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cell culture 212 human luad cell lines  (ATCC)


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    ATCC cell culture 212 human luad cell lines
    Cell Culture 212 Human Luad Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 2635 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cell+culture+luad+cell+lines/NCI-H460/pm41491958-72-2-26
    Average 98 stars, based on 2635 article reviews
    cell culture 212 human luad cell lines - by Bioz Stars, 2026-10
    98/100 stars

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    Cell Culture:

    Article Title: LncRNA LINC00520 Aggravates Cell Proliferation and Migration in Lung Adenocarcinoma via a Positive Feedback Loop
    Article Snippet: .. Cell culture LUAD cell lines (A549, H1975, H2030, H1435) and a normal human bronchial epithelial cell (BEAS-2B) were provided by the American Type Culture Collection (ATCC; Gaithersburg, MD, USA). .. Brie y, all cells applied in this study were maintained in Dulbecco’s modi ed Eagle’s medium (DMEM; Gibco, Waltham, MA, USA) containing 10% fetal bovine serum (FBS; Gibco, Waltham, MA, USA), 100 U/ml penicillin (Sigma-Aldrich, USA), and 100 mg/ml streptomycin (Sigma-Aldrich, USA) at 37 °C with 5% CO2.

    Article Title: The recruitment of CD8 + T cells through YBX1 stabilization abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma.
    Article Snippet: .. MATERIALS AND METHODS Cell lines and cell culture LUAD cell lines (A549 and PC9) were obtained from the American Type Culture Collection (ATCC). .. A549 cells were cultured in RPMI-1640(KeyGen, China) supplemented with 10% fetal bovine serum (FBS; Life Technologies) while PC9 cells were maintained in DMEM (KeyGen, China).

    Article Title: B3GNT3 as a prognostic biomarker and correlation with immune cell infiltration in lung adenocarcinoma
    Article Snippet: .. Cell culture LUAD cell lines (A549 and PC9) and human bronchial epithelial cell line BEAS-2B were purchased from the American Type Culture Collection. .. Cells were maintained in Dulbecco’s Modified Eagle Medium supplemented with 10% fetal bovine serum (Gibco, CA, USA) at 37 °C in a humidified incubator with 5% CO 2 at 37 °C.



