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ATCC experimental models pc9 cell line ecacc 90071810 nci h1975 cell line atcc crl 5908 hcc4006 cell line atcc crl
Experimental Models Pc9 Cell Line Ecacc 90071810 Nci H1975 Cell Line Atcc Crl 5908 Hcc4006 Cell Line Atcc Crl, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1722 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pc9+cell+line/NCI-H1975/pm41023502-214-12-22
Average 97 stars, based on 1722 article reviews

experimental models pc9 cell line ecacc 90071810 nci h1975 cell line atcc crl 5908 hcc4006 cell line atcc crl - by Bioz Stars, 2026-11

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Article Title: Gilteritinib overcomes lorlatinib resistance in ALK -rearranged cancer
Article Snippet: Each experiment was designed with proper controls, and samples for comparison were collected and analyzed under the same conditions Primary antibodies for western blot: anti-ALK Ab: Cell Signaling Technology, Cat# 3633, Lot: 9 anti-phospho-ALK Ab (Y1604): Cell Signaling Technology, Cat# 3Y1282/1283); Cell Signaling Technology, Cat# 9687, Lot: 1 anti-S6 ribosomal protein Ab: Cell Signaling Technology, Cat# 217, Lot: 10 anti-phospho-S6 ribosomal protein Ab: Cell Signaling Technology, Cat# 5364, Lot: 8 anti-p42/44 ERK/MAPK Ab: Cell Signaling Technology, Cat# 9102, Lot: 27 anti-phospho-p42/44 ERK/MAPK Ab: Cell Signaling Technology, Cat# 9101, Lot: 30 anti-AKT Ab: Cell Signaling Technology, Cat# 4691, Lot: 20 anti-phospho-AKT Ab: Cell Signaling Technology, Cat# 4060, Lot: 25 anti-EGFR Ab: Cell Signaling Technology, Cat# 4267, Lot: 17 anti-phospho-EGFR Ab: Abcam, Cat# ab5644, Lot: GR3333992-1 anti-MEK1/2 Ab: Cell Signaling Technology, Cat# 9122, Lot: 12 anti-phospho-MEK1/2 Ab: Cell Signaling Technology, Cat# 9121, Lot: 56 anti-PARP Ab: Cell Signaling Technology, Cat# 9542, Lot: 15 anti-AXL Ab: Cell Signaling Technology, Cat# 4566, Lot: 2 anti-phospho-AXL Ab: Cell Signaling Technology, Cat# 5724, Lot:1 anti-KRAS Ab: Sigma-Aldrich, Cat# WH0003845M1, Lot: J5281-S2 anti-NTRK1 Ab: Cell Signaling Technology, Cat# 4609, Lot: 3 anti-phospho-NTRK1 Ab: Cell Signaling Technology, Cat# 4621, Lot: 3 3 n atu re research | rep o rtin g su m m ary A p ril2020 Validation Eukaryotic cell lines Policy information about cell lines Cell line source(s) Authentication Mycoplasma contamination Commonly misidentified lines (See ICLAC register) Animals and other organisms Policy information about studies involving animals; ARRIVE guidelines recommended for reporting animal research Laboratory animals Wild animals Field-collected samples Ethics oversight Note that full information on the approval of the study protocol must also be provided in the manuscript. anti-STAT3 Ab: Cell Signaling Technology, Cat# 4904, Lot: 7 anti-phospho-STAT3 Ab: Cell Signaling Technology, Cat# 9145, Lot: 22 anti-GAPDH Ab: Millipore, Cat# MAB374, Lot: 3527693 Secondary antibodies for western blot: anti-rabbit IgG Ab: Sigma-Aldrich, Cat# NA934V, Lot: 17197685 anti-mouse IgG Ab: Sigma-Aldrich, Cat# NA931V, Lot: 17061154 All antibodies were obtained commercially and had been validated by the companies. .. 293FT cell line (purchased from Thermo Fischer Scientific) Ba/F3 cell line (purchased from Riken BRC cell bank) NIH3T3 cell line (kindly gifted by Dr Tsuruo T) A431 cell line (kindly gifted by Dr Tsuruo T) H2228 cell line (purchased from ATCC) H3122 cell line (kindly gifted by Dr. Engelman JA) KM12 cell line (obtained from NCI) HCC827 cell line (purchased from ATCC) PC9 cell line (kindly gifted by Dr. Nishio K) A549 cell line (obtained from NCI) H460 cell line (obtained from NCI) HCC78 cell line (purchased from DSMZ) KARPAS299 cell line (purchased from ECACC) TIG-3 cell line (kindly gifted by Dr. Kaji K) JFCR-018-1 cells were established from EML4-ALK positive NSCLC patient JFCR-028-3 cells were established from EML4-ALK positive NSCLC patient MCC-003 cells were established from EML4-ALK positive NSCLC patient JFCR-168 cells were established from CD74-ROS1 positive NSCLC patient JFCR-256-3 cells were established from BRAF V600E positive NSCLC patient MR347 cells were established from EML4-ALK positive NSCLC patient JFCR-098 cells were established from EML4-ALK positive NSCLC patient Patient derived cell lines were confirmed by the sequencing of driver oncogenes. ..

