hcc827  (ATCC)

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: Glycolysis gatekeeper PDK1 was an essential regulator of gefitinib resistance in lung cancer. (A) The PC-9 and PC-9/G cells were treated with various concentrations of gefitinib for 72 h, and cell viabilities were detected by CCK-8 assay. (B) PC-9/G cells induced higher glucose consumption and lactate production rates compared with PC-9 cells. (C) The mRNA and protein expression levels of PDK1 were tested by quantitative reverse transcription PCR and Western blotting in PC-9 and PC-9/G cell lines. (D) The protein expression levels of PDK1 were tested by Western blotting in PC-9, PC-9/OR, HCC827, and HCC827/OR cell lines. (E) Indicated cells were treated with gefitinib of different concentrations for 72 h, and PDK1 knockdown in PC-9/G cells rendered cells more sensitive to gefitinib, while forced expression of PDK1 in PC-9 cells made cells more resistant to gefitinib. (F) The apoptosis rates were determined by flow cytometry, and PDK1 knockdown in PC-9/G cells induced higher apoptosis rates. 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: The NSCLC cell lines PC-9 and HCC827 were purchased from the American Type Culture Collection.

Techniques: CCK-8 Assay, Expressing, Reverse Transcription, Western Blot, Knockdown, Flow Cytometry, Standard Deviation

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: Histone demethylase KDM3A induced the expression levels of PDK1 via H3K9me1 and H3K9me2 demethylation. (A) The analysis results of gene correlation analysis from the LUNG CANCER EXPLORER database showed that KDM3A was positively correlated with PDK1. (B) The Starbase database also confirmed that there was a positive correlation between KDM3A and PDK1. (C) The mRNA and protein expression levels of KDM3A were tested by quantitative reverse transcription PCR and Western blotting in PC-9 and PC-9/G cells. (D) The protein expression levels of KDM3A were tested by Western blotting in PC-9, PC-9/OR, HCC827, and HCC827/OR cell lines. (E) After silencing KDM3A in PC-9/G cells, the sensitivity of the cells to gefitinib increased. (F) The apoptosis rates were determined by flow cytometry, and KDM3A knockdown in PC-9/G cells induced higher apoptosis rates. (G) KDM3A knockdown in PC-9/G cells reduced the expression levels of PDK1, while the expression levels of H3K9me1 and H3K9me2 were increased. (H) The ENCODE database showed there were binding peaks of H3K9me1, H3K9me2, and KDM3A at the promoter region of PDK1. (I) Chromatin immunoprecipitation assay was conducted to determine the binding sites of KDM3A at the promoter region of the PDK1 gene. Cross-linked and sheared chromatin was immunoprecipitated with anti-KDM3A/histone H3 antibody or IgG, and quantitative reverse transcription PCR was used to detect the enrichment percentages. 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: The NSCLC cell lines PC-9 and HCC827 were purchased from the American Type Culture Collection.

Techniques: Expressing, Reverse Transcription, Western Blot, Flow Cytometry, Knockdown, Binding Assay, Chromatin Immunoprecipitation, Immunoprecipitation, Standard Deviation

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: The NSCLC cell lines PC-9 and HCC827 were purchased from the American Type Culture Collection.

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

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of osimertinib on viability and tripartite motif containing 59 (TRIM59) expression, and the effects of eugenol on the viability and apoptosis of osimertinib-induced non-drug-resistant lung cancer cells and drug-resistant lung cancer cells. (a) Chemical structure of eugenol. (b, c) The resistance of lung cancer cells and drug-resistant cell lines to osimertinib, detected the activity by cell counting kit-8 (CCK-8) assay and calculated half maximal inhibitory concentration (IC50). (d–f) Western Blotting was used to detect the expression of TRIM59 in the cells of each group with different concentrations of osimertinib. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as an internal reference. (g–h) The viability of each group was detected by CCK-8 assay. (i–l) The apoptosis of each group was detected by flow cytometry assay. *** P < 0.001, vs. PC9; ++ P < 0.01, +++ P < 0.001, vs. HCC827; ^ P < 0.05, ^^ P < 0.01, ^^^ P < 0.001, vs. 0; ### P < 0.001, vs. PC9-AR; &&& P < 0.001, vs. HCC827-AR; △△△ P < 0.001, vs. PC9+Eugenol; ΩΩΩ P < 0.001, vs. HCC827+Eugenol.

Article Snippet: PC9 cells and HCC827 cells were treated with osimertinib (AZD9291; S7297, Selleck, Shanghai, China) to construct drug-resistant cell lines (PC9-AR and HCC827-AR) [ ].

Techniques: Expressing, Activity Assay, Cell Counting, CCK-8 Assay, Concentration Assay, Western Blot, Flow Cytometry

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on the proliferation, invasion, and migration of osimertinib-induced non-drug-resistant lung cancer cells and drug-resistant lung cancer cells. (a–d) The colony formation assay was used to examine the ability of cells to form colonies. (e–i) Transwell was used to detect cell migration and invasion ability. Magnification: 250×, scale bar: 50 μm. *** P < 0.001, vs. PC9; ++ P < 0.01, +++ P < 0.001, vs. HCC827; ### P < 0.001, vs. P C9-AR; &&& P < 0.001, vs. HCC827-AR; △△ P < 0.01, △△△ P < 0.001, vs. PC9+Eugenol; Ω P < 0.05, ΩΩ P < 0.01, vs. HCC827+Eugenol.

Article Snippet: PC9 cells and HCC827 cells were treated with osimertinib (AZD9291; S7297, Selleck, Shanghai, China) to construct drug-resistant cell lines (PC9-AR and HCC827-AR) [ ].

Techniques: Migration, Colony Assay

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on glucose consumption, lactic acid release, glycolysis, and TRIM59/extracellular signal-regulated kinase (ERK) expression in osimertinib-induced non-drug-resistant lung cancer cells and drug-resistant lung cancer cells. (a, b) Eugenol could reduce the glucose consumption of cells in each group. (c, d) Eugenol could reduce lactate release content. (e–i) Western blotting was used to detect the expression of glycolysis-related proteins, cellular-myelocytomatosis oncogene (c-Myc), and lactate dehydrogenase A (LDHA). GAPDH as an internal reference. (j–n) Western blotting was used to detect the expression of TRIM59/ERK in the resistance of lung cancer cells and drug-resistant cell lines to osimertinib that they were treated with eugenol. GAPDH as an internal reference. * P < 0.05, ** P < 0.01, *** P < 0.001, vs. PC; + P < 0.05, ++ P < 0.01, +++ P < 0.001, vs. HCC827; ## P < 0.01, ### P < 0.001, vs. PC9-AR; && P < 0.01, &&& P < 0.001, vs. HCC827-AR; △ P < 0.05, △△ P < 0.01, △△△ P < 0.001, vs. PC9+Eugenol; Ω P < 0.05, ΩΩ P < 0.01, vs. HCC827+Eugenol. GAPDH, glyceraldehyde-3-phosphate dehydrogenase; TRIM59, tripartite motif containing 59.

Article Snippet: PC9 cells and HCC827 cells were treated with osimertinib (AZD9291; S7297, Selleck, Shanghai, China) to construct drug-resistant cell lines (PC9-AR and HCC827-AR) [ ].

Techniques: Expressing, Western Blot

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Silencing of TRIM59 enhanced the effect of eugenol on the viability, glucose consumption, lactic acid release, and glycolysis expression of osimertinib-induced drug-resistant lung cancer cells. (a, b) siTRIM59 was transfected into the PC9-AR and HCC827-AR cells, the transfection efficiency was detected by qRT-PCR. GAPDH as an internal reference. (c, d) Cell viability that PC9-AR and HCC827-AR cells was treated with eugenol and transfected with siTRIM59 was detected by CCK-8. (e, f) A kit was used to detect the glucose uptake of cells in drug-resistant cell was treated with eugenol and transfected with siTRIM59. (g, h) The detection of intracellular lactate release was detected. (i–m) Western blotting was used to detect the expression of glycolysis-related proteins in the cells of each treatment group. GAPDH as an internal reference. * * P < 0.01, ** * P < 0.001, vs. PC9-AR+siNC; ++ P < 0.01, +++ P < 0.001, vs. HCC827-AR+siNC; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. PC9-AR+Eugenol; & P < 0.05, && P < 0.01, &&& P < 0.001, vs. HCC827-AR+Eugenol. CCK-8, cell counting kit-8; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; qRT-PCR, quantitative reverse transcription PCR; TRIM59, tripartite motif containing 59.

Article Snippet: PC9 cells and HCC827 cells were treated with osimertinib (AZD9291; S7297, Selleck, Shanghai, China) to construct drug-resistant cell lines (PC9-AR and HCC827-AR) [ ].

Techniques: Expressing, Transfection, Quantitative RT-PCR, CCK-8 Assay, Western Blot, Cell Counting, Reverse Transcription

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Silencing of TRIM59 enhanced the effect of eugenol on the TRIM59/ERK expression of osimertinib-induced drug-resistant lung cancer cells. (a–e) Western Blotting was used to detect the expression of TRIM59 and ERK-related proteins in osimertinib-induced PC9 and HCC827 cells. GAPDH as an internal reference. * P < 0.05, * * P < 0.01, vs. PC9-AR+siNC; ++ P < 0.01, +++ P < 0.001, vs. HCC827-AR+siNC; # P < 0.05, ### P < 0.001, vs. PC9-AR+Eugenol; && P < 0.01, &&& P < 0.001, vs. HCC827-AR+Eugenol. ERK, extracellular signal-regulated kinase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; TRIM59, tripartite motif containing 59.

Article Snippet: PC9 cells and HCC827 cells were treated with osimertinib (AZD9291; S7297, Selleck, Shanghai, China) to construct drug-resistant cell lines (PC9-AR and HCC827-AR) [ ].

Techniques: Expressing, Western Blot

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on the proliferation of osimertinib-induced drug-resistant lung cancer cells by regulating TRIM59/ERK expression. (a–c) Drug-resistant cell was treated with ERK inhibitor (LY3214996) and transfected with TRIM59 overexpression vector, the colony formation assay was used to detect the colony formation ability of PC9 and HCC827 cells. *** P < 0.001, vs. vector; + P < 0.05, +++ P < 0.001, vs. Eugenol; ### P < 0.001, vs. Eugenol+TRIM59; ^ P < 0.05, vs. Eugenol+LY3214996. ERK, extracellular signal-regulated kinase; TRIM59, tripartite motif containing 59.

Article Snippet: PC9 cells and HCC827 cells were treated with osimertinib (AZD9291; S7297, Selleck, Shanghai, China) to construct drug-resistant cell lines (PC9-AR and HCC827-AR) [ ].

Techniques: Expressing, Transfection, Over Expression, Plasmid Preparation, Colony Assay

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on the invasion and migration of osimertinib-induced drug-resistant lung cancer cells by regulating TRIM59/ERK expression. (a–c) Transwell was used to detect the migration and invasion ability of PC9-AR cells transfected with TRIM59 overexpression vector. Magnification: 250×, scale bar: 50 μm. (d–f) Transwell was used to detect the migration and invasion ability of HCC827-AR cells transfected with TRIM59 overexpression vector. Magnification: 250×, scale bar: 50 μm. *** P < 0.001, vs. vector; ++ P < 0.01, +++ P < 0.001, vs. Eugenol; ### P < 0.001, vs. Eugenol+TRIM59; ^ P < 0.05, ^^ P < 0.01, vs. Eugenol+LY3214996. ERK, extracellular signal-regulated kinase; TRIM59, tripartite motif containing 59.

Article Snippet: PC9 cells and HCC827 cells were treated with osimertinib (AZD9291; S7297, Selleck, Shanghai, China) to construct drug-resistant cell lines (PC9-AR and HCC827-AR) [ ].

Techniques: Migration, Expressing, Transfection, Over Expression, Plasmid Preparation

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on TRIM59/ERK expression in osimertinib-induced drug-resistant lung cancer cells by regulating TRIM59/ERK expression. (a–c) Western Blotting was used to detect the expression of TRIM59 and ERK-related proteins in osimertinib-induced PC9 Cells. GAPDH as an internal reference. (d–f) Western Blotting was used to detect the expression of TRIM59 and ERK-related proteins in osimertinib-induced HCC827 Cells. GAPDH as an internal reference. *** P < 0.001, vs. vector; ++ P < 0.01, +++ P < 0.001, vs. Eugenol; ^^ P < 0.01 vs. Eugenol+LY3214996; ### P < 0.001, vs. Eugenol+TRIM59. ERK, extracellular signal-regulated kinase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; TRIM59, tripartite motif containing 59.

Article Snippet: PC9 cells and HCC827 cells were treated with osimertinib (AZD9291; S7297, Selleck, Shanghai, China) to construct drug-resistant cell lines (PC9-AR and HCC827-AR) [ ].

Techniques: Expressing, Western Blot, Plasmid Preparation

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of osimertinib on viability and tripartite motif containing 59 (TRIM59) expression, and the effects of eugenol on the viability and apoptosis of osimertinib-induced non-drug-resistant lung cancer cells and drug-resistant lung cancer cells. (a) Chemical structure of eugenol. (b, c) The resistance of lung cancer cells and drug-resistant cell lines to osimertinib, detected the activity by cell counting kit-8 (CCK-8) assay and calculated half maximal inhibitory concentration (IC50). (d–f) Western Blotting was used to detect the expression of TRIM59 in the cells of each group with different concentrations of osimertinib. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as an internal reference. (g–h) The viability of each group was detected by CCK-8 assay. (i–l) The apoptosis of each group was detected by flow cytometry assay. *** P < 0.001, vs. PC9; ++ P < 0.01, +++ P < 0.001, vs. HCC827; ^ P < 0.05, ^^ P < 0.01, ^^^ P < 0.001, vs. 0; ### P < 0.001, vs. PC9-AR; &&& P < 0.001, vs. HCC827-AR; △△△ P < 0.001, vs. PC9+Eugenol; ΩΩΩ P < 0.001, vs. HCC827+Eugenol.

Article Snippet: Lung adenocarcinoma cell line HCC827 was ordered from the American Type Culture Collection (CRL-2868, Manassas, Virginia, USA).

Techniques: Expressing, Activity Assay, Cell Counting, CCK-8 Assay, Concentration Assay, Western Blot, Flow Cytometry

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on the proliferation, invasion, and migration of osimertinib-induced non-drug-resistant lung cancer cells and drug-resistant lung cancer cells. (a–d) The colony formation assay was used to examine the ability of cells to form colonies. (e–i) Transwell was used to detect cell migration and invasion ability. Magnification: 250×, scale bar: 50 μm. *** P < 0.001, vs. PC9; ++ P < 0.01, +++ P < 0.001, vs. HCC827; ### P < 0.001, vs. P C9-AR; &&& P < 0.001, vs. HCC827-AR; △△ P < 0.01, △△△ P < 0.001, vs. PC9+Eugenol; Ω P < 0.05, ΩΩ P < 0.01, vs. HCC827+Eugenol.

Article Snippet: Lung adenocarcinoma cell line HCC827 was ordered from the American Type Culture Collection (CRL-2868, Manassas, Virginia, USA).

Techniques: Migration, Colony Assay

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on glucose consumption, lactic acid release, glycolysis, and TRIM59/extracellular signal-regulated kinase (ERK) expression in osimertinib-induced non-drug-resistant lung cancer cells and drug-resistant lung cancer cells. (a, b) Eugenol could reduce the glucose consumption of cells in each group. (c, d) Eugenol could reduce lactate release content. (e–i) Western blotting was used to detect the expression of glycolysis-related proteins, cellular-myelocytomatosis oncogene (c-Myc), and lactate dehydrogenase A (LDHA). GAPDH as an internal reference. (j–n) Western blotting was used to detect the expression of TRIM59/ERK in the resistance of lung cancer cells and drug-resistant cell lines to osimertinib that they were treated with eugenol. GAPDH as an internal reference. * P < 0.05, ** P < 0.01, *** P < 0.001, vs. PC; + P < 0.05, ++ P < 0.01, +++ P < 0.001, vs. HCC827; ## P < 0.01, ### P < 0.001, vs. PC9-AR; && P < 0.01, &&& P < 0.001, vs. HCC827-AR; △ P < 0.05, △△ P < 0.01, △△△ P < 0.001, vs. PC9+Eugenol; Ω P < 0.05, ΩΩ P < 0.01, vs. HCC827+Eugenol. GAPDH, glyceraldehyde-3-phosphate dehydrogenase; TRIM59, tripartite motif containing 59.

Article Snippet: Lung adenocarcinoma cell line HCC827 was ordered from the American Type Culture Collection (CRL-2868, Manassas, Virginia, USA).

Techniques: Expressing, Western Blot

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Silencing of TRIM59 enhanced the effect of eugenol on the viability, glucose consumption, lactic acid release, and glycolysis expression of osimertinib-induced drug-resistant lung cancer cells. (a, b) siTRIM59 was transfected into the PC9-AR and HCC827-AR cells, the transfection efficiency was detected by qRT-PCR. GAPDH as an internal reference. (c, d) Cell viability that PC9-AR and HCC827-AR cells was treated with eugenol and transfected with siTRIM59 was detected by CCK-8. (e, f) A kit was used to detect the glucose uptake of cells in drug-resistant cell was treated with eugenol and transfected with siTRIM59. (g, h) The detection of intracellular lactate release was detected. (i–m) Western blotting was used to detect the expression of glycolysis-related proteins in the cells of each treatment group. GAPDH as an internal reference. * * P < 0.01, ** * P < 0.001, vs. PC9-AR+siNC; ++ P < 0.01, +++ P < 0.001, vs. HCC827-AR+siNC; # P < 0.05, ## P < 0.01, ### P < 0.001, vs. PC9-AR+Eugenol; & P < 0.05, && P < 0.01, &&& P < 0.001, vs. HCC827-AR+Eugenol. CCK-8, cell counting kit-8; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; qRT-PCR, quantitative reverse transcription PCR; TRIM59, tripartite motif containing 59.

Article Snippet: Lung adenocarcinoma cell line HCC827 was ordered from the American Type Culture Collection (CRL-2868, Manassas, Virginia, USA).

Techniques: Expressing, Transfection, Quantitative RT-PCR, CCK-8 Assay, Western Blot, Cell Counting, Reverse Transcription

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Silencing of TRIM59 enhanced the effect of eugenol on the TRIM59/ERK expression of osimertinib-induced drug-resistant lung cancer cells. (a–e) Western Blotting was used to detect the expression of TRIM59 and ERK-related proteins in osimertinib-induced PC9 and HCC827 cells. GAPDH as an internal reference. * P < 0.05, * * P < 0.01, vs. PC9-AR+siNC; ++ P < 0.01, +++ P < 0.001, vs. HCC827-AR+siNC; # P < 0.05, ### P < 0.001, vs. PC9-AR+Eugenol; && P < 0.01, &&& P < 0.001, vs. HCC827-AR+Eugenol. ERK, extracellular signal-regulated kinase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; TRIM59, tripartite motif containing 59.

Article Snippet: Lung adenocarcinoma cell line HCC827 was ordered from the American Type Culture Collection (CRL-2868, Manassas, Virginia, USA).

Techniques: Expressing, Western Blot

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on the proliferation of osimertinib-induced drug-resistant lung cancer cells by regulating TRIM59/ERK expression. (a–c) Drug-resistant cell was treated with ERK inhibitor (LY3214996) and transfected with TRIM59 overexpression vector, the colony formation assay was used to detect the colony formation ability of PC9 and HCC827 cells. *** P < 0.001, vs. vector; + P < 0.05, +++ P < 0.001, vs. Eugenol; ### P < 0.001, vs. Eugenol+TRIM59; ^ P < 0.05, vs. Eugenol+LY3214996. ERK, extracellular signal-regulated kinase; TRIM59, tripartite motif containing 59.

Article Snippet: Lung adenocarcinoma cell line HCC827 was ordered from the American Type Culture Collection (CRL-2868, Manassas, Virginia, USA).

Techniques: Expressing, Transfection, Over Expression, Plasmid Preparation, Colony Assay

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on the invasion and migration of osimertinib-induced drug-resistant lung cancer cells by regulating TRIM59/ERK expression. (a–c) Transwell was used to detect the migration and invasion ability of PC9-AR cells transfected with TRIM59 overexpression vector. Magnification: 250×, scale bar: 50 μm. (d–f) Transwell was used to detect the migration and invasion ability of HCC827-AR cells transfected with TRIM59 overexpression vector. Magnification: 250×, scale bar: 50 μm. *** P < 0.001, vs. vector; ++ P < 0.01, +++ P < 0.001, vs. Eugenol; ### P < 0.001, vs. Eugenol+TRIM59; ^ P < 0.05, ^^ P < 0.01, vs. Eugenol+LY3214996. ERK, extracellular signal-regulated kinase; TRIM59, tripartite motif containing 59.

Article Snippet: Lung adenocarcinoma cell line HCC827 was ordered from the American Type Culture Collection (CRL-2868, Manassas, Virginia, USA).

Techniques: Migration, Expressing, Transfection, Over Expression, Plasmid Preparation

Journal: Anti-Cancer Drugs

Article Title: Eugenol as a game-changer: overcoming osimertinib resistance in non-small cell lung cancer by inhibiting glycolysis via the tripartite motif containing 59/extracellular signal-regulated kinase pathway

doi: 10.1097/CAD.0000000000001793

Figure Lengend Snippet: Effects of eugenol on TRIM59/ERK expression in osimertinib-induced drug-resistant lung cancer cells by regulating TRIM59/ERK expression. (a–c) Western Blotting was used to detect the expression of TRIM59 and ERK-related proteins in osimertinib-induced PC9 Cells. GAPDH as an internal reference. (d–f) Western Blotting was used to detect the expression of TRIM59 and ERK-related proteins in osimertinib-induced HCC827 Cells. GAPDH as an internal reference. *** P < 0.001, vs. vector; ++ P < 0.01, +++ P < 0.001, vs. Eugenol; ^^ P < 0.01 vs. Eugenol+LY3214996; ### P < 0.001, vs. Eugenol+TRIM59. ERK, extracellular signal-regulated kinase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; TRIM59, tripartite motif containing 59.

Article Snippet: Lung adenocarcinoma cell line HCC827 was ordered from the American Type Culture Collection (CRL-2868, Manassas, Virginia, USA).

Techniques: Expressing, Western Blot, Plasmid Preparation