sw48 human colorectal cancer cell lines  (ATCC)

Journal: Genes

Article Title: Isoform-Specific Transcriptomic Effects of miR-133A1 , miR-133A2 , and miR-133B in a Colorectal Cancer Cell Line

doi: 10.3390/genes16111322

Figure Lengend Snippet: Functional categorization of differentially expressed genes regulated by miR-133 isoforms. ( A ) Schematic representation of mature miR-133 isoform sequences. miR-133A1 and miR-133A2 are identical, while miR-133B contains a G→A substitution at position 22. The seed region (positions 2–8, dashed purple box) is identical across all isoforms. ( B ) qRT-PCR validation of miR-133 overexpression in SW48 cells. Data represent mean ± SD (n = 3). (** p < 0.01, *** p < 0.001 vs. vector control). DOX(−): non-induced; DOX(+): doxycycline-induced. (C-E) Functional categorization of differentially expressed genes in miR-133A1 ( C ), miR-133A2 ( D ), and miR-133B ( E ) stable cell lines. Pie charts show proportional distribution across biological processes; bar graphs show directional regulation (red: upregulated; blue: downregulated).

Article Snippet: Human colorectal cancer SW48 cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA; Cat. No. CCL-231) and maintained in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; HyClone, Logan, UT, USA), 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 °C in a humidified atmosphere with 5% CO 2 .

Techniques: Functional Assay, Quantitative RT-PCR, Biomarker Discovery, Over Expression, Plasmid Preparation, Control, Stable Transfection

Journal: Genes

Article Title: Isoform-Specific Transcriptomic Effects of miR-133A1 , miR-133A2 , and miR-133B in a Colorectal Cancer Cell Line

doi: 10.3390/genes16111322

Figure Lengend Snippet: Comparative analysis of differentially expressed genes regulated by miR-133 isoforms. ( A ) Venn diagram showing the overlap of differentially expressed genes among SW48-KI133A1, SW48-KI133A2, and SW48-KI133B cells compared with parental SW48 controls. Numbers indicate isoform-specific and shared upregulated (red) and downregulated (blue) genes. ( B – D ) Scatter plots depicting log2-normalized expression changes in SW48-KI133A1 ( B ), SW48-KI133A2 ( C ), and SW48-KI133B ( D ) relative to SW48 control cells. Red dots represent significantly upregulated genes, while blue dots indicate significantly downregulated genes. The results highlight both common and isoform-specific transcriptional signatures regulated by miR-133 isoforms.

Article Snippet: Human colorectal cancer SW48 cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA; Cat. No. CCL-231) and maintained in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; HyClone, Logan, UT, USA), 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 °C in a humidified atmosphere with 5% CO 2 .

Techniques: Expressing, Control

Journal: Genes

Article Title: Isoform-Specific Transcriptomic Effects of miR-133A1 , miR-133A2 , and miR-133B in a Colorectal Cancer Cell Line

doi: 10.3390/genes16111322

Figure Lengend Snippet: Hierarchical clustering and correlation analysis of differentially expressed genes in miR-133 isoform-expressing SW48 cells. ( A ) Heatmaps showing hierarchical clustering of differentially expressed genes at three-fold change thresholds (>1.5, >2.0, and >3.0) for SW48-KI 133A1 , SW48-KI 133A2 , and SW48-KI 133B cells compared with parental SW48 controls. Rows represent individual genes, and columns represent two independent biological replicates. Red indicates upregulated genes, and blue indicates downregulated genes. At higher thresholds, core isoform-specific genes (labeled on the right) are highlighted. KI 133A1 and KI 133A2 show similar expression patterns, whereas KI 133B displays a distinct transcriptional profile. ( B ) Pearson correlation matrix (left) and scatter plots (right) of all biological replicates across samples. Strong correlations (r = 0.95–0.99) confirm high reproducibility between replicates and support the robustness of differential expression analysis. These results indicate that the observed transcriptomic differences among isoforms are biologically reproducible rather than experimental noise. Asterisks indicate statistical significance (*** p < 0.001).

Article Snippet: Human colorectal cancer SW48 cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA; Cat. No. CCL-231) and maintained in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; HyClone, Logan, UT, USA), 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 °C in a humidified atmosphere with 5% CO 2 .