Article Title: Long Noncoding RNA TALAM1 Is a Transcriptional Target of the RUNX2 Transcription Factor in Lung Adenocarcinoma
Article Snippet: The human alveolar basal epithelial cell adenocarcinoma cell line A549 (ATCC ® CCL-185TM) was cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 5% antibiotic solution (ampicillin and streptomycin). .. The PC9 cell line (ATCC CRM HTB-174D TM ) is derived from the lung tissue of a human patient with adenocarcinoma (undifferentiated type) (ECACC 2019). ..

Article Title: Long Noncoding RNA TALAM1 Is a Transcriptional Target of the RUNX2 Transcription Factor in Lung Adenocarcinoma.
Article Snippet: The human alveolar basal epithelial cell adenocarcinoma cell line A549 (ATCC® CCL185TM) was cultured in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 5% antibiotic solution (ampicillin and streptomycin). .. The PC9 cell line (ATCC CRM HTB-174DTM) is derived from the lung tissue of a human patient with adenocarcinoma (undifferentiated type) (ECACC 2019). ..

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USP5 promotes malignant proliferation and tumor growth in LUAD (A) Western blot analysis of USP5 protein levels in H1299, PC9, and H1650 cells following lentiviral-mediated knockdown or overexpression. (B) Representative images and quantification of EdU incorporation assays evaluating proliferative activity upon USP5 modulation. (C) Cell viability measured by CCK-8 assays in LUAD cells with USP5 knockdown or overexpression over time. (D) Colony formation capacity of LUAD cells after USP5 modulation (representative images and quantified results). (E) Representative excised tumors from nude mice at the experimental endpoint (day 24 post-injection). (F) Tumor volume measured every 4 days from day 7 post-injection. (G) Final tumor weights and volumes from the xenograft mouse model. Data are expressed as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; triplicate experiments.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: USP5 promotes malignant proliferation and tumor growth in LUAD (A) Western blot analysis of USP5 protein levels in H1299, PC9, and H1650 cells following lentiviral-mediated knockdown or overexpression. (B) Representative images and quantification of EdU incorporation assays evaluating proliferative activity upon USP5 modulation. (C) Cell viability measured by CCK-8 assays in LUAD cells with USP5 knockdown or overexpression over time. (D) Colony formation capacity of LUAD cells after USP5 modulation (representative images and quantified results). (E) Representative excised tumors from nude mice at the experimental endpoint (day 24 post-injection). (F) Tumor volume measured every 4 days from day 7 post-injection. (G) Final tumor weights and volumes from the xenograft mouse model. Data are expressed as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; triplicate experiments.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Western Blot, Knockdown, Over Expression, Activity Assay, CCK-8 Assay, Injection

USP5 drives aggressive malignant phenotypes in LUAD by enhancing invasion, suppressing apoptosis, and inducing EMT (A) Wound healing assays demonstrating that USP5 knockdown impairs migration in H1299 cells, while its overexpression enhances migration in H1650 cells. Scale bars: 100 μm. (B) Transwell invasion assays showing that USP5 knockdown reduces invasion, whereas its overexpression increases invasion in the respective cell lines. Scale bars: 100 μm. (C) Flow cytometric analysis indicating that USP5 knockdown promotes apoptosis in H1299 and PC9 cells. (D) Western blot analysis of epithelial-mesenchymal transition and apoptosis-related protein expression following USP5 knockdown in H1299 cells. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: USP5 drives aggressive malignant phenotypes in LUAD by enhancing invasion, suppressing apoptosis, and inducing EMT (A) Wound healing assays demonstrating that USP5 knockdown impairs migration in H1299 cells, while its overexpression enhances migration in H1650 cells. Scale bars: 100 μm. (B) Transwell invasion assays showing that USP5 knockdown reduces invasion, whereas its overexpression increases invasion in the respective cell lines. Scale bars: 100 μm. (C) Flow cytometric analysis indicating that USP5 knockdown promotes apoptosis in H1299 and PC9 cells. (D) Western blot analysis of epithelial-mesenchymal transition and apoptosis-related protein expression following USP5 knockdown in H1299 cells. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Knockdown, Migration, Over Expression, Western Blot, Expressing, Control

