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colorectal cancer cell line sw48  (ATCC)


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    ATCC colorectal cancer cell line sw48
    Generation and functional validation of miR-196 knockout <t>SW48</t> cells. ( A ) Sequence alignment of miR-196A and miR-196B showing a high degree of similarity between the two miRNA isoforms. ( B ) Quantitative RT-PCR analysis of miR-196 expression in parental SW48 cells and in miR-196A-KO or miR-196B-KO cells. Relative expression levels were normalized to an internal control RNA and presented as fold change compared with control cells. ( C ) Cell proliferation assay showing the relative growth rates of control, miR-196A-KO, and miR-196B-KO SW48 cells. Data represent the mean ± SD from independent experiments. Statistical significance is indicated (* p < 0.05, *** p < 0.001).
    Colorectal Cancer Cell Line Sw48, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 818 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/colorectal cancer cell line sw48/product/ATCC
    Average 96 stars, based on 818 article reviews
    colorectal cancer cell line sw48 - by Bioz Stars, 2026-05
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    Images

    1) Product Images from "Transcriptomic Profiling Reveals Isoform-Specific Regulatory Roles of miR-196A and miR-196B in Colorectal Cancer Cells"

    Article Title: Transcriptomic Profiling Reveals Isoform-Specific Regulatory Roles of miR-196A and miR-196B in Colorectal Cancer Cells

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms27093959

    Generation and functional validation of miR-196 knockout SW48 cells. ( A ) Sequence alignment of miR-196A and miR-196B showing a high degree of similarity between the two miRNA isoforms. ( B ) Quantitative RT-PCR analysis of miR-196 expression in parental SW48 cells and in miR-196A-KO or miR-196B-KO cells. Relative expression levels were normalized to an internal control RNA and presented as fold change compared with control cells. ( C ) Cell proliferation assay showing the relative growth rates of control, miR-196A-KO, and miR-196B-KO SW48 cells. Data represent the mean ± SD from independent experiments. Statistical significance is indicated (* p < 0.05, *** p < 0.001).
    Figure Legend Snippet: Generation and functional validation of miR-196 knockout SW48 cells. ( A ) Sequence alignment of miR-196A and miR-196B showing a high degree of similarity between the two miRNA isoforms. ( B ) Quantitative RT-PCR analysis of miR-196 expression in parental SW48 cells and in miR-196A-KO or miR-196B-KO cells. Relative expression levels were normalized to an internal control RNA and presented as fold change compared with control cells. ( C ) Cell proliferation assay showing the relative growth rates of control, miR-196A-KO, and miR-196B-KO SW48 cells. Data represent the mean ± SD from independent experiments. Statistical significance is indicated (* p < 0.05, *** p < 0.001).

    Techniques Used: Functional Assay, Biomarker Discovery, Knock-Out, Sequencing, Quantitative RT-PCR, Expressing, Control, Proliferation Assay

    Identification of differentially expressed genes following deletion of miR-196 isoforms in SW48 cells. ( A ) Volcano plot showing the distribution of differentially expressed genes (DEGs) in miR-196 knockout cells compared with control SW48 cells. Significantly up-regulated and down-regulated genes are highlighted based on predefined statistical thresholds. ( B ) Summary of DEGs identified in the transcriptomic analysis, showing the numbers of significantly up-regulated and down-regulated genes in miR-196 knockout cells relative to control cells. The vertical dashed lines indicate the fold-change thresholds, and the horizontal dashed line represents the statistical significance threshold (adjusted p -value cutoff). The grey shaded area indicates genes that are not significantly differentially expressed. ( C ) Venn diagram illustrating the overlap of DEGs between miR-196A-KO and miR-196B-KO cells. A subset of genes was commonly regulated by both miR-196 isoforms, while additional genes were uniquely altered in each knockout condition.
    Figure Legend Snippet: Identification of differentially expressed genes following deletion of miR-196 isoforms in SW48 cells. ( A ) Volcano plot showing the distribution of differentially expressed genes (DEGs) in miR-196 knockout cells compared with control SW48 cells. Significantly up-regulated and down-regulated genes are highlighted based on predefined statistical thresholds. ( B ) Summary of DEGs identified in the transcriptomic analysis, showing the numbers of significantly up-regulated and down-regulated genes in miR-196 knockout cells relative to control cells. The vertical dashed lines indicate the fold-change thresholds, and the horizontal dashed line represents the statistical significance threshold (adjusted p -value cutoff). The grey shaded area indicates genes that are not significantly differentially expressed. ( C ) Venn diagram illustrating the overlap of DEGs between miR-196A-KO and miR-196B-KO cells. A subset of genes was commonly regulated by both miR-196 isoforms, while additional genes were uniquely altered in each knockout condition.