Techniques: Expressing, Labeling, Quantitative Proteomics

Journal: Genes

Article Title: Isoform-Specific Transcriptomic Effects of miR-133A1 , miR-133A2 , and miR-133B in a Colorectal Cancer Cell Line

doi: 10.3390/genes16111322

Figure Lengend Snippet: Comparative GO and KEGG enrichment analysis of differentially expressed genes across miR-133 isoforms. The upper panel presents a merged visualization of enriched GO categories (BP: Biological Process, CC: Cellular Component, MF: Molecular Function) combining data from all three miR-133 isoforms in a single integrated bar plot. The lower panel displays KEGG pathway enrichment analysis. Bar plots show enrichment in SW48-KI 133A1 (red/pink bars), SW48-KI 133A2 (blue/light blue bars), and SW48-KI 133B (dark blue/yellow bars) compared with parental SW48 controls. For each isoform, darker-colored bars represent downregulated gene sets and lighter-colored bars represent upregulated gene sets. Bars are grouped by functional category to facilitate direct comparison across the three isoforms. The side-by-side presentation reveals highly convergent enrichment patterns across all three miR-133 isoforms, with consistent regulation of cell proliferation, metal ion homeostasis, extracellular components, protein binding functions, and cancer-associated signaling pathways.

Article Snippet: Human colorectal cancer SW48 cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA; Cat. No. CCL-231) and maintained in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; HyClone, Logan, UT, USA), 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 °C in a humidified atmosphere with 5% CO 2 .

Techniques: Functional Assay, Comparison, Protein Binding, Protein-Protein interactions

Journal: Genes

Article Title: Isoform-Specific Transcriptomic Effects of miR-133A1 , miR-133A2 , and miR-133B in a Colorectal Cancer Cell Line

doi: 10.3390/genes16111322

Figure Lengend Snippet: Heatmap representation of fold change values for representative genes regulated by miR-133 isoforms. Heatmaps show the relative expression (fold change) of selected genes in SW48-KI 133-A1 , SW48-KI 133-A2 , and SW48-KI 133-B compared with parental SW48 controls. Red indicates upregulation (fold change > 1.5), and blue indicates downregulation (fold change < 0.67). ( A ) Apoptosis-related genes. ( B ) Cell cycle genes. ( C ) Cell migration genes. ( D ) Immune response genes. ( E ) Cell differentiation genes. ( F ) Angiogenesis-related gene. ( G ) Inflammatory response genes. Note that some panels share common genes (e.g., PPIA) as these genes are functionally involved in multiple biological processes.

Article Snippet: Human colorectal cancer SW48 cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA; Cat. No. CCL-231) and maintained in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; HyClone, Logan, UT, USA), 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 °C in a humidified atmosphere with 5% CO 2 .

Techniques: Expressing, Migration, Cell Differentiation

Journal: BioMed Research International

Article Title: SEMA4D Knockdown Attenuates β -Catenin-Dependent Tumor Progression in Colorectal Cancer

doi: 10.1155/2021/8507373

Figure Lengend Snippet: Effect of siRNA SEMA4D on SW48 cells viability. (a) MTT analysis of SW48 cells in the presence and absence of siRNA SEMA4D. (b) Cells were transfected with SEMA4D siRNA and scrambled siRNA and untransfected as control. RT-qPCR analysis revealed the downregulation of SEMA4D in siRNA SEMA4D transfected cells. (c) The effect of siRNA SEMA4D on the proliferation of SW48 cells was analyzed by colony formation assay. The findings are expressed as mean ± standard deviation (SD) of three independent experiments. ∗∗∗ P < 0.001 compared with control.

Article Snippet: As a model of colon cancer cells, the SW48 human colorectal cancer cell line, purchased from the National Cell Bank of Pasteur Institute (Tehran, Iran), was used.

Techniques: Transfection, Control, Quantitative RT-PCR, Colony Assay, Standard Deviation

Journal: BioMed Research International

Article Title: SEMA4D Knockdown Attenuates β -Catenin-Dependent Tumor Progression in Colorectal Cancer

doi: 10.1155/2021/8507373

Figure Lengend Snippet: Effect of siRNA SEMA4D on SW48 cells apoptosis. (a) Induction of apoptosis was measured by flow cytometry analysis after 72 h in the presence and absence of siRNA SEMA4D. (b) mRNA levels of caspase 3, P53, Bcl2, and Bax were analyzed by qRT-PCR in transfected and untransfected SW48 cells. GAPDH was employed as an internal control. The data are expressed as mean ± standard deviation, and each experiment was repeated three times. ∗∗∗ P < 0.001 vs. control group.