USP5 interacts with and post-transcriptionally stabilizes CD73 in LUAD (A) Co-immunoprecipitation (CoIP) of USP5 from H1299 lysates followed by mass spectrometry (MS) analysis of Coomassie-stained bands identifies CD73 as a potential interacting partner. (B) Specificity control: CoIP shows no interaction between USP5 and the glycolytic enzymes TPI1, PKM, or PGK1. (C and D) Endogenous coIP confirms the USP5-CD73 interaction in H1299 LUAD cells (C) and PC9 LUAD cells (D). (E–G) Exogenous coIP validates the direct interaction in HEK-293T cells (E and F) and LUAD cells (G) co-expressing Flag-USP5 and His-CD73. (H) USP5 and CD73 protein levels are coordinately upregulated in LUAD cell lines compared to normal bronchial epithelial cells (HBE135-E6E7). (I) USP5 knockdown or overexpression does not alter CD73 mRNA levels (RT-qPCR). (J–M) USP5 positively regulates CD73 protein expression, as shown by its levels upon USP5 knockdown or overexpression. (J and K) CD73 levels decreased upon USP5 knockdown. (L and M) CD73 levels increased upon USP5 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: USP5 interacts with and post-transcriptionally stabilizes CD73 in LUAD (A) Co-immunoprecipitation (CoIP) of USP5 from H1299 lysates followed by mass spectrometry (MS) analysis of Coomassie-stained bands identifies CD73 as a potential interacting partner. (B) Specificity control: CoIP shows no interaction between USP5 and the glycolytic enzymes TPI1, PKM, or PGK1. (C and D) Endogenous coIP confirms the USP5-CD73 interaction in H1299 LUAD cells (C) and PC9 LUAD cells (D). (E–G) Exogenous coIP validates the direct interaction in HEK-293T cells (E and F) and LUAD cells (G) co-expressing Flag-USP5 and His-CD73. (H) USP5 and CD73 protein levels are coordinately upregulated in LUAD cell lines compared to normal bronchial epithelial cells (HBE135-E6E7). (I) USP5 knockdown or overexpression does not alter CD73 mRNA levels (RT-qPCR). (J–M) USP5 positively regulates CD73 protein expression, as shown by its levels upon USP5 knockdown or overexpression. (J and K) CD73 levels decreased upon USP5 knockdown. (L and M) CD73 levels increased upon USP5 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Immunoprecipitation, Mass Spectrometry, Staining, Control, Expressing, Knockdown, Over Expression, Quantitative RT-PCR

USP5 reprograms glycolytic metabolism in LUAD (A) Principal component analysis of global metabolic profiles shows a clear separation between the control and USP5-knockdown H1299 cells. (B and C) Unsupervised analysis identifies significantly altered metabolites upon USP5 knockdown, displayed in a volcano plot (B) and heatmap (C). (D) Targeted metabolomics reveals an impaired glycolytic flux in USP5-knockdown cells, as indicated by the concurrent depletion of key glycolytic intermediates, including glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), pyruvate, and lactate. (E–I) Functional assessment of glycolysis using a Seahorse XF Analyzer. USP5 knockdown reduces the proton efflux rate (PER), basal glycolysis, and compensatory glycolysis in H1299 cells (E), PC9 cells (F), and HCC827-OR cells (I); USP5 overexpression enhances these parameters in H1650 cells (G) and HCC827 cells (H). (J) Consistent with the functional data, extracellular lactate secretion decreased by USP5 knockdown and increased by USP5 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: USP5 reprograms glycolytic metabolism in LUAD (A) Principal component analysis of global metabolic profiles shows a clear separation between the control and USP5-knockdown H1299 cells. (B and C) Unsupervised analysis identifies significantly altered metabolites upon USP5 knockdown, displayed in a volcano plot (B) and heatmap (C). (D) Targeted metabolomics reveals an impaired glycolytic flux in USP5-knockdown cells, as indicated by the concurrent depletion of key glycolytic intermediates, including glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), pyruvate, and lactate. (E–I) Functional assessment of glycolysis using a Seahorse XF Analyzer. USP5 knockdown reduces the proton efflux rate (PER), basal glycolysis, and compensatory glycolysis in H1299 cells (E), PC9 cells (F), and HCC827-OR cells (I); USP5 overexpression enhances these parameters in H1650 cells (G) and HCC827 cells (H). (J) Consistent with the functional data, extracellular lactate secretion decreased by USP5 knockdown and increased by USP5 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Control, Knockdown, Functional Assay, Over Expression