    Techniques Used: Knock-Out, Control

    Functional enrichment analysis of differentially expressed genes following miR-196A or miR-196B deletion. ( A ) Functional categorization of differentially expressed genes (DEGs) identified in miR-196A-KO cells compared with control SW48 cells. The pie chart shows the percentage distribution of genes associated with major biological processes. The percentages may exceed 100% because individual genes can be associated with multiple functional categories and are therefore counted in more than one category. ( B ) Distribution of significantly up-regulated and down-regulated genes in each functional category in miR-196A-KO cells. ( C ) Expression profiles of representative genes altered in miR-196A-KO cells. Each point represents normalized RNA-seq expression values from independent samples. ( D ) Functional classification of DEGs identified in miR-196B-KO cells relative to control cells. The percentages may exceed 100% because individual genes can be associated with multiple functional categories and are therefore counted in more than one category. ( E ) Numbers of significantly up-regulated and down-regulated genes in each functional category in miR-196B-KO cells. ( F ) Expression patterns of representative genes affected by miR-196B deletion.
    Figure Legend Snippet: Functional enrichment analysis of differentially expressed genes following miR-196A or miR-196B deletion. ( A ) Functional categorization of differentially expressed genes (DEGs) identified in miR-196A-KO cells compared with control SW48 cells. The pie chart shows the percentage distribution of genes associated with major biological processes. The percentages may exceed 100% because individual genes can be associated with multiple functional categories and are therefore counted in more than one category. ( B ) Distribution of significantly up-regulated and down-regulated genes in each functional category in miR-196A-KO cells. ( C ) Expression profiles of representative genes altered in miR-196A-KO cells. Each point represents normalized RNA-seq expression values from independent samples. ( D ) Functional classification of DEGs identified in miR-196B-KO cells relative to control cells. The percentages may exceed 100% because individual genes can be associated with multiple functional categories and are therefore counted in more than one category. ( E ) Numbers of significantly up-regulated and down-regulated genes in each functional category in miR-196B-KO cells. ( F ) Expression patterns of representative genes affected by miR-196B deletion.

    Techniques Used: Functional Assay, Control, Expressing, RNA Sequencing

    Hierarchical clustering and reproducibility assessment of RNA-seq data from miR-196 knockout SW48 cells. ( A – C ) Heatmap visualization of differentially expressed genes between miR-196 knockout cells and parental SW48 cells using fold-change thresholds of >1.5 ( A ), >2.0 ( B ), and >3.0 ( C ). Hierarchical clustering reveals distinct expression patterns associated with miR-196 deletion. ( D ) Pearson correlation heatmap showing strong correlations among biological replicates and experimental groups. Color intensity represents the Pearson correlation coefficient (r), ranging from −1 to 1, where values closer to 1 indicate stronger similarity between samples. The numerical values in each cell correspond to the correlation coefficients. ( E ) Pairwise scatter plot matrix demonstrating high concordance in gene expression profiles across samples. The red line represents the linear regression fit. Asterisks (***) indicate statistical significance ( p < 0.001).
    Figure Legend Snippet: Hierarchical clustering and reproducibility assessment of RNA-seq data from miR-196 knockout SW48 cells. ( A – C ) Heatmap visualization of differentially expressed genes between miR-196 knockout cells and parental SW48 cells using fold-change thresholds of >1.5 ( A ), >2.0 ( B ), and >3.0 ( C ). Hierarchical clustering reveals distinct expression patterns associated with miR-196 deletion. ( D ) Pearson correlation heatmap showing strong correlations among biological replicates and experimental groups. Color intensity represents the Pearson correlation coefficient (r), ranging from −1 to 1, where values closer to 1 indicate stronger similarity between samples. The numerical values in each cell correspond to the correlation coefficients. ( E ) Pairwise scatter plot matrix demonstrating high concordance in gene expression profiles across samples. The red line represents the linear regression fit. Asterisks (***) indicate statistical significance ( p < 0.001).

    Techniques Used: RNA Sequencing, Knock-Out, Expressing, Gene Expression

    Functional enrichment analysis of genes altered following miR-196 deletion. Gene Ontology (GO) and KEGG pathway enrichment analyses were performed using differentially expressed genes identified from RNA-seq analysis of miR-196A-KO and miR-196B-KO SW48 cells. ( A ) Bubble plot showing significantly enriched GO terms and KEGG pathways in miR-196A-KO cells. Functional categories are grouped into biological process (BP), cellular component (CC), molecular function (MF), and KEGG pathways. Bubble size represents the number of genes associated with each term, and color intensity indicates the −log10( p -value). ( B ) Bubble plot showing enriched GO terms and KEGG pathways in miR-196B-KO cells using the same criteria. ( C ) Distribution of up-regulated and down-regulated genes contributing to each enriched functional category in miR-196A-KO cells. ( D ) Distribution of up-regulated and down-regulated genes contributing to each enriched functional category in miR-196B-KO cells.
    Figure Legend Snippet: Functional enrichment analysis of genes altered following miR-196 deletion. Gene Ontology (GO) and KEGG pathway enrichment analyses were performed using differentially expressed genes identified from RNA-seq analysis of miR-196A-KO and miR-196B-KO SW48 cells. ( A ) Bubble plot showing significantly enriched GO terms and KEGG pathways in miR-196A-KO cells. Functional categories are grouped into biological process (BP), cellular component (CC), molecular function (MF), and KEGG pathways. Bubble size represents the number of genes associated with each term, and color intensity indicates the −log10( p -value). ( B ) Bubble plot showing enriched GO terms and KEGG pathways in miR-196B-KO cells using the same criteria. ( C ) Distribution of up-regulated and down-regulated genes contributing to each enriched functional category in miR-196A-KO cells. ( D ) Distribution of up-regulated and down-regulated genes contributing to each enriched functional category in miR-196B-KO cells.