Article Snippet: As a model of colon cancer cells, the SW48 human colorectal cancer cell line, purchased from the National Cell Bank of Pasteur Institute (Tehran, Iran), was used.

Techniques: Flow Cytometry, Quantitative RT-PCR, Transfection, Control, Standard Deviation

Journal: BioMed Research International

Article Title: SEMA4D Knockdown Attenuates β -Catenin-Dependent Tumor Progression in Colorectal Cancer

doi: 10.1155/2021/8507373

Figure Lengend Snippet: Effect of SEMA4D silencing on cell migration. (a) Representative image of SW48 cell migration in the absence and presence of siRNA SEMA4D at 0 h, 24 h, and 48 h. The scratched areas were measured in three random fields in each group. (b) The effect of siRNA SEMA4D on MMP-2 and MMP-9 activity, which was evaluated by gelatin zymography. Gelatinolytic activity of MMP-2 and MMP-9 is revealed in polyacrylamide gel by white banding. (c) The MMP-2 and MMP-9 gene expression was analyzed by real-time PCR. Data are represented as mean ± standard deviation ∗∗∗ P < 0.001 vs. control group.

Article Snippet: As a model of colon cancer cells, the SW48 human colorectal cancer cell line, purchased from the National Cell Bank of Pasteur Institute (Tehran, Iran), was used.

Techniques: Migration, Activity Assay, Zymography, Gene Expression, Real-time Polymerase Chain Reaction, Standard Deviation, Control

Journal: BMC Cancer

Article Title: Ras-ERK1/2 signaling contributes to the development of colorectal cancer via regulating H3K9ac

doi: 10.1186/s12885-018-5199-3

Figure Lengend Snippet: Ras-ERK1/2 repressed H3K9 acetylation in SW48 cells. SW48 cells were transfected with empty pEGFP vector, pEGFP-K-Ras-WT (wild type) or pEGFP-K-Ras G12V/T35S construct. Protein levels of a p-ERK1/2 and b and c H3K9ac were measured by Western blot analysis. ** P < 0.01. Four inhibitors specific for ERK1/2, MAPK, PI3K and JNK pathways, i.e., SCH772984, SB203580, LY294002 and SP600125 were used to treat cells. Protein levels of d H3K9ac and e p-ERK1/2 were measured by Western blot analysis

Article Snippet: Human colorectal cancer cell line SW48 purchased from American Type Culture Collection (Catalogue number: CCL-231TM, ATCC, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco, Grand Island, NY, USA) supplemented with 10% heat-inactivated fetal bovine serum (FBS, Gibco).

Techniques: Transfection, Plasmid Preparation, Construct, Western Blot

Journal: BMC Cancer

Article Title: Ras-ERK1/2 signaling contributes to the development of colorectal cancer via regulating H3K9ac

doi: 10.1186/s12885-018-5199-3

Figure Lengend Snippet: Ras-ERK1/2 repressed H3K9 acetylation to promote the growth and migration of SW48 cells. a SW48 cells were transfected with pEGFP-H3, pEGFP-K-Ras G12V/T35S plus pEGFP-H3, or pEGFP-K-Ras G12V/T35S plus pEGFP-H3K9Q (with increasing amount 0.5, 1, and 2 g). a Transfection efficiency was tested by Western blot. b MTT assay was performed to assess cell viability. Subsequently, pEGFP-H3, pEGFP-K-Ras G12V/T35S plus pEGFP-H3, or pEGFP-K-Ras G12V/T35S plus pEGFP-H3K9Q (2 g) was transfected into cell, and c number of colonies and d cell migration were respectively determined by colony formation assay and transwell assay. ** P < 0.01; *** P < 0.001

Article Snippet: Human colorectal cancer cell line SW48 purchased from American Type Culture Collection (Catalogue number: CCL-231TM, ATCC, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco, Grand Island, NY, USA) supplemented with 10% heat-inactivated fetal bovine serum (FBS, Gibco).