The USP5-CD73 axis drives glycolytic flux by modulating key glycolytic effectors (A) USP5 knockdown reduces, while its overexpression increases, the protein levels of CD73, phosphorylated EGFR ( p -EGFR), and key glycolytic enzymes. (B) CD73 knockdown recapitulates the effect of USP5 knockdown on p -EGFR and glycolytic effector expression. (C) Osimertinib-resistant HCC827-RO cells exhibit elevated levels of USP5, CD73, p -EGFR, and glycolytic proteins compared to their sensitive counterparts. (D and E) Functional assessment of glycolysis using a Seahorse XF Analyzer. (D) CD73 knockdown reduces the proton efflux rate (PER), basal glycolysis, and compensatory glycolysis in H1299 cells. (E) CD73 knockdown reduces the PER, basal glycolysis, and compensatory glycolysis in PC9 cells. (F and G) Reconstitution of CD73 expression in USP5-knockdown H1299 cells (F) and USP5-knockdown PC9 cells (G) rescues the impaired glycolytic function. (H and I) Consistent with the functional assays, CD73 knockdown decreases extracellular lactate secretion (H), while CD73 overexpression restores extracellular lactate secretion (I) in USP5-deficient cells. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: The USP5-CD73 axis drives glycolytic flux by modulating key glycolytic effectors (A) USP5 knockdown reduces, while its overexpression increases, the protein levels of CD73, phosphorylated EGFR ( p -EGFR), and key glycolytic enzymes. (B) CD73 knockdown recapitulates the effect of USP5 knockdown on p -EGFR and glycolytic effector expression. (C) Osimertinib-resistant HCC827-RO cells exhibit elevated levels of USP5, CD73, p -EGFR, and glycolytic proteins compared to their sensitive counterparts. (D and E) Functional assessment of glycolysis using a Seahorse XF Analyzer. (D) CD73 knockdown reduces the proton efflux rate (PER), basal glycolysis, and compensatory glycolysis in H1299 cells. (E) CD73 knockdown reduces the PER, basal glycolysis, and compensatory glycolysis in PC9 cells. (F and G) Reconstitution of CD73 expression in USP5-knockdown H1299 cells (F) and USP5-knockdown PC9 cells (G) rescues the impaired glycolytic function. (H and I) Consistent with the functional assays, CD73 knockdown decreases extracellular lactate secretion (H), while CD73 overexpression restores extracellular lactate secretion (I) in USP5-deficient cells. Data are presented as the mean ± SD from n = 3 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus the respective control group.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Knockdown, Over Expression, Expressing, Functional Assay, Control

CD73 is a critical downstream effector for USP5-mediated oncogenic phenotypes in LUAD (A and C) USP5 knockdown in H1299 cells (A) and PC9 cells (C) impairs migration, invasion, and colony formation. These phenotypic defects are rescued by the concomitant overexpression of CD73, as assessed by transwell, wound healing, and colony formation assays (scale bars: 100 μm). (B and D) Cell viability (CCK-8 assays) in H1299 cells (B) and PC9 cells (D) is reduced upon USP5 knockdown but is restored by CD73 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Statistical comparisons are shown for relevant groups.

Journal: iScience

Article Title: USP5-mediated CD73 deubiquitination drives osimertinib resistance via PI3K/AKT and glycolysis activation in LUAD

doi: 10.1016/j.isci.2026.114916

Figure Lengend Snippet: CD73 is a critical downstream effector for USP5-mediated oncogenic phenotypes in LUAD (A and C) USP5 knockdown in H1299 cells (A) and PC9 cells (C) impairs migration, invasion, and colony formation. These phenotypic defects are rescued by the concomitant overexpression of CD73, as assessed by transwell, wound healing, and colony formation assays (scale bars: 100 μm). (B and D) Cell viability (CCK-8 assays) in H1299 cells (B) and PC9 cells (D) is reduced upon USP5 knockdown but is restored by CD73 overexpression. Data are presented as the mean ± SD from n = 3 independent experiments; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Statistical comparisons are shown for relevant groups.