    Techniques Used: Functional Assay, RNA Sequencing

    Differential gene expression patterns in miR-196A-KO and miR-196B-KO SW48 cells. Radar charts display the top ten most highly upregulated and downregulated genes in each knockout condition. Left panels show average normalized expression values (log2); right panels show fold change relative to parental SW48 cells (SW48-vector). ( A ) Top ten upregulated genes in miR-196A-KO cells, including RIMS2 , ADGRL2 , and LAMA2 . ( B ) Top ten upregulated genes in miR-196B-KO cells, including PCCA , LAMA2 , and AKAP12 . ( C ) Top ten downregulated genes in miR-196A-KO cells, including KRT14 , KLK11 , and KRT16 . ( D ) Top ten downregulated genes in miR-196B-KO cells, including KRT16 , KRT14 , and KRT19 . ( E ) qPCR validation of selected miR-196-associated genes ( NT5E , PRRX1 , KITLG , CLDN4 , and FLG ) in parental SW48 and miR-196 isoform knockout cells, showing isoform-dependent differences in gene expression. Data are presented as mean ± SD ( n = 3).
    Figure Legend Snippet: Differential gene expression patterns in miR-196A-KO and miR-196B-KO SW48 cells. Radar charts display the top ten most highly upregulated and downregulated genes in each knockout condition. Left panels show average normalized expression values (log2); right panels show fold change relative to parental SW48 cells (SW48-vector). ( A ) Top ten upregulated genes in miR-196A-KO cells, including RIMS2 , ADGRL2 , and LAMA2 . ( B ) Top ten upregulated genes in miR-196B-KO cells, including PCCA , LAMA2 , and AKAP12 . ( C ) Top ten downregulated genes in miR-196A-KO cells, including KRT14 , KLK11 , and KRT16 . ( D ) Top ten downregulated genes in miR-196B-KO cells, including KRT16 , KRT14 , and KRT19 . ( E ) qPCR validation of selected miR-196-associated genes ( NT5E , PRRX1 , KITLG , CLDN4 , and FLG ) in parental SW48 and miR-196 isoform knockout cells, showing isoform-dependent differences in gene expression. Data are presented as mean ± SD ( n = 3).

    Techniques Used: Gene Expression, Knock-Out, Expressing, Plasmid Preparation, Biomarker Discovery



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    Knockdown of RPS4X expression reduced tumor stemness. (A) The RPS4X gene expression level was assessed by qPCR. GAPDH served as an internal parameter (n = 3). (B) The cell proliferation ability of <t>SW48</t> was determined using the CCK-8 assay (n = 3). (C–D) Cell migration and invasion ability of SW48 were evaluated (n = 3). Data are presented as mean ± SD. *P < 0.05 (E–F) Cell apoptotic rate of SW48 was evaluated (n = 3). Data are presented as mean ± SD. **P < 0.01. (G) Tumor growth curve and RPS4X down-regulation in tumors from mice (n = 5 per group). Data are presented as mean ± SD. *P < 0.05 **P < 0.01 ***P < 0.001. (H) Representative images showing the tumors harvested from SW48-bearing mice (n = 5 per group). (I)Weight of the harvested tumors from tumor-bearing mice (n = 5 per group). Data are presented as mean ± SD. **P < 0.01.
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    Image Search Results


    Generation and functional validation of miR-196 knockout SW48 cells. ( A ) Sequence alignment of miR-196A and miR-196B showing a high degree of similarity between the two miRNA isoforms. ( B ) Quantitative RT-PCR analysis of miR-196 expression in parental SW48 cells and in miR-196A-KO or miR-196B-KO cells. Relative expression levels were normalized to an internal control RNA and presented as fold change compared with control cells. ( C ) Cell proliferation assay showing the relative growth rates of control, miR-196A-KO, and miR-196B-KO SW48 cells. Data represent the mean ± SD from independent experiments. Statistical significance is indicated (* p < 0.05, *** p < 0.001).

    Journal: International Journal of Molecular Sciences

    Article Title: Transcriptomic Profiling Reveals Isoform-Specific Regulatory Roles of miR-196A and miR-196B in Colorectal Cancer Cells

    doi: 10.3390/ijms27093959

    Figure Lengend Snippet: Generation and functional validation of miR-196 knockout SW48 cells. ( A ) Sequence alignment of miR-196A and miR-196B showing a high degree of similarity between the two miRNA isoforms. ( B ) Quantitative RT-PCR analysis of miR-196 expression in parental SW48 cells and in miR-196A-KO or miR-196B-KO cells. Relative expression levels were normalized to an internal control RNA and presented as fold change compared with control cells. ( C ) Cell proliferation assay showing the relative growth rates of control, miR-196A-KO, and miR-196B-KO SW48 cells. Data represent the mean ± SD from independent experiments. Statistical significance is indicated (* p < 0.05, *** p < 0.001).