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    Fig. 1 Existence of immune environment abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma. A Relative expression levels of MIR155HG in <t>LUAD</t> tissues (n = 514) and normal tissues (n = 59) from TCGA database. B Relative expression levels of MIR155HG in tumor tissues (n = 30 tumors) and normal tissues (n = 30 samples) from LUAD patients. C Kaplan–Meier survival curves of OS from TCGA database according to MIR155HG levels in LUAD tissues. D Prognostic values of MIR155HG in LUAD using probes of 229437_s_at. E Enriched GO pathway analysis on MIR155HG-related gene signature. F Schematic view of mice model in BALB/c nude mice and PBMC- transferred NCG mice respectively. G Tumor growth curves of sh-NC and <t>sh-MIR155HG-transfected</t> <t>A549</t> cells in BALB/c nude mice. H Tumor growth curves of Vector and MIR155HG-transfected A549 cells in BALB/c nude mice. I Tumor growth curves and tumor volumes of sh-NC and sh-MIR155HG-transfected A549 cells in PBMC-transferred NCG mice. J Tumor growth curves and tumor volumes of Vector and MIR155HG- transfected A549 cells in PBMC-transferred NCG mice. Results are presented as mean ± SEM, n = 5. ns, not significant; **p < 0.01, ***p < 0.001.
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    Fig. 1 Existence of immune environment abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma. A Relative expression levels of MIR155HG in <t>LUAD</t> tissues (n = 514) and normal tissues (n = 59) from TCGA database. B Relative expression levels of MIR155HG in tumor tissues (n = 30 tumors) and normal tissues (n = 30 samples) from LUAD patients. C Kaplan–Meier survival curves of OS from TCGA database according to MIR155HG levels in LUAD tissues. D Prognostic values of MIR155HG in LUAD using probes of 229437_s_at. E Enriched GO pathway analysis on MIR155HG-related gene signature. F Schematic view of mice model in BALB/c nude mice and PBMC- transferred NCG mice respectively. G Tumor growth curves of sh-NC and <t>sh-MIR155HG-transfected</t> <t>A549</t> cells in BALB/c nude mice. H Tumor growth curves of Vector and MIR155HG-transfected A549 cells in BALB/c nude mice. I Tumor growth curves and tumor volumes of sh-NC and sh-MIR155HG-transfected A549 cells in PBMC-transferred NCG mice. J Tumor growth curves and tumor volumes of Vector and MIR155HG- transfected A549 cells in PBMC-transferred NCG mice. Results are presented as mean ± SEM, n = 5. ns, not significant; **p < 0.01, ***p < 0.001.
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    Fig. 1 Existence of immune environment abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma. A Relative expression levels of MIR155HG in <t>LUAD</t> tissues (n = 514) and normal tissues (n = 59) from TCGA database. B Relative expression levels of MIR155HG in tumor tissues (n = 30 tumors) and normal tissues (n = 30 samples) from LUAD patients. C Kaplan–Meier survival curves of OS from TCGA database according to MIR155HG levels in LUAD tissues. D Prognostic values of MIR155HG in LUAD using probes of 229437_s_at. E Enriched GO pathway analysis on MIR155HG-related gene signature. F Schematic view of mice model in BALB/c nude mice and PBMC- transferred NCG mice respectively. G Tumor growth curves of sh-NC and <t>sh-MIR155HG-transfected</t> <t>A549</t> cells in BALB/c nude mice. H Tumor growth curves of Vector and MIR155HG-transfected A549 cells in BALB/c nude mice. I Tumor growth curves and tumor volumes of sh-NC and sh-MIR155HG-transfected A549 cells in PBMC-transferred NCG mice. J Tumor growth curves and tumor volumes of Vector and MIR155HG- transfected A549 cells in PBMC-transferred NCG mice. Results are presented as mean ± SEM, n = 5. ns, not significant; **p < 0.01, ***p < 0.001.
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    ATCC cell culture luad cell line a549
    SMARCA4 restoration in <t>A549</t> cells reduces cell viability and changes the miRNome. (A) Resazurin assay at different time points after transfection of A549 with empty vector (EV) or the SMARCA4 plasmid (SMARCA4). (B) Clonogenic assay after 14 days of SMARCA4 restoration in A549. Upper panel: Colony number quantification; lower panel: Representative images of each condition after the staining with crystal violet. (C) Volcano plot with the differentially expressed miRNAs upon SMARCA4 restoration. miRNAs with a FDR <0.05 and an absolute log2 FC >1 are displayed with a diamond (NS, non-significant; FDR, false discovery rate; FC, fold change). (D) Top three significantly enriched pathways of the dysregulated miRNAs upon SMARCA4 restoration. For each pathway, we represented the number of genes that are targets of at least seven miRNAs of our dysregulated miRNAs. (E) miR-222 relative expression levels after 24 and 48 h of restoration of SMARCA4 in A549. Values represent mean ± SD (n ≥ 3). *Two-tailed t-test P < 0.05; **P < 0.01; ***P < 0.001.
    Cell Culture Luad Cell Line A549, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Fig. 1 Existence of immune environment abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma. A Relative expression levels of MIR155HG in LUAD tissues (n = 514) and normal tissues (n = 59) from TCGA database. B Relative expression levels of MIR155HG in tumor tissues (n = 30 tumors) and normal tissues (n = 30 samples) from LUAD patients. C Kaplan–Meier survival curves of OS from TCGA database according to MIR155HG levels in LUAD tissues. D Prognostic values of MIR155HG in LUAD using probes of 229437_s_at. E Enriched GO pathway analysis on MIR155HG-related gene signature. F Schematic view of mice model in BALB/c nude mice and PBMC- transferred NCG mice respectively. G Tumor growth curves of sh-NC and sh-MIR155HG-transfected A549 cells in BALB/c nude mice. H Tumor growth curves of Vector and MIR155HG-transfected A549 cells in BALB/c nude mice. I Tumor growth curves and tumor volumes of sh-NC and sh-MIR155HG-transfected A549 cells in PBMC-transferred NCG mice. J Tumor growth curves and tumor volumes of Vector and MIR155HG- transfected A549 cells in PBMC-transferred NCG mice. Results are presented as mean ± SEM, n = 5. ns, not significant; **p < 0.01, ***p < 0.001.