Article Snippet: PC9 cell line , ServiceBio Co., Ltd. (Hubei, China) , Cat#STCC10210P.

Techniques: Knockdown, Migration, Over Expression, CCK-8 Assay

NTRK2 promotes malignant behavior of LUAD cells in vitro . (A) The expression of NTRK2 was verified by qRT-PCR at the transcriptional level in A549, A549/Taxol and PC9 cells. (B) Western blotting analysis was performed to validate the expression of NTRK2 protein in the above cells. (C) MTT showing the effect of NTRK2 knockdown on the proliferation of A549, A549/Taxol and PC9 cells. Data are shown as mean ± SD. Statistical analysis was performed by two-way ANOVA. (D) The effect of NTRK2 knockdown on colony formation ability of the above cells. The right histograms showed the number of colonies for each cell line as indicated. (E) Relative mRNA expression level of NTRK2 was determined by qRT-PCR in A549 and PC9 cells transfected with an empty vector (Vector) or an NTRK2-overexpressing plasmid (oe-NTRK2). (F) Protein expression level of NTRK2 was analyzed by Western blotting in the same set of transfected cells. (G) Cell proliferation was assessed by MTT assay in A549 and PC9 cells following NTRK2 overexpression. Data are presented as the mean ± SD. Statistical analysis was performed by two-way ANOVA. (H) The promoting effect of NTRK2 overexpression on colony formation in A549 and PC9 cells. The effect of NTRK2 knockdown on cell cycle distributions (I) and apoptosis (J) was examined by the flow cytometry. The histograms of cell cycle distributions and apoptosis are presented on the right side of their respective representative graphs. Data are presented as the mean ± SD. β-actin was used as an internal control for qRT-PCR. GAPDH was adopted as the internal control for Western blotting. * P < 0.05; ** P < 0.01; *** P < 0.001.

Journal: Translational Oncology

Article Title: NTRK2 promotes malignant progression and paclitaxel resistance of lung adenocarcinoma through targeting MYC/ABCF1 axis

doi: 10.1016/j.tranon.2025.102655

Figure Lengend Snippet: NTRK2 promotes malignant behavior of LUAD cells in vitro . (A) The expression of NTRK2 was verified by qRT-PCR at the transcriptional level in A549, A549/Taxol and PC9 cells. (B) Western blotting analysis was performed to validate the expression of NTRK2 protein in the above cells. (C) MTT showing the effect of NTRK2 knockdown on the proliferation of A549, A549/Taxol and PC9 cells. Data are shown as mean ± SD. Statistical analysis was performed by two-way ANOVA. (D) The effect of NTRK2 knockdown on colony formation ability of the above cells. The right histograms showed the number of colonies for each cell line as indicated. (E) Relative mRNA expression level of NTRK2 was determined by qRT-PCR in A549 and PC9 cells transfected with an empty vector (Vector) or an NTRK2-overexpressing plasmid (oe-NTRK2). (F) Protein expression level of NTRK2 was analyzed by Western blotting in the same set of transfected cells. (G) Cell proliferation was assessed by MTT assay in A549 and PC9 cells following NTRK2 overexpression. Data are presented as the mean ± SD. Statistical analysis was performed by two-way ANOVA. (H) The promoting effect of NTRK2 overexpression on colony formation in A549 and PC9 cells. The effect of NTRK2 knockdown on cell cycle distributions (I) and apoptosis (J) was examined by the flow cytometry. The histograms of cell cycle distributions and apoptosis are presented on the right side of their respective representative graphs. Data are presented as the mean ± SD. β-actin was used as an internal control for qRT-PCR. GAPDH was adopted as the internal control for Western blotting. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: Human LUAD cell lines PC9, A549 and its taxol-resistant strain A549/Taxol were purchased from Procell Life Science & Technology Co.,Ltd (Wuhan, China).

