hct 116 colon cancer cell line  (ATCC)

Journal: RSC Advances

Article Title: Synthesis, structural characterization and molecular docking analysis of novel β-ketoiminato palladium( ii ) complexes with anticancer properties

doi: 10.1039/d5ra09325b

Figure Lengend Snippet: Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 and HCT-116 cell lines.

Article Snippet: Cancer cell lines were obtained from the ATCC (Manassas, VA), MCF7 human breast cancer cell line (ATCC® HTB-22TM, USA), HCT-116 colon cancer cell line (ATCC CCL-247TM, USA) and human skin fibroblast (ATCC® PCS-201-012TM).

Techniques:

Journal: RSC Advances

Article Title: Synthesis, structural characterization and molecular docking analysis of novel β-ketoiminato palladium( ii ) complexes with anticancer properties

doi: 10.1039/d5ra09325b

Figure Lengend Snippet: Combined histogram displaying the binding energy scores of the Pd( ii ) complexes 4 and 5 against the KRAS-G13D, PIK3CA-H1047R and ATM-A112V targeted proteins in HCT-116.

Article Snippet: Cancer cell lines were obtained from the ATCC (Manassas, VA), MCF7 human breast cancer cell line (ATCC® HTB-22TM, USA), HCT-116 colon cancer cell line (ATCC CCL-247TM, USA) and human skin fibroblast (ATCC® PCS-201-012TM).

Techniques: Binding Assay

Journal: International Journal of Molecular Sciences

Article Title: Anticancer Activity of the Antimicrobial Myristoylated Peptide Myr-B in HeLa Cells: Cytotoxic, Membrane-Disruptive and Proteomic Insights

doi: 10.3390/ijms27093918

Figure Lengend Snippet: The cytotoxic effect of Myr-B peptide against human colon cancer Caco-2 cells. Cell viability was assessed using the MTT assay for the Caco-2 cell line after 3 h and 24 h of incubation with N-myristoylated Myr-B peptide ( a ) and corresponding non-myristoylated Pep-B peptide ( b ). Data are expressed as a percentage of viable cells in the presence of different peptide concentrations (2.5–50 µM) compared to untreated Caco-2 cells (negative control). Positive control represents cells treated with 2% NaN 3 . Untreated cells serve as negative control. All experiments were performed using two independent replicates, each with at least three repeats. Statistical significance was assessed using one-way ANOVA followed by Dunnett’s post hoc test (GraphPad Prism 11.0). Difference from the negative control was considered statistically significant as follows: ** adjusted p -value < 0.01; **** p -value < 0.0001.

Article Snippet: The human colon cancer Caco-2 cell line (ATCC HTB-37) was cultured in DMEM supplemented with 10% ( v / v ) FBS, 1% ( w / v ) glutamine, 1% ( w / v ) penicillin–streptomycin, 1% Non-Essential Amino Acids and 1% sodium pyruvate and maintained at 37 °C in a humidified incubator with 5% CO 2 [ ].

Techniques: MTT Assay, Incubation, Negative Control, Positive Control

Journal: International Journal of Molecular Sciences

Article Title: Anticancer Activity of the Antimicrobial Myristoylated Peptide Myr-B in HeLa Cells: Cytotoxic, Membrane-Disruptive and Proteomic Insights

doi: 10.3390/ijms27093918

Figure Lengend Snippet: Evaluation of Myr-B peptide-induced death of human cervical cancer HeLa ( a ) and colon cancer Caco-2 ( b ) cells. Cell membrane integrity was assessed through lactate dehydrogenase (LDH) release from untreated HeLa or Caco-2 cells (negative control) after 3 h exposure of HeLa and Caco-2 cells to their respective IC 50 doses of Myr-B peptide (38 μM and 50 μM, respectively) and from HeLa or Caco-2 cells treated with a lysis solution to release all LDH (positive control). The exposure to Pep-B was carried out under the same conditions as the corresponding treatment with the Myr-B peptide for each cancer cell line. Statistical significance was assessed using one-way ANOVA followed by Dunnett’s post hoc test (GraphPad Prism 11.0). Difference from the negative control was considered statistically significant as follows: * adjusted p -value < 0.05; *** p -value < 0.001; **** p -value < 0.0001.