    Journal: Cell death discovery

    Article Title: The recruitment of CD8 + T cells through YBX1 stabilization abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma.

    doi: 10.1038/s41420-024-02102-3

    Figure Lengend Snippet: Fig. 1 Existence of immune environment abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma. A Relative expression levels of MIR155HG in LUAD tissues (n = 514) and normal tissues (n = 59) from TCGA database. B Relative expression levels of MIR155HG in tumor tissues (n = 30 tumors) and normal tissues (n = 30 samples) from LUAD patients. C Kaplan–Meier survival curves of OS from TCGA database according to MIR155HG levels in LUAD tissues. D Prognostic values of MIR155HG in LUAD using probes of 229437_s_at. E Enriched GO pathway analysis on MIR155HG-related gene signature. F Schematic view of mice model in BALB/c nude mice and PBMC- transferred NCG mice respectively. G Tumor growth curves of sh-NC and sh-MIR155HG-transfected A549 cells in BALB/c nude mice. H Tumor growth curves of Vector and MIR155HG-transfected A549 cells in BALB/c nude mice. I Tumor growth curves and tumor volumes of sh-NC and sh-MIR155HG-transfected A549 cells in PBMC-transferred NCG mice. J Tumor growth curves and tumor volumes of Vector and MIR155HG- transfected A549 cells in PBMC-transferred NCG mice. Results are presented as mean ± SEM, n = 5. ns, not significant; **p < 0.01, ***p < 0.001.

    Article Snippet: MATERIALS AND METHODS Cell lines and cell culture LUAD cell lines (A549 and PC9) were obtained from the American Type Culture Collection (ATCC).

    Techniques: Expressing, Transfection, Plasmid Preparation

    Fig. 2 MIR155HG is positively associated with CD8+ T cells infiltrating in vivo and in vitro. A Representative H&E staining and computational staining images of LUAD from TCGA, which were retrieved from the CANCER Digital Slide Archive and TCIA, respectively. Normalized MIR155HG expression and TIL percentage values are shown above corresponding images. B Quantification of estimated TIL proportions in MIR155HGhi and MIR155HGlo LUAD patients. C Correlations of MIR155HG levels with the percentages of TILs in LUAD tissues. D Correlations of normalized MIR155HG expression with predicted immune cell fractions in LUAD. E Immunofluorescence in 94 LUAD patient tissue microarrays and correlations between MIR155HG and CD8+ T cells infiltration. F Representative images and quantification of CD8 IHC staining in NCG mice tumors with MIR155HG knockdown or overexpression; Scale bar, 100 μm. G Schematic view of T cell chemotaxis assay. H CD3+CD8+ T cells in A549 and PC9 cells with MIR155HG knockdown or overexpression detected flow cytometry analysis. Results are presented as mean ± SEM, n = 3. *p < 0.05, **p < 0.01.

    Journal: Cell death discovery

    Article Title: The recruitment of CD8 + T cells through YBX1 stabilization abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma.

    doi: 10.1038/s41420-024-02102-3

    Figure Lengend Snippet: Fig. 2 MIR155HG is positively associated with CD8+ T cells infiltrating in vivo and in vitro. A Representative H&E staining and computational staining images of LUAD from TCGA, which were retrieved from the CANCER Digital Slide Archive and TCIA, respectively. Normalized MIR155HG expression and TIL percentage values are shown above corresponding images. B Quantification of estimated TIL proportions in MIR155HGhi and MIR155HGlo LUAD patients. C Correlations of MIR155HG levels with the percentages of TILs in LUAD tissues. D Correlations of normalized MIR155HG expression with predicted immune cell fractions in LUAD. E Immunofluorescence in 94 LUAD patient tissue microarrays and correlations between MIR155HG and CD8+ T cells infiltration. F Representative images and quantification of CD8 IHC staining in NCG mice tumors with MIR155HG knockdown or overexpression; Scale bar, 100 μm. G Schematic view of T cell chemotaxis assay. H CD3+CD8+ T cells in A549 and PC9 cells with MIR155HG knockdown or overexpression detected flow cytometry analysis. Results are presented as mean ± SEM, n = 3. *p < 0.05, **p < 0.01.