Techniques: Migration, Transfection, Western Blot, MTT Assay, Colony Assay, Transwell Assay

Journal: BMC Cancer

Article Title: Ras-ERK1/2 signaling contributes to the development of colorectal cancer via regulating H3K9ac

doi: 10.1186/s12885-018-5199-3

Figure Lengend Snippet: Ras-ERK1/2 repressed H3K9 acetylation to affect the transcription of Ras downstream genes. SW48 cells were transfected with pEGFP-H3, pEGFP-K-Ras G12V/T35S plus pEGFP-H3, or pEGFP-K-Ras G12V/T35S plus pEGFP-H3K9Q. a RT-qPCR was performed to assess the expression levels of these genes. b ChIP was conducted to assess the levels of H3K9ac when different genes were expressed. * P < 0.05; ** P < 0.01; *** P < 0.001

Article Snippet: Human colorectal cancer cell line SW48 purchased from American Type Culture Collection (Catalogue number: CCL-231TM, ATCC, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco, Grand Island, NY, USA) supplemented with 10% heat-inactivated fetal bovine serum (FBS, Gibco).

Techniques: Transfection, Quantitative RT-PCR, Expressing

Journal: BMC Cancer

Article Title: Ras-ERK1/2 signaling contributes to the development of colorectal cancer via regulating H3K9ac

doi: 10.1186/s12885-018-5199-3

Figure Lengend Snippet: Silence of HDAC2 recovered H3K9 acetylation and SW48 cells phenotype. a The efficiency of siRNA-mediated HDAC2 silence was determined. b SW40 cells were transfected as indicated. The expression changes of H3K9ac were detected by Western blot analysis. c Cell viability, d migration, e cell cycle progression, and f several gene transcription were respectively assessed by MTT assay, transwell assay, flow cytometry and RT-qPCR. * P < 0.05; ** P < 0.01; *** P < 0.001

Article Snippet: Human colorectal cancer cell line SW48 purchased from American Type Culture Collection (Catalogue number: CCL-231TM, ATCC, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco, Grand Island, NY, USA) supplemented with 10% heat-inactivated fetal bovine serum (FBS, Gibco).

Techniques: Transfection, Expressing, Western Blot, Migration, MTT Assay, Transwell Assay, Flow Cytometry, Quantitative RT-PCR

Journal: BMC Cancer

Article Title: Ras-ERK1/2 signaling contributes to the development of colorectal cancer via regulating H3K9ac

doi: 10.1186/s12885-018-5199-3

Figure Lengend Snippet: Ras-ERK1/2 repressed H3K9 acetylation in SW48 cells via degradation of PCAF. a The mRNA level of PCAF after the indicated transfected was tested. b and c Western blot analysis was performed to measure the expression of PCAF, HDAC2, and H3K9ac following the indicated transfection. Anti-HA antibody was used for testing the exogenous levels of PCAF and HDAC2. d ChIP analysis for testing PCAF levels when different genes were expressed. e 25 μM of MG132 was used to treat cells, after which Western blot was performed to reassess PCAF level. Protein expression of H3K9ac was monitored in the f absence or g presence of MG132. ** P < 0.01; *** P < 0.001

Article Snippet: Human colorectal cancer cell line SW48 purchased from American Type Culture Collection (Catalogue number: CCL-231TM, ATCC, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco, Grand Island, NY, USA) supplemented with 10% heat-inactivated fetal bovine serum (FBS, Gibco).

Techniques: Transfection, Western Blot, Expressing

Journal: BMC Cancer

Article Title: Ras-ERK1/2 signaling contributes to the development of colorectal cancer via regulating H3K9ac

doi: 10.1186/s12885-018-5199-3

Figure Lengend Snippet: Ras-ERK1/2 regulated H3K9ac via MDM2-mediated PCAF degradation. SW48 cells were transfected with pEGFP-K-Ras G12V/T35S , PCAF-HA, MDM2-His (with increasing amount 0.5, 1, and 2 g) and pEGFP-N1. a Exogenous and b endogenous expression of PCAF was measured by Western blot. SW48 cells were transfected either by MDM2-His (2 g) or by MDM2 mutated type (MDM2-MU), then c exogenous and d endogenous expression of PCAF were reassessed. Anti-His and anti-HA antibodies were used for testing the exogenous levels of MDM2 and PCAF, respectively. e MDM2 and H3K9ac expression in cells transfected with pEGFP-K-Ras G12V/T35S or pEGFP-N1. f The protein level of MDM2 after siRNA transfection was tested. g After the indicated transfection, H3K9ac level was tested by Western blot

Article Snippet: Human colorectal cancer cell line SW48 purchased from American Type Culture Collection (Catalogue number: CCL-231TM, ATCC, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco, Grand Island, NY, USA) supplemented with 10% heat-inactivated fetal bovine serum (FBS, Gibco).