Techniques: In Vitro, Expressing, Quantitative RT-PCR, Western Blot, Knockdown, Transfection, Plasmid Preparation, MTT Assay, Over Expression, Flow Cytometry, Control

NTRK2 reduces the response of LUAD cells to paclitaxel in vitro. NTRK2-knockdown A549 and A549/Taxol cells (A), NTRK2-overexpressing A549 and PC9 cells (B) as well as control cells were subjected to dose-dependent paclitaxel treatment for 48 h. The cell viability was assessed via MTT assay, and the Reed-Muench method was adopted to calculate IC 50 values. (C) The cells with NTRK2 knockdown or overexpression mentioned above and their control cells were subjected to treatment with paclitaxel at indicated concentrations for a duration of 4 days or treatment with DMSO. MTT assays were conducted to evaluate the time-dependent proliferation of these cells. Data are shown as mean ± SD. Statistical analysis was performed by two-way ANOVA. NTRK2-knockdown A549/Taxol (D) and NTRK2-overexpressing A549 cells (E) were treated with paclitaxel at indicated concentrations to evaluate the effect of NTRK2 expression on the inhibitory effect of paclitaxel on clone formation. A549/Taxol cells with NTRK2 knockdown were treated with paclitaxel or DMSO for 24 h, and cell cycle distributions (F) and apoptosis (G) were analyzed by the flow cytometry. ** P < 0.01; *** P < 0.001.

Journal: Translational Oncology

Article Title: NTRK2 promotes malignant progression and paclitaxel resistance of lung adenocarcinoma through targeting MYC/ABCF1 axis

doi: 10.1016/j.tranon.2025.102655

Figure Lengend Snippet: NTRK2 reduces the response of LUAD cells to paclitaxel in vitro. NTRK2-knockdown A549 and A549/Taxol cells (A), NTRK2-overexpressing A549 and PC9 cells (B) as well as control cells were subjected to dose-dependent paclitaxel treatment for 48 h. The cell viability was assessed via MTT assay, and the Reed-Muench method was adopted to calculate IC 50 values. (C) The cells with NTRK2 knockdown or overexpression mentioned above and their control cells were subjected to treatment with paclitaxel at indicated concentrations for a duration of 4 days or treatment with DMSO. MTT assays were conducted to evaluate the time-dependent proliferation of these cells. Data are shown as mean ± SD. Statistical analysis was performed by two-way ANOVA. NTRK2-knockdown A549/Taxol (D) and NTRK2-overexpressing A549 cells (E) were treated with paclitaxel at indicated concentrations to evaluate the effect of NTRK2 expression on the inhibitory effect of paclitaxel on clone formation. A549/Taxol cells with NTRK2 knockdown were treated with paclitaxel or DMSO for 24 h, and cell cycle distributions (F) and apoptosis (G) were analyzed by the flow cytometry. ** P < 0.01; *** P < 0.001.

Article Snippet: Human LUAD cell lines PC9, A549 and its taxol-resistant strain A549/Taxol were purchased from Procell Life Science & Technology Co.,Ltd (Wuhan, China).

Techniques: In Vitro, Knockdown, Control, MTT Assay, Endpoint Dilution Assay, Over Expression, Expressing, Flow Cytometry

ABCF1 is a key target of NTRK2 in mediating resistance to paclitaxel in LUAD cells. The mRNA (A) and protein (B) expression levels of NTRK2 and ABCF1 in A549 and A549/Taxol cells were measured by qRT-PCR and Western blotting analysis, respectively. (C) Representative immunohistochemical staining of NTRK2 and ABCF1 in LUAD tissues (Case 1), paclitaxel-resistant LUAD tissues (Case 2) and their matched noncancerous lung tissues (MN). Scale bars: 50 μm. qRT-PCR (D) and Western blotting (E) analysis results showing the effect of NTRK2 knockdown on ABCF1 expression in A549 and A549/Taxol cell lines. qRT-PCR (F) and Western blotting (G) analysis results showing the effect of ectopic expression of NTRK2 on ABCF1 expression in A549 and PC9 cells. (H) ABCF1-knockdown A549, A549/Taxol cells and control cells were subjected to dose-dependent paclitaxel treatment for 48 h. The cell viability was assessed via MTT assay, and the Reed-Muench method was adopted to calculate IC 50 values. (I) Knockdown of ABCF1 in A549 cells cooperated with overexpressing NTRK2 and their control cells were subjected to 0, 5 and 10 nM paclitaxel treatment for 48 h. The relative cell viability was assessed by MTT assay. β-actin served as an internal control for qRT-PCR. GAPDH was the internal reference for Western blotting. Data are expressed as mean ± SD. All above experiments were independently repeated in triplicate. * P < 0.05; ** P < 0.01; *** P < 0.001.