    Article Snippet: MATERIALS AND METHODS Cell lines and cell culture LUAD cell lines (A549 and PC9) were obtained from the American Type Culture Collection (ATCC).

    Techniques: In Vivo, In Vitro, Staining, Expressing, Immunohistochemistry, Knockdown, Over Expression, Chemotaxis Assay, Cytometry

    Fig. 3 MIR155HG regulates CCL5 expression in LUAD. A Heatmap of upregulated/downregulated genes in MIR155G-overexpressed A549 cells compared with parental A549 cells by RNA-sequence. B Volcano plot for the DEGs in MIR155G-overexpressed versus vector A549 cells. C GSEA plots of Cytokine-cytokine receptor interaction pathway-related signatures. D mRNA levels of several chemokine in Vector and MIR155HG-transfected A549 cells by qRT-PCR. E mRNA levels of CCL5 in Vector and MIR155HG-transfected A549 and PC9 cells by qRT-PCR. F ELISA detection of CCL5 in A549 and PC9 cells with MIR155HG knockdown or overexpressed. G Increased recruitment of CD3+CD8+ T cells in MIR155HG-overexpressing A549 and PC9 cells was abolished by CCL5 knockdown by flow cytometry analysis. Results are presented as mean ± SEM, n = 3. **p < 0.01, ***p < 0.001.

    Journal: Cell death discovery

    Article Title: The recruitment of CD8 + T cells through YBX1 stabilization abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma.

    doi: 10.1038/s41420-024-02102-3

    Figure Lengend Snippet: Fig. 3 MIR155HG regulates CCL5 expression in LUAD. A Heatmap of upregulated/downregulated genes in MIR155G-overexpressed A549 cells compared with parental A549 cells by RNA-sequence. B Volcano plot for the DEGs in MIR155G-overexpressed versus vector A549 cells. C GSEA plots of Cytokine-cytokine receptor interaction pathway-related signatures. D mRNA levels of several chemokine in Vector and MIR155HG-transfected A549 cells by qRT-PCR. E mRNA levels of CCL5 in Vector and MIR155HG-transfected A549 and PC9 cells by qRT-PCR. F ELISA detection of CCL5 in A549 and PC9 cells with MIR155HG knockdown or overexpressed. G Increased recruitment of CD3+CD8+ T cells in MIR155HG-overexpressing A549 and PC9 cells was abolished by CCL5 knockdown by flow cytometry analysis. Results are presented as mean ± SEM, n = 3. **p < 0.01, ***p < 0.001.

    Article Snippet: MATERIALS AND METHODS Cell lines and cell culture LUAD cell lines (A549 and PC9) were obtained from the American Type Culture Collection (ATCC).

    Techniques: Expressing, Sequencing, Plasmid Preparation, Transfection, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Knockdown, Cytometry

    Fig. 5 MIR155HG promotes CCL5 transcription through YBX1 in LUAD. A The human CCL5 proximal promoter (−1 to −2 kb) was divided into seven different segments. B ChIP analysis was used to study the potential binding of YBX1 in A549 cells. YBX1 bound to the designated regions (C1, containing the Y-box sequence). ChIP assays were performed using a YBX1-specific antibody, R-IgG was the ChIP control. C Three different luciferase vectors constructed according to CCL5 promoter C1 region were co-transfected with si-YBX1 into A549 cells. The relative firefly/Renilla luciferase activities were analyzed in the cells 24 h after transfection. D Increased CCL5 expression in MIR155HG-overexpressing A549 cells was abolished by YBX1 knockdown by qRT-PCR. E Increased secretion levels of CCL5 in MIR155HG-overexpressing A549 cells were abolished by YBX1 knockdown by ELISA assay. F Increased recruitment of CD3+CD8+ T cells in MIR155HG-overexpressing A549 cells was abolished by YBX1 knockdown by flow cytometry analysis. Results are presented as mean ± SEM, n = 3. *p < 0.05, **p < 0.01, ***p < 0.001.