    Article Snippet: The human colorectal cancer cell line SW48 (ATCC Cat. No. CCL-231) was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Functional Assay, Biomarker Discovery, Knock-Out, Sequencing, Quantitative RT-PCR, Expressing, Control, Proliferation Assay

    Identification of differentially expressed genes following deletion of miR-196 isoforms in SW48 cells. ( A ) Volcano plot showing the distribution of differentially expressed genes (DEGs) in miR-196 knockout cells compared with control SW48 cells. Significantly up-regulated and down-regulated genes are highlighted based on predefined statistical thresholds. ( B ) Summary of DEGs identified in the transcriptomic analysis, showing the numbers of significantly up-regulated and down-regulated genes in miR-196 knockout cells relative to control cells. The vertical dashed lines indicate the fold-change thresholds, and the horizontal dashed line represents the statistical significance threshold (adjusted p -value cutoff). The grey shaded area indicates genes that are not significantly differentially expressed. ( C ) Venn diagram illustrating the overlap of DEGs between miR-196A-KO and miR-196B-KO cells. A subset of genes was commonly regulated by both miR-196 isoforms, while additional genes were uniquely altered in each knockout condition.

    Journal: International Journal of Molecular Sciences

    Article Title: Transcriptomic Profiling Reveals Isoform-Specific Regulatory Roles of miR-196A and miR-196B in Colorectal Cancer Cells

    doi: 10.3390/ijms27093959

    Figure Lengend Snippet: Identification of differentially expressed genes following deletion of miR-196 isoforms in SW48 cells. ( A ) Volcano plot showing the distribution of differentially expressed genes (DEGs) in miR-196 knockout cells compared with control SW48 cells. Significantly up-regulated and down-regulated genes are highlighted based on predefined statistical thresholds. ( B ) Summary of DEGs identified in the transcriptomic analysis, showing the numbers of significantly up-regulated and down-regulated genes in miR-196 knockout cells relative to control cells. The vertical dashed lines indicate the fold-change thresholds, and the horizontal dashed line represents the statistical significance threshold (adjusted p -value cutoff). The grey shaded area indicates genes that are not significantly differentially expressed. ( C ) Venn diagram illustrating the overlap of DEGs between miR-196A-KO and miR-196B-KO cells. A subset of genes was commonly regulated by both miR-196 isoforms, while additional genes were uniquely altered in each knockout condition.

    Article Snippet: The human colorectal cancer cell line SW48 (ATCC Cat. No. CCL-231) was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Knock-Out, Control

    Functional enrichment analysis of differentially expressed genes following miR-196A or miR-196B deletion. ( A ) Functional categorization of differentially expressed genes (DEGs) identified in miR-196A-KO cells compared with control SW48 cells. The pie chart shows the percentage distribution of genes associated with major biological processes. The percentages may exceed 100% because individual genes can be associated with multiple functional categories and are therefore counted in more than one category. ( B ) Distribution of significantly up-regulated and down-regulated genes in each functional category in miR-196A-KO cells. ( C ) Expression profiles of representative genes altered in miR-196A-KO cells. Each point represents normalized RNA-seq expression values from independent samples. ( D ) Functional classification of DEGs identified in miR-196B-KO cells relative to control cells. The percentages may exceed 100% because individual genes can be associated with multiple functional categories and are therefore counted in more than one category. ( E ) Numbers of significantly up-regulated and down-regulated genes in each functional category in miR-196B-KO cells. ( F ) Expression patterns of representative genes affected by miR-196B deletion.

    Journal: International Journal of Molecular Sciences

    Article Title: Transcriptomic Profiling Reveals Isoform-Specific Regulatory Roles of miR-196A and miR-196B in Colorectal Cancer Cells

    doi: 10.3390/ijms27093959

    Figure Lengend Snippet: Functional enrichment analysis of differentially expressed genes following miR-196A or miR-196B deletion. ( A ) Functional categorization of differentially expressed genes (DEGs) identified in miR-196A-KO cells compared with control SW48 cells. The pie chart shows the percentage distribution of genes associated with major biological processes. The percentages may exceed 100% because individual genes can be associated with multiple functional categories and are therefore counted in more than one category. ( B ) Distribution of significantly up-regulated and down-regulated genes in each functional category in miR-196A-KO cells. ( C ) Expression profiles of representative genes altered in miR-196A-KO cells. Each point represents normalized RNA-seq expression values from independent samples. ( D ) Functional classification of DEGs identified in miR-196B-KO cells relative to control cells. The percentages may exceed 100% because individual genes can be associated with multiple functional categories and are therefore counted in more than one category. ( E ) Numbers of significantly up-regulated and down-regulated genes in each functional category in miR-196B-KO cells. ( F ) Expression patterns of representative genes affected by miR-196B deletion.

    Article Snippet: The human colorectal cancer cell line SW48 (ATCC Cat. No. CCL-231) was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Functional Assay, Control, Expressing, RNA Sequencing

    Hierarchical clustering and reproducibility assessment of RNA-seq data from miR-196 knockout SW48 cells. ( A – C ) Heatmap visualization of differentially expressed genes between miR-196 knockout cells and parental SW48 cells using fold-change thresholds of >1.5 ( A ), >2.0 ( B ), and >3.0 ( C ). Hierarchical clustering reveals distinct expression patterns associated with miR-196 deletion. ( D ) Pearson correlation heatmap showing strong correlations among biological replicates and experimental groups. Color intensity represents the Pearson correlation coefficient (r), ranging from −1 to 1, where values closer to 1 indicate stronger similarity between samples. The numerical values in each cell correspond to the correlation coefficients. ( E ) Pairwise scatter plot matrix demonstrating high concordance in gene expression profiles across samples. The red line represents the linear regression fit. Asterisks (***) indicate statistical significance ( p < 0.001).