Article Snippet: The human colon cancer Caco-2 cell line (ATCC HTB-37) was cultured in DMEM supplemented with 10% ( v / v ) FBS, 1% ( w / v ) glutamine, 1% ( w / v ) penicillin–streptomycin, 1% Non-Essential Amino Acids and 1% sodium pyruvate and maintained at 37 °C in a humidified incubator with 5% CO 2 [ ].

Techniques: Membrane, Negative Control, Lysis, Positive Control

Journal: International Journal of Molecular Sciences

Article Title: Anticancer Activity of the Antimicrobial Myristoylated Peptide Myr-B in HeLa Cells: Cytotoxic, Membrane-Disruptive and Proteomic Insights

doi: 10.3390/ijms27093918

Figure Lengend Snippet: SEM analysis of Myr-B peptide-induced effects on human colon cancer Caco-2 cells. SEM micrographs (acquired and processed using JEOL inTouchScope Interface software) of untreated Caco-2 cells (negative control) ( a , b ), Caco-2 cells after 3 h exposure to 50 μM Myr-B ( c , d ) and 50 μM Pep-B ( e , f ) and Caco-2 cells treated with 2% NaN 3 (positive control) ( g , h ). Magnification and scale bars = ( a – d ) 1500× and 10 μm, respectively; ( e – h ) 10,000× and 1 μm, respectively.

Article Snippet: The human colon cancer Caco-2 cell line (ATCC HTB-37) was cultured in DMEM supplemented with 10% ( v / v ) FBS, 1% ( w / v ) glutamine, 1% ( w / v ) penicillin–streptomycin, 1% Non-Essential Amino Acids and 1% sodium pyruvate and maintained at 37 °C in a humidified incubator with 5% CO 2 [ ].

Techniques: Software, Negative Control, Positive Control

Journal: Cell Reports Medicine

Article Title: Immunogenic tumor cell death and T-cell-derived IFN-γ elicit tumoricidal macrophages to potentiate OX40 immunotherapy

doi: 10.1016/j.xcrm.2026.102699

Figure Lengend Snippet: scRNA-seq reveals differential immune infiltration in αOX40-treated tumors based on response (A) Schematic of the bilateral MC38 tumor model assessing αOX40 response. Humanized OX40 mice received three doses of αOX40, followed by resection of the left tumor for scRNA-seq and flow cytometry analysis. Contralateral tumor dynamics and survival were monitored longitudinally. (B) UMAP visualization of scRNA-seq data from immune cells in MC38-bearing mice following αOX40 treatment. Cells are color-coded by annotated cell type. (C) Heatmap depicting nine transcriptionally distinct immune cell subpopulations. (D) Pie chart shows the relative abundance of nine immune cell clusters in αOX40 responders and nonresponders. (E) Flow cytometry analysis of tumor-infiltrating immune cell frequencies in αOX40-treated MC38-bearing mice. Frequencies of CD4 + T cells, CD8 + T cells, and macrophages were quantified after the third αOX40 dose (control, n = 5 mice; mice with a robust therapeutic response named as responder, n = 4 mice; mice with minimal to no response named as nonresponder, n = 4 mice). Data represent mean ± SD from one of two independent experiments (E). Statistical significance was determined using one-way ANOVA with multiple comparisons. ∗∗ p < 0.01.

Article Snippet: The mouse colon cancer MC38 cell line (Cat. NO. NM-S13) and the pancreatic cancer KPC cell line (Cat. NO. NM-YD04) were purchased from Shanghai Model Organisms Center, Inc.

Techniques: Flow Cytometry, Control, Clinical Proteomics

Journal: Cell Reports Medicine

Article Title: Immunogenic tumor cell death and T-cell-derived IFN-γ elicit tumoricidal macrophages to potentiate OX40 immunotherapy

doi: 10.1016/j.xcrm.2026.102699

Figure Lengend Snippet: NOS2-expressing macrophages is associated with response to αOX40 therapy (A) UMAP of monocytes/macrophages subclusters from scRNA-seq data in αOX40-treated MC38-bearing mice. (B) Representative marker genes in the monocyte/macrophage subclusters. (C) Pie chart showing the proportional distribution of monocyte/macrophage subsets of responders and nonresponders. (