    Journal: Cell death discovery

    Article Title: The recruitment of CD8 + T cells through YBX1 stabilization abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma.

    doi: 10.1038/s41420-024-02102-3

    Figure Lengend Snippet: Fig. 5 MIR155HG promotes CCL5 transcription through YBX1 in LUAD. A The human CCL5 proximal promoter (−1 to −2 kb) was divided into seven different segments. B ChIP analysis was used to study the potential binding of YBX1 in A549 cells. YBX1 bound to the designated regions (C1, containing the Y-box sequence). ChIP assays were performed using a YBX1-specific antibody, R-IgG was the ChIP control. C Three different luciferase vectors constructed according to CCL5 promoter C1 region were co-transfected with si-YBX1 into A549 cells. The relative firefly/Renilla luciferase activities were analyzed in the cells 24 h after transfection. D Increased CCL5 expression in MIR155HG-overexpressing A549 cells was abolished by YBX1 knockdown by qRT-PCR. E Increased secretion levels of CCL5 in MIR155HG-overexpressing A549 cells were abolished by YBX1 knockdown by ELISA assay. F Increased recruitment of CD3+CD8+ T cells in MIR155HG-overexpressing A549 cells was abolished by YBX1 knockdown by flow cytometry analysis. Results are presented as mean ± SEM, n = 3. *p < 0.05, **p < 0.01, ***p < 0.001.

    Article Snippet: MATERIALS AND METHODS Cell lines and cell culture LUAD cell lines (A549 and PC9) were obtained from the American Type Culture Collection (ATCC).

    Techniques: Binding Assay, Sequencing, Control, Luciferase, Construct, Transfection, Expressing, Knockdown, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Cytometry

    Fig. 7 MIR155HG correlates with the efficacy of PD-L1 mAb therapy in LUAD patients and improves antitumor effect of PD-L1 blockade in vivo. A Correlations of MIR155HG expression with CCL5 and PD-L1 expression in LUAD from TCGA database. B Representative images of immunofluorescence in 94 LUAD patient tissue microarrays and correlations between MIR155HG, CCL5 and PD-L1. C Correlations of MIR155HG expression with CCL5 and PD-L1 expression in microarrays. D Kaplan–Meier survival curves of survival probability according to MIR155HG-related gene signature in LUAD cohorts (GSE136961, GSE13522). E Relative MIR155HG expression between response and non- response in GSE135222. F Schematic view of mice model in PBMC-transferred NCG mice with PD-L1 mAb treatment. G Tumor growth curves and tumor volumes of Vector and MIR155HG-transfected A549 cells with PD-L1 mAb treatment in PBMC-transferred NCG mice. H Graphic abstract. Results are presented as mean ± SEM, n = 5. *p < 0.05, ***p < 0.001.

    Journal: Cell death discovery

    Article Title: The recruitment of CD8 + T cells through YBX1 stabilization abrogates tumor intrinsic oncogenic role of MIR155HG in lung adenocarcinoma.

    doi: 10.1038/s41420-024-02102-3

    Figure Lengend Snippet: Fig. 7 MIR155HG correlates with the efficacy of PD-L1 mAb therapy in LUAD patients and improves antitumor effect of PD-L1 blockade in vivo. A Correlations of MIR155HG expression with CCL5 and PD-L1 expression in LUAD from TCGA database. B Representative images of immunofluorescence in 94 LUAD patient tissue microarrays and correlations between MIR155HG, CCL5 and PD-L1. C Correlations of MIR155HG expression with CCL5 and PD-L1 expression in microarrays. D Kaplan–Meier survival curves of survival probability according to MIR155HG-related gene signature in LUAD cohorts (GSE136961, GSE13522). E Relative MIR155HG expression between response and non- response in GSE135222. F Schematic view of mice model in PBMC-transferred NCG mice with PD-L1 mAb treatment. G Tumor growth curves and tumor volumes of Vector and MIR155HG-transfected A549 cells with PD-L1 mAb treatment in PBMC-transferred NCG mice. H Graphic abstract. Results are presented as mean ± SEM, n = 5. *p < 0.05, ***p < 0.001.