Journal: Translational Oncology

Article Title: NTRK2 promotes malignant progression and paclitaxel resistance of lung adenocarcinoma through targeting MYC/ABCF1 axis

doi: 10.1016/j.tranon.2025.102655

Figure Lengend Snippet: ABCF1 is a key target of NTRK2 in mediating resistance to paclitaxel in LUAD cells. The mRNA (A) and protein (B) expression levels of NTRK2 and ABCF1 in A549 and A549/Taxol cells were measured by qRT-PCR and Western blotting analysis, respectively. (C) Representative immunohistochemical staining of NTRK2 and ABCF1 in LUAD tissues (Case 1), paclitaxel-resistant LUAD tissues (Case 2) and their matched noncancerous lung tissues (MN). Scale bars: 50 μm. qRT-PCR (D) and Western blotting (E) analysis results showing the effect of NTRK2 knockdown on ABCF1 expression in A549 and A549/Taxol cell lines. qRT-PCR (F) and Western blotting (G) analysis results showing the effect of ectopic expression of NTRK2 on ABCF1 expression in A549 and PC9 cells. (H) ABCF1-knockdown A549, A549/Taxol cells and control cells were subjected to dose-dependent paclitaxel treatment for 48 h. The cell viability was assessed via MTT assay, and the Reed-Muench method was adopted to calculate IC 50 values. (I) Knockdown of ABCF1 in A549 cells cooperated with overexpressing NTRK2 and their control cells were subjected to 0, 5 and 10 nM paclitaxel treatment for 48 h. The relative cell viability was assessed by MTT assay. β-actin served as an internal control for qRT-PCR. GAPDH was the internal reference for Western blotting. Data are expressed as mean ± SD. All above experiments were independently repeated in triplicate. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: Human LUAD cell lines PC9, A549 and its taxol-resistant strain A549/Taxol were purchased from Procell Life Science & Technology Co.,Ltd (Wuhan, China).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Immunohistochemical staining, Staining, Knockdown, Control, MTT Assay, Endpoint Dilution Assay

NTRK2 increases ABCF1 expression through MYC. (A) Western blotting analysis showing the effect of NTRK2 knockdown on the activity of PI3K/AKT and MAPK/ERK pathways and MYC expression in A549, A549/Taxol and PC9 cells. (B) The effect of NTRK2 overexpression on the activity of PI3K/AKT and MAPK/ERK pathways and MYC expression in A549 and PC9 cells. The effect of MYC inhibitor 10058-F4 on cell proliferation (C) and colony formation (D) of A549 cells cooperated with overexpressing NTRK2 . (E) Analysis the correlation between MYC and ABCF1 in lung cancer tissues (the data from TCGA and GTEx datasets). A549 and PC9 cells were treated with 60 μM 10058-F4 or DMSO for 24 h, and the mRNA (F) and protein (G) expression of MYC and ABCF1 were detected. A549 and PC9 cells were transfected with an empty vector (Vector) or an MYC-overexpressing plasmid (oe-MYC), the mRNA (H) and protein (I) expression levels of MYC and ABCF1 were determined by qRT-PCR and Western blotting assays. (J) The impact of MYC overexpression on the promoter activity of the wild-type (WT) and mutant (Mut) ABCF1 was evaluated using a luciferase reporter system in A549 and PC9 cells. ABCF1-Luc reporter activity was normalized to Renilla activity (Luc/Renilla). The Luc/Renilla activity was represented as means ± SD (n = 3). (K) ChIP-qPCR assay shows MYC binding to three different regions of ABCF1 promoter in A549 and PC9 cells ( n = 3). (L) qRT-PCR assay was performed to detect the mRNA expression of both MYC (left panel) and ABCF1 (right panel) in NTRK2-overexpressed cells after treating with 10058-F4 or DMSO. (M) Western blotting analysis of NTRK2, MYC and ABCF1 in NTRK2-overexpressed A549 and PC9 cells treated with 60 μM 10058-F4. β-actin was the normalized control for qRT-PCR and GAPDH served as the internal reference for Western blotting analysis. Data are shown as the mean ± SD. All above experiments were independently repeated in triplicate. ** P < 0.01; *** P < 0.001.