    Journal: International Journal of Molecular Sciences

    Article Title: Transcriptomic Profiling Reveals Isoform-Specific Regulatory Roles of miR-196A and miR-196B in Colorectal Cancer Cells

    doi: 10.3390/ijms27093959

    Figure Lengend Snippet: Hierarchical clustering and reproducibility assessment of RNA-seq data from miR-196 knockout SW48 cells. ( A – C ) Heatmap visualization of differentially expressed genes between miR-196 knockout cells and parental SW48 cells using fold-change thresholds of >1.5 ( A ), >2.0 ( B ), and >3.0 ( C ). Hierarchical clustering reveals distinct expression patterns associated with miR-196 deletion. ( D ) Pearson correlation heatmap showing strong correlations among biological replicates and experimental groups. Color intensity represents the Pearson correlation coefficient (r), ranging from −1 to 1, where values closer to 1 indicate stronger similarity between samples. The numerical values in each cell correspond to the correlation coefficients. ( E ) Pairwise scatter plot matrix demonstrating high concordance in gene expression profiles across samples. The red line represents the linear regression fit. Asterisks (***) indicate statistical significance ( p < 0.001).

    Article Snippet: The human colorectal cancer cell line SW48 (ATCC Cat. No. CCL-231) was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: RNA Sequencing, Knock-Out, Expressing, Gene Expression

    Functional enrichment analysis of genes altered following miR-196 deletion. Gene Ontology (GO) and KEGG pathway enrichment analyses were performed using differentially expressed genes identified from RNA-seq analysis of miR-196A-KO and miR-196B-KO SW48 cells. ( A ) Bubble plot showing significantly enriched GO terms and KEGG pathways in miR-196A-KO cells. Functional categories are grouped into biological process (BP), cellular component (CC), molecular function (MF), and KEGG pathways. Bubble size represents the number of genes associated with each term, and color intensity indicates the −log10( p -value). ( B ) Bubble plot showing enriched GO terms and KEGG pathways in miR-196B-KO cells using the same criteria. ( C ) Distribution of up-regulated and down-regulated genes contributing to each enriched functional category in miR-196A-KO cells. ( D ) Distribution of up-regulated and down-regulated genes contributing to each enriched functional category in miR-196B-KO cells.

    Journal: International Journal of Molecular Sciences

    Article Title: Transcriptomic Profiling Reveals Isoform-Specific Regulatory Roles of miR-196A and miR-196B in Colorectal Cancer Cells

    doi: 10.3390/ijms27093959

    Figure Lengend Snippet: Functional enrichment analysis of genes altered following miR-196 deletion. Gene Ontology (GO) and KEGG pathway enrichment analyses were performed using differentially expressed genes identified from RNA-seq analysis of miR-196A-KO and miR-196B-KO SW48 cells. ( A ) Bubble plot showing significantly enriched GO terms and KEGG pathways in miR-196A-KO cells. Functional categories are grouped into biological process (BP), cellular component (CC), molecular function (MF), and KEGG pathways. Bubble size represents the number of genes associated with each term, and color intensity indicates the −log10( p -value). ( B ) Bubble plot showing enriched GO terms and KEGG pathways in miR-196B-KO cells using the same criteria. ( C ) Distribution of up-regulated and down-regulated genes contributing to each enriched functional category in miR-196A-KO cells. ( D ) Distribution of up-regulated and down-regulated genes contributing to each enriched functional category in miR-196B-KO cells.

    Article Snippet: The human colorectal cancer cell line SW48 (ATCC Cat. No. CCL-231) was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Functional Assay, RNA Sequencing

    Differential gene expression patterns in miR-196A-KO and miR-196B-KO SW48 cells. Radar charts display the top ten most highly upregulated and downregulated genes in each knockout condition. Left panels show average normalized expression values (log2); right panels show fold change relative to parental SW48 cells (SW48-vector). ( A ) Top ten upregulated genes in miR-196A-KO cells, including RIMS2 , ADGRL2 , and LAMA2 . ( B ) Top ten upregulated genes in miR-196B-KO cells, including PCCA , LAMA2 , and AKAP12 . ( C ) Top ten downregulated genes in miR-196A-KO cells, including KRT14 , KLK11 , and KRT16 . ( D ) Top ten downregulated genes in miR-196B-KO cells, including KRT16 , KRT14 , and KRT19 . ( E ) qPCR validation of selected miR-196-associated genes ( NT5E , PRRX1 , KITLG , CLDN4 , and FLG ) in parental SW48 and miR-196 isoform knockout cells, showing isoform-dependent differences in gene expression. Data are presented as mean ± SD ( n = 3).