    Article Snippet: MATERIALS AND METHODS Cell lines and cell culture LUAD cell lines (A549 and PC9) were obtained from the American Type Culture Collection (ATCC).

    Techniques: In Vivo, Expressing, Plasmid Preparation, Transfection

    SMARCA4 restoration in A549 cells reduces cell viability and changes the miRNome. (A) Resazurin assay at different time points after transfection of A549 with empty vector (EV) or the SMARCA4 plasmid (SMARCA4). (B) Clonogenic assay after 14 days of SMARCA4 restoration in A549. Upper panel: Colony number quantification; lower panel: Representative images of each condition after the staining with crystal violet. (C) Volcano plot with the differentially expressed miRNAs upon SMARCA4 restoration. miRNAs with a FDR <0.05 and an absolute log2 FC >1 are displayed with a diamond (NS, non-significant; FDR, false discovery rate; FC, fold change). (D) Top three significantly enriched pathways of the dysregulated miRNAs upon SMARCA4 restoration. For each pathway, we represented the number of genes that are targets of at least seven miRNAs of our dysregulated miRNAs. (E) miR-222 relative expression levels after 24 and 48 h of restoration of SMARCA4 in A549. Values represent mean ± SD (n ≥ 3). *Two-tailed t-test P < 0.05; **P < 0.01; ***P < 0.001.

    Journal: Human Molecular Genetics

    Article Title: The SWI/SNF complex regulates the expression of miR-222, a tumor suppressor microRNA in lung adenocarcinoma

    doi: 10.1093/hmg/ddab187

    Figure Lengend Snippet: SMARCA4 restoration in A549 cells reduces cell viability and changes the miRNome. (A) Resazurin assay at different time points after transfection of A549 with empty vector (EV) or the SMARCA4 plasmid (SMARCA4). (B) Clonogenic assay after 14 days of SMARCA4 restoration in A549. Upper panel: Colony number quantification; lower panel: Representative images of each condition after the staining with crystal violet. (C) Volcano plot with the differentially expressed miRNAs upon SMARCA4 restoration. miRNAs with a FDR <0.05 and an absolute log2 FC >1 are displayed with a diamond (NS, non-significant; FDR, false discovery rate; FC, fold change). (D) Top three significantly enriched pathways of the dysregulated miRNAs upon SMARCA4 restoration. For each pathway, we represented the number of genes that are targets of at least seven miRNAs of our dysregulated miRNAs. (E) miR-222 relative expression levels after 24 and 48 h of restoration of SMARCA4 in A549. Values represent mean ± SD (n ≥ 3). *Two-tailed t-test P < 0.05; **P < 0.01; ***P < 0.001.

    Article Snippet: Cell culture LUAD cell line A549 was purchased from the American Type Culture Collection, and it was tested to be free of mycoplasma contamination.

    Techniques: Resazurin Assay, Transfection, Plasmid Preparation, Clonogenic Assay, Staining, Expressing, Two Tailed Test

    SMARCA4 binds to the enhancer of miR-222 in a time-dependent manner. (A) Overview of the miR-222 genomic context including ChIP-Seq profiles of H3K4me3, H3K27ac and H3K4me1 in the A549 cell line (Supplementary Material S1). High levels of H3K27ac and H3K4me1 and low levels of H3K4me3 are characteristic of enhancer regions. (B) Analysis by ChIP-qPCR of SMARCA4 or SMARCA2 binding to the enhancer of miR-222 after 24 and 48 h of SMARCA4 restoration in A549. (C) Quantification of SMARCA4 protein levels relative to ACTB expression in transfected A549 cells after 24 and 48 h of SMARCA4 restoration. Values represent mean ± SD (n ≥ 3). *Two-tailed t-test P < 0.05; **P < 0.01.