Journal: Translational Oncology

Article Title: NTRK2 promotes malignant progression and paclitaxel resistance of lung adenocarcinoma through targeting MYC/ABCF1 axis

doi: 10.1016/j.tranon.2025.102655

Figure Lengend Snippet: NTRK2 increases ABCF1 expression through MYC. (A) Western blotting analysis showing the effect of NTRK2 knockdown on the activity of PI3K/AKT and MAPK/ERK pathways and MYC expression in A549, A549/Taxol and PC9 cells. (B) The effect of NTRK2 overexpression on the activity of PI3K/AKT and MAPK/ERK pathways and MYC expression in A549 and PC9 cells. The effect of MYC inhibitor 10058-F4 on cell proliferation (C) and colony formation (D) of A549 cells cooperated with overexpressing NTRK2 . (E) Analysis the correlation between MYC and ABCF1 in lung cancer tissues (the data from TCGA and GTEx datasets). A549 and PC9 cells were treated with 60 μM 10058-F4 or DMSO for 24 h, and the mRNA (F) and protein (G) expression of MYC and ABCF1 were detected. A549 and PC9 cells were transfected with an empty vector (Vector) or an MYC-overexpressing plasmid (oe-MYC), the mRNA (H) and protein (I) expression levels of MYC and ABCF1 were determined by qRT-PCR and Western blotting assays. (J) The impact of MYC overexpression on the promoter activity of the wild-type (WT) and mutant (Mut) ABCF1 was evaluated using a luciferase reporter system in A549 and PC9 cells. ABCF1-Luc reporter activity was normalized to Renilla activity (Luc/Renilla). The Luc/Renilla activity was represented as means ± SD (n = 3). (K) ChIP-qPCR assay shows MYC binding to three different regions of ABCF1 promoter in A549 and PC9 cells ( n = 3). (L) qRT-PCR assay was performed to detect the mRNA expression of both MYC (left panel) and ABCF1 (right panel) in NTRK2-overexpressed cells after treating with 10058-F4 or DMSO. (M) Western blotting analysis of NTRK2, MYC and ABCF1 in NTRK2-overexpressed A549 and PC9 cells treated with 60 μM 10058-F4. β-actin was the normalized control for qRT-PCR and GAPDH served as the internal reference for Western blotting analysis. Data are shown as the mean ± SD. All above experiments were independently repeated in triplicate. ** P < 0.01; *** P < 0.001.

Article Snippet: Human LUAD cell lines PC9, A549 and its taxol-resistant strain A549/Taxol were purchased from Procell Life Science & Technology Co.,Ltd (Wuhan, China).

Techniques: Expressing, Western Blot, Knockdown, Activity Assay, Over Expression, Transfection, Plasmid Preparation, Quantitative RT-PCR, Mutagenesis, Luciferase, ChIP-qPCR, Binding Assay, Control

Inhibition rates of various concentrations of cisplatin on PC9 and PC9/S100A6 cells at 24h ( a ), 48h ( b ), and 72h ( c ).

Journal: Cancer Management and Research

Article Title: S100A6 Induces the Resistance to Gefitinib in Human Lung Adenocarcinoma PC9 Cell Lines with EGFR 19 Exon Mutations

doi: 10.2147/CMAR.S533644

Figure Lengend Snippet: Inhibition rates of various concentrations of cisplatin on PC9 and PC9/S100A6 cells at 24h ( a ), 48h ( b ), and 72h ( c ).

Article Snippet: The lung adenocarcinoma cell line PC9, with EGFR 19 exon mutation, and normal lung epithelial cell (BEAS-2B) were purchased from the Procell Life Science & Technology Co., Ltd (Wuhan, China).

Techniques: Inhibition

Inhibition rate of various concentrations of gefitinib on PC9 and PC9/S100A6 cells at 48h ( a ) and 72h ( b ).

Journal: Cancer Management and Research

Article Title: S100A6 Induces the Resistance to Gefitinib in Human Lung Adenocarcinoma PC9 Cell Lines with EGFR 19 Exon Mutations

doi: 10.2147/CMAR.S533644

Figure Lengend Snippet: Inhibition rate of various concentrations of gefitinib on PC9 and PC9/S100A6 cells at 48h ( a ) and 72h ( b ).

Techniques: Inhibition

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experimental models pc9 cell line ecacc 90071810 nci h1975 cell line atcc crl 5908 hcc4006 cell line atcc crl (ATCC)

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