    Journal: International Journal of Molecular Sciences

    Article Title: Transcriptomic Profiling Reveals Isoform-Specific Regulatory Roles of miR-196A and miR-196B in Colorectal Cancer Cells

    doi: 10.3390/ijms27093959

    Figure Lengend Snippet: Differential gene expression patterns in miR-196A-KO and miR-196B-KO SW48 cells. Radar charts display the top ten most highly upregulated and downregulated genes in each knockout condition. Left panels show average normalized expression values (log2); right panels show fold change relative to parental SW48 cells (SW48-vector). ( A ) Top ten upregulated genes in miR-196A-KO cells, including RIMS2 , ADGRL2 , and LAMA2 . ( B ) Top ten upregulated genes in miR-196B-KO cells, including PCCA , LAMA2 , and AKAP12 . ( C ) Top ten downregulated genes in miR-196A-KO cells, including KRT14 , KLK11 , and KRT16 . ( D ) Top ten downregulated genes in miR-196B-KO cells, including KRT16 , KRT14 , and KRT19 . ( E ) qPCR validation of selected miR-196-associated genes ( NT5E , PRRX1 , KITLG , CLDN4 , and FLG ) in parental SW48 and miR-196 isoform knockout cells, showing isoform-dependent differences in gene expression. Data are presented as mean ± SD ( n = 3).

    Article Snippet: The human colorectal cancer cell line SW48 (ATCC Cat. No. CCL-231) was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Gene Expression, Knock-Out, Expressing, Plasmid Preparation, Biomarker Discovery

    Knockdown of PRMT6 significantly inhibits colorectal tumor proliferation in vivo. ( A ) Representative images of tumors from mice injected with SW48 cells stably expressing shNC or shPRMT6. (B) Tumor growth curves showing the growth rates of tumors derived from mice injected with shNC or shPRMT6 cells. (C) Scatter plot of tumor weights from mice injected with shNC or shPRMT6 cells. (D) Kaplan-Meier survival curves for mice bearing tumors from the three experimental groups. (E) Representative images of immunohistochemistry (IHC) assays showing PRMT6, c-MYC, and Ki-67 expression in tumors. (F) Western blot analysis to detect the expression levels of intratumoral PRMT6, c-MYC, and Ki-67. (G) Working model: PRMT6 mono-methylated c-MYC at arginine 371 site, which suppressed the poly-ubiquitin level of c-MYC, and then promoted colorectal cancer progress. Student’s t-test was employed for statistical analysis, and all Western blot experiments were performed in triplicate

    Journal: Journal of Translational Medicine

    Article Title: PRMT6 promotes colorectal cancer progress via activating MYC signaling

    doi: 10.1186/s12967-025-06097-y

    Figure Lengend Snippet: Knockdown of PRMT6 significantly inhibits colorectal tumor proliferation in vivo. ( A ) Representative images of tumors from mice injected with SW48 cells stably expressing shNC or shPRMT6. (B) Tumor growth curves showing the growth rates of tumors derived from mice injected with shNC or shPRMT6 cells. (C) Scatter plot of tumor weights from mice injected with shNC or shPRMT6 cells. (D) Kaplan-Meier survival curves for mice bearing tumors from the three experimental groups. (E) Representative images of immunohistochemistry (IHC) assays showing PRMT6, c-MYC, and Ki-67 expression in tumors. (F) Western blot analysis to detect the expression levels of intratumoral PRMT6, c-MYC, and Ki-67. (G) Working model: PRMT6 mono-methylated c-MYC at arginine 371 site, which suppressed the poly-ubiquitin level of c-MYC, and then promoted colorectal cancer progress. Student’s t-test was employed for statistical analysis, and all Western blot experiments were performed in triplicate

    Article Snippet: RKO and SW48 cancer cell lines were acquired from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Knockdown, In Vivo, Injection, Stable Transfection, Expressing, Derivative Assay, Immunohistochemistry, Western Blot, Methylation, Ubiquitin Proteomics

    Knockdown of RPS4X expression reduced tumor stemness. (A) The RPS4X gene expression level was assessed by qPCR. GAPDH served as an internal parameter (n = 3). (B) The cell proliferation ability of SW48 was determined using the CCK-8 assay (n = 3). (C–D) Cell migration and invasion ability of SW48 were evaluated (n = 3). Data are presented as mean ± SD. *P < 0.05 (E–F) Cell apoptotic rate of SW48 was evaluated (n = 3). Data are presented as mean ± SD. **P < 0.01. (G) Tumor growth curve and RPS4X down-regulation in tumors from mice (n = 5 per group). Data are presented as mean ± SD. *P < 0.05 **P < 0.01 ***P < 0.001. (H) Representative images showing the tumors harvested from SW48-bearing mice (n = 5 per group). (I)Weight of the harvested tumors from tumor-bearing mice (n = 5 per group). Data are presented as mean ± SD. **P < 0.01.

    Journal: Heliyon

    Article Title: Exercise potentially prevents colorectal cancer liver metastases by suppressing tumor epithelial cell stemness via RPS4X downregulation

    doi: 10.1016/j.heliyon.2024.e26604

    Figure Lengend Snippet: Knockdown of RPS4X expression reduced tumor stemness. (A) The RPS4X gene expression level was assessed by qPCR. GAPDH served as an internal parameter (n = 3). (B) The cell proliferation ability of SW48 was determined using the CCK-8 assay (n = 3). (C–D) Cell migration and invasion ability of SW48 were evaluated (n = 3). Data are presented as mean ± SD. *P < 0.05 (E–F) Cell apoptotic rate of SW48 was evaluated (n = 3). Data are presented as mean ± SD. **P < 0.01. (G) Tumor growth curve and RPS4X down-regulation in tumors from mice (n = 5 per group). Data are presented as mean ± SD. *P < 0.05 **P < 0.01 ***P < 0.001. (H) Representative images showing the tumors harvested from SW48-bearing mice (n = 5 per group). (I)Weight of the harvested tumors from tumor-bearing mice (n = 5 per group). Data are presented as mean ± SD. **P < 0.01.