    Journal: Human Molecular Genetics

    Article Title: The SWI/SNF complex regulates the expression of miR-222, a tumor suppressor microRNA in lung adenocarcinoma

    doi: 10.1093/hmg/ddab187

    Figure Lengend Snippet: SMARCA4 binds to the enhancer of miR-222 in a time-dependent manner. (A) Overview of the miR-222 genomic context including ChIP-Seq profiles of H3K4me3, H3K27ac and H3K4me1 in the A549 cell line (Supplementary Material S1). High levels of H3K27ac and H3K4me1 and low levels of H3K4me3 are characteristic of enhancer regions. (B) Analysis by ChIP-qPCR of SMARCA4 or SMARCA2 binding to the enhancer of miR-222 after 24 and 48 h of SMARCA4 restoration in A549. (C) Quantification of SMARCA4 protein levels relative to ACTB expression in transfected A549 cells after 24 and 48 h of SMARCA4 restoration. Values represent mean ± SD (n ≥ 3). *Two-tailed t-test P < 0.05; **P < 0.01.

    Article Snippet: Cell culture LUAD cell line A549 was purchased from the American Type Culture Collection, and it was tested to be free of mycoplasma contamination.

    Techniques: ChIP-sequencing, ChIP-qPCR, Binding Assay, Expressing, Transfection, Two Tailed Test

    Schematic overview of the regulation of miR-222 by the SWI/SNF complex. Upper panel: After 24 h of SMARCA4 re-expression in A549 cells, there are high levels of SMARCA4 and it is included in the SWI/SNF complex. There is a predominance of SWI/SNF complexes with SMARCA4 and this type of complexes induces miR-222 expression. Lower panel: After longer times of transfection, SMARCA4 levels in A549 decrease, and SWI/SNF complexes with SMARCA2 are predominant. This complex impairs miR-222 expression. Both figures were made using BioRender (https://app.biorender.com/).

    Journal: Human Molecular Genetics

    Article Title: The SWI/SNF complex regulates the expression of miR-222, a tumor suppressor microRNA in lung adenocarcinoma

    doi: 10.1093/hmg/ddab187

    Figure Lengend Snippet: Schematic overview of the regulation of miR-222 by the SWI/SNF complex. Upper panel: After 24 h of SMARCA4 re-expression in A549 cells, there are high levels of SMARCA4 and it is included in the SWI/SNF complex. There is a predominance of SWI/SNF complexes with SMARCA4 and this type of complexes induces miR-222 expression. Lower panel: After longer times of transfection, SMARCA4 levels in A549 decrease, and SWI/SNF complexes with SMARCA2 are predominant. This complex impairs miR-222 expression. Both figures were made using BioRender (https://app.biorender.com/).

    Article Snippet: Cell culture LUAD cell line A549 was purchased from the American Type Culture Collection, and it was tested to be free of mycoplasma contamination.

    Techniques: Expressing, Transfection

    miR-222 behaves as a tumor suppressor miRNA by decreasing cell viability and colony formation. (A) Relative miR-222 expression levels after transfection of A549 cells with either a negative control mimic or a miR-222 mimic. (B) Resazurin assay at different time points after transfection of A549 with negative control mimic or miR-222 mimic. (C) Clonogenic assay after 14 days of transfection of A549 with negative control mimic or miR-222 mimic. Left: Colony number quantification. Right: Representative images of each condition after the staining with crystal violet. Values represent mean ± SD (n ≥ 3). *Two-tailed t-test P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Journal: Human Molecular Genetics

    Article Title: The SWI/SNF complex regulates the expression of miR-222, a tumor suppressor microRNA in lung adenocarcinoma

    doi: 10.1093/hmg/ddab187

    Figure Lengend Snippet: miR-222 behaves as a tumor suppressor miRNA by decreasing cell viability and colony formation. (A) Relative miR-222 expression levels after transfection of A549 cells with either a negative control mimic or a miR-222 mimic. (B) Resazurin assay at different time points after transfection of A549 with negative control mimic or miR-222 mimic. (C) Clonogenic assay after 14 days of transfection of A549 with negative control mimic or miR-222 mimic. Left: Colony number quantification. Right: Representative images of each condition after the staining with crystal violet. Values represent mean ± SD (n ≥ 3). *Two-tailed t-test P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Article Snippet: Cell culture LUAD cell line A549 was purchased from the American Type Culture Collection, and it was tested to be free of mycoplasma contamination.

    Techniques: Expressing, Transfection, Negative Control, Resazurin Assay, Clonogenic Assay, Staining, Two Tailed Test