Techniques: Transfection, Expressing, Western Blot

Journal: Iranian Journal of Medical Sciences

Article Title: The Effects of NDRG2 Overexpression on Cell Proliferation and Invasiveness of SW48 Colorectal Cancer Cell Line

doi:

Figure Lengend Snippet: GFP-tagged NDRG2 overexpressed in the SW48 cells. Green fluorescence represented the successful transfection and overexpression of GFP-tagged NDRG2. The exogenously introduced NDRG2 was localized in the cytoplasm of the SW48 cells.

Article Snippet: The human colorectal cancer cell line SW48 was purchased from the cell bank of the Pasteur institute of Iran (ATCC number: CCL-231).

Techniques: Fluorescence, Transfection, Over Expression

Journal: Iranian Journal of Medical Sciences

Article Title: The Effects of NDRG2 Overexpression on Cell Proliferation and Invasiveness of SW48 Colorectal Cancer Cell Line

doi:

Figure Lengend Snippet: NDRG2 overexpression reduced SW48 cell viability. Cell viability was determined by MTT assay. Compared with the control and mock group, overexpression of NDRG2 significantly inhibited the proliferation of SW48 cells at 4 to 7 days after stable transfection. The results are the mean±SD of at least three independent experiments (*P<0.001 compare to WT group, by two-way repeated measures ANOVA).

Article Snippet: The human colorectal cancer cell line SW48 was purchased from the cell bank of the Pasteur institute of Iran (ATCC number: CCL-231).

Techniques: Over Expression, MTT Assay, Control, Stable Transfection

Journal: Iranian Journal of Medical Sciences

Article Title: The Effects of NDRG2 Overexpression on Cell Proliferation and Invasiveness of SW48 Colorectal Cancer Cell Line

doi:

Figure Lengend Snippet: NDRG2 overexpression reduced migration of SW48 cell. Cell migration was determined by transwell assay. Compared with the control and mock group, overexpression of NDRG2 significantly decreased the number of migrated SW48 cells. The results are the mean±SD of at least three independent experiments (*P<0.001 compare to WT group).

Article Snippet: The human colorectal cancer cell line SW48 was purchased from the cell bank of the Pasteur institute of Iran (ATCC number: CCL-231).

Techniques: Over Expression, Migration, Transwell Assay, Control

Journal: Iranian Journal of Medical Sciences

Article Title: The Effects of NDRG2 Overexpression on Cell Proliferation and Invasiveness of SW48 Colorectal Cancer Cell Line

doi:

Figure Lengend Snippet: NDRG2 overexpression reduced invasion of SW48 cell. Cell invasion was determined by matrigel-transwell assay. Compared with the control and mock group, overexpression of NDRG2 significantly decreased the number of invaded SW48 cells. The results are the mean±SD of at least three independent experiments (*P<0.001 compare to WT group).

Article Snippet: The human colorectal cancer cell line SW48 was purchased from the cell bank of the Pasteur institute of Iran (ATCC number: CCL-231).

Techniques: Over Expression, Transwell Assay, Control

Journal: Iranian Journal of Medical Sciences

Article Title: The Effects of NDRG2 Overexpression on Cell Proliferation and Invasiveness of SW48 Colorectal Cancer Cell Line

doi:

Figure Lengend Snippet: NDRG2 overexpression reduced SW48 cells cell motility. The cell motility of stably transfected pCMV6-AC-GFP-NDRG2 cells (NDRG2 group) and pCMV6-AC-GFP transfected cells (mock group) was determined by wound migration assay. A: Representative photographs taken at 0 h and 24 h after scratch creating (40×). B: Percent of wound closure was measured at 0 h and 24 h after scratch creating using image J software. The experiments were performed in triplicate (*P<0.01).

Article Snippet: The human colorectal cancer cell line SW48 was purchased from the cell bank of the Pasteur institute of Iran (ATCC number: CCL-231).

Techniques: Over Expression, Stable Transfection, Transfection, Migration, Software