    Article Snippet: SW48 (catalog KG536) cancer cell lines were purchased from KeyGEN.

    Techniques: Knockdown, Expressing, Gene Expression, CCK-8 Assay, Migration

    HRMA derivative plot for KRAS mutation detection . (A1) Derivative plot generated after ARMS amplification for the detection of KRAS G12V and (B1) KRAS G12D mutations. (A2) Average intensity of the melting peak generated after ARMS-HRMA reaction for the detection of G12V and (B2) G12D mutations in G12V/G12V (SW480) (green line), wt/wt (SW48) (gray line), and G12D/wt (LS174T) (yellow line). **** P value < 0.0001 using Mann–Whitney test. Error bars represent the standard error mean of the average result of at least 8 replicates

    Journal: Analytical and Bioanalytical Chemistry

    Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

    doi: 10.1007/s00216-023-04696-6

    Figure Lengend Snippet: HRMA derivative plot for KRAS mutation detection . (A1) Derivative plot generated after ARMS amplification for the detection of KRAS G12V and (B1) KRAS G12D mutations. (A2) Average intensity of the melting peak generated after ARMS-HRMA reaction for the detection of G12V and (B2) G12D mutations in G12V/G12V (SW480) (green line), wt/wt (SW48) (gray line), and G12D/wt (LS174T) (yellow line). **** P value < 0.0001 using Mann–Whitney test. Error bars represent the standard error mean of the average result of at least 8 replicates

    Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

    Techniques: Mutagenesis, Generated, Amplification, MANN-WHITNEY

    ARMS-HRMA for the detection of KRAS G12V mutation . A HRMA derivative plot for KRAS G12V mutation analysis for the tumor samples T1 (blue green line), T2 (yellow line), T3 (blue line), and T4 (dark gray line). Cell lines SW480 (turquoise line) and SW48 (gray line) as G12V positive and negative controls, respectively. B Difference plot. The difference plot shows the melting curve of each tumor sample subtracted from the SW48 cell line. C Chromograms for SS results for KRAS codon 12 (wt: GGT). Sequence obtained with forward primer. Arrows indicate the mutations at positions 2 of codon 12 of KRAS . Sanger sequencing showed a G to T transversion at position 2 of codon 2 (G12V: GGT > GTT) in tumors T1 and T3, and a G to A transition (G12D: GGT > GAT) in tumor T2. T4 has a wt KRAS codon 12

    Journal: Analytical and Bioanalytical Chemistry

    Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

    doi: 10.1007/s00216-023-04696-6

    Figure Lengend Snippet: ARMS-HRMA for the detection of KRAS G12V mutation . A HRMA derivative plot for KRAS G12V mutation analysis for the tumor samples T1 (blue green line), T2 (yellow line), T3 (blue line), and T4 (dark gray line). Cell lines SW480 (turquoise line) and SW48 (gray line) as G12V positive and negative controls, respectively. B Difference plot. The difference plot shows the melting curve of each tumor sample subtracted from the SW48 cell line. C Chromograms for SS results for KRAS codon 12 (wt: GGT). Sequence obtained with forward primer. Arrows indicate the mutations at positions 2 of codon 12 of KRAS . Sanger sequencing showed a G to T transversion at position 2 of codon 2 (G12V: GGT > GTT) in tumors T1 and T3, and a G to A transition (G12D: GGT > GAT) in tumor T2. T4 has a wt KRAS codon 12

    Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

    Techniques: Mutagenesis, Sequencing

    ARMS-HRMA for the detection of KRAS G12V mutation in tumor samples. A G12V mutation scoring for the set of 30 tumor samples, based on the intensity of the melting peak at 79.5 °C. The dark blue bars represent tumor samples scored as G12V non-mutated. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The blue green bar represents tumor samples scored as G12V mutated; the light gray bar represents the SW48 cell line as the control for G12V non-mutated samples; the turquoise bar represents the SW480 cell line as the control for G12V mutated samples. The dagger represents samples scored as G12V mutated with non-concordant result based on SS. Error bars represent the standard error mean of the average result of at least 4 replicates

    Journal: Analytical and Bioanalytical Chemistry

    Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

    doi: 10.1007/s00216-023-04696-6

    Figure Lengend Snippet: ARMS-HRMA for the detection of KRAS G12V mutation in tumor samples. A G12V mutation scoring for the set of 30 tumor samples, based on the intensity of the melting peak at 79.5 °C. The dark blue bars represent tumor samples scored as G12V non-mutated. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The blue green bar represents tumor samples scored as G12V mutated; the light gray bar represents the SW48 cell line as the control for G12V non-mutated samples; the turquoise bar represents the SW480 cell line as the control for G12V mutated samples. The dagger represents samples scored as G12V mutated with non-concordant result based on SS. Error bars represent the standard error mean of the average result of at least 4 replicates

    Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

    Techniques: Mutagenesis, MANN-WHITNEY, Control

    ARMS-HRMA for KRAS G12D mutation detection. A Derivative plot generated after ARMS amplification for the detection of KRAS G12D mutation in LS174T (wt/G12D) (yellow line) and SW48 (wt/wt) (gray line) cell lines and four tumor samples (T2 (dark yellow line), T3 (blue line), T4 (dark blue line), and T5 (brown line)). B G12D mutation scoring for the set of 30 tumor samples, based on the intensity of the melting peak at 79.5 °C; the dagger represents samples scored as G12D mutated with non-concordant result based on SS, and the asterisk represents samples with non-concordant results by both ddPCR and SS. C Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The dark gray bar represents tumor samples scored as G12D non-mutated; the dark yellow bar represents tumor samples scored as G12D mutated; the light gray SW48 cell line as control for G12D non-mutated samples; the light yellow bar represents the LS174T cell line as the control for G12D mutated samples. Error bars represent the standard error mean of the average result of at least 4 replicates

    Journal: Analytical and Bioanalytical Chemistry

    Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

    doi: 10.1007/s00216-023-04696-6

    Figure Lengend Snippet: ARMS-HRMA for KRAS G12D mutation detection. A Derivative plot generated after ARMS amplification for the detection of KRAS G12D mutation in LS174T (wt/G12D) (yellow line) and SW48 (wt/wt) (gray line) cell lines and four tumor samples (T2 (dark yellow line), T3 (blue line), T4 (dark blue line), and T5 (brown line)). B G12D mutation scoring for the set of 30 tumor samples, based on the intensity of the melting peak at 79.5 °C; the dagger represents samples scored as G12D mutated with non-concordant result based on SS, and the asterisk represents samples with non-concordant results by both ddPCR and SS. C Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The dark gray bar represents tumor samples scored as G12D non-mutated; the dark yellow bar represents tumor samples scored as G12D mutated; the light gray SW48 cell line as control for G12D non-mutated samples; the light yellow bar represents the LS174T cell line as the control for G12D mutated samples. Error bars represent the standard error mean of the average result of at least 4 replicates

    Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

    Techniques: Mutagenesis, Generated, Amplification, MANN-WHITNEY, Control

    ARMS-HRMA detection of KRAS G12V mutation in plasma samples. A G12V mutation scoring for the set of 30 plasma samples, based on the intensity of the melting peak at 79.5 °C. The dark blue bars represent tumor samples scored as G12V non-mutated. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The dark blue bar represents plasma samples scored as G12V mutated; the dark gray bar represents the SW48 cell line as the control for G12V non-mutated samples; the blue bar represents the SW480 cell line as the control for G12V mutated samples. The dagger represents samples scored as G12V mutated with non-concordant result based on SS. Error bars represent the standard error mean of the average result of at least 4 replicates

    Journal: Analytical and Bioanalytical Chemistry

    Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

    doi: 10.1007/s00216-023-04696-6

    Figure Lengend Snippet: ARMS-HRMA detection of KRAS G12V mutation in plasma samples. A G12V mutation scoring for the set of 30 plasma samples, based on the intensity of the melting peak at 79.5 °C. The dark blue bars represent tumor samples scored as G12V non-mutated. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The dark blue bar represents plasma samples scored as G12V mutated; the dark gray bar represents the SW48 cell line as the control for G12V non-mutated samples; the blue bar represents the SW480 cell line as the control for G12V mutated samples. The dagger represents samples scored as G12V mutated with non-concordant result based on SS. Error bars represent the standard error mean of the average result of at least 4 replicates

    Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

    Techniques: Mutagenesis, Clinical Proteomics, MANN-WHITNEY, Control

    ARMS-HRMA for KRAS G12D mutation detection on plasma samples. A Derivative plot generated after ARMS amplification for the detection of KRAS G12D mutation in plasma sample P7. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. C Mutation scoring for the set of 24 plasma samples, based on the average intensity of the melting peak at 79.5 °C/80 °C. The dark gray bar represents plasma samples scored as G12D non-mutated; the dark yellow bar represents plasma samples scored as G12D mutated; the light gray bar represents the SW48 cell line as the control for G12D non-mutated samples; the yellow bar represents the LS174T cell line as the control for G12D mutated samples. The asterisk represents samples scored as G12D mutated with non-concordant result based on SS and ddPCR

    Journal: Analytical and Bioanalytical Chemistry

    Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

    doi: 10.1007/s00216-023-04696-6

    Figure Lengend Snippet: ARMS-HRMA for KRAS G12D mutation detection on plasma samples. A Derivative plot generated after ARMS amplification for the detection of KRAS G12D mutation in plasma sample P7. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. C Mutation scoring for the set of 24 plasma samples, based on the average intensity of the melting peak at 79.5 °C/80 °C. The dark gray bar represents plasma samples scored as G12D non-mutated; the dark yellow bar represents plasma samples scored as G12D mutated; the light gray bar represents the SW48 cell line as the control for G12D non-mutated samples; the yellow bar represents the LS174T cell line as the control for G12D mutated samples. The asterisk represents samples scored as G12D mutated with non-concordant result based on SS and ddPCR

    Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

    Techniques: Mutagenesis, Clinical Proteomics, Generated, Amplification, MANN-WHITNEY, Control