody levels were enriched on PDK1 mRNA, but were significantly decreased after METTL16 silencing. Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Journal: Genes & Diseases

    Article Title: PDK1 elevation was induced by epigenetic modifications of KDM3A and METTL16 to mediate TKI resistance and cancer development

    doi: 10.1016/j.gendis.2025.101947

    Figure Lengend Snippet: RNA m 6 A methyltransferase METTL16 enhanced the mRNA stability of PDK1 and induced gefitinib resistance in lung cancer. (A) The level of total M 6 A in PC-9 and PC-9/G cells was detected by dot blotting. (B) The mRNA and protein expression levels of METTL16 were tested by quantitative reverse transcription PCR and Western blotting in PC-9 and PC-9/G cells. (C) The protein expression levels of METTL16 were tested by Western blotting in PC-9, PC-9/OR, HCC827, and HCC827/OR cell lines. (D) After silencing METTL16 in PC-9G cells, the sensitivity to gefitinib increased. (E) The apoptosis rates were determined by flow cytometry, and METTL16 knockdown in PC-9/G cells induced higher apoptosis rates. (F) 3-DAA treatment in PC-9 and PC-9/G cells reduced the expression levels of PDK1. (G) Overexpression of METTL16 in PC-9 cells showed increased expression of PDK1, and knockdown of METTL16 in PC-9/G cells showed reduced expression of PDK1. (H) PDK1 mRNA levels were determined by semi-PCR in PC-9/G cells (control and METTL16-silenced) after actinomycin D treatment (normalized to 0 h). (I) Relative wild-type (WT) or mutated (Mut) luciferase activities in METTL16-overexpressed PC-9 cells were determined by normalizing the values to those of the negative control group. (J) The RNA immunoprecipitation assay showed that total m 6 A antibody levels were enriched on PDK1 mRNA, but were significantly decreased after METTL16 silencing. Data were statistically analyzed with Student’s t -test, and values were shown as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Article Snippet: 5 μg/mL actinomycin D (MedChemExpress, Shanghai, China) was used to treat indicated cells for 0 h, 2 h, 4 h, 6 h, 8 h, and 16 h, followed by RNA extraction.

    Techniques: Expressing, Reverse Transcription, Western Blot, Flow Cytometry, Knockdown, Over Expression, Control, Luciferase, Negative Control, RNA Immunoprecipitation, Standard Deviation