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Sangon Biotech hcc827 cells
Hcc827 Cells, supplied by Sangon Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hcc827+cells/cells+hcc827/pm42097097-104-7-12
Average 86 stars, based on 1 article reviews
hcc827 cells - by Bioz Stars, 2026-09
86/100 stars

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Transfection:

Article Title: Single-cell and spatial transcriptomic profiling of POU5F1 in Lung Adenocarcinoma: Dynamics, spatial niche, and prognosis via multi-algorithm ML.
Article Snippet: .. siRNA transfection was performed on NCI-H1975 and HCC827 cells. siRNA reagents from Sangon Biotech were used for transient knockdown of POU5F1 gene expression, with a negative control siRNA (si-NC) established. .. The procedure was as follows: When cells in six-well plates reached 80% confluence, lipo3000 transfection reagent and siRNA were diluted in Opti-MEM medium (Thermo Fisher).

Knockdown:

Article Title: Single-cell and spatial transcriptomic profiling of POU5F1 in Lung Adenocarcinoma: Dynamics, spatial niche, and prognosis via multi-algorithm ML.
Article Snippet: .. siRNA transfection was performed on NCI-H1975 and HCC827 cells. siRNA reagents from Sangon Biotech were used for transient knockdown of POU5F1 gene expression, with a negative control siRNA (si-NC) established. .. The procedure was as follows: When cells in six-well plates reached 80% confluence, lipo3000 transfection reagent and siRNA were diluted in Opti-MEM medium (Thermo Fisher).

Gene Expression:

Article Title: Single-cell and spatial transcriptomic profiling of POU5F1 in Lung Adenocarcinoma: Dynamics, spatial niche, and prognosis via multi-algorithm ML.
Article Snippet: .. siRNA transfection was performed on NCI-H1975 and HCC827 cells. siRNA reagents from Sangon Biotech were used for transient knockdown of POU5F1 gene expression, with a negative control siRNA (si-NC) established. .. The procedure was as follows: When cells in six-well plates reached 80% confluence, lipo3000 transfection reagent and siRNA were diluted in Opti-MEM medium (Thermo Fisher).

Negative Control:

Article Title: Single-cell and spatial transcriptomic profiling of POU5F1 in Lung Adenocarcinoma: Dynamics, spatial niche, and prognosis via multi-algorithm ML.
Article Snippet: .. siRNA transfection was performed on NCI-H1975 and HCC827 cells. siRNA reagents from Sangon Biotech were used for transient knockdown of POU5F1 gene expression, with a negative control siRNA (si-NC) established. .. The procedure was as follows: When cells in six-well plates reached 80% confluence, lipo3000 transfection reagent and siRNA were diluted in Opti-MEM medium (Thermo Fisher).



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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. <t>HCC827;</t> ^ 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.
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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. <t>HCC827;</t> ^ 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.
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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. <t>HCC827;</t> ^ 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.
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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. <t>HCC827;</t> ^ 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.
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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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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

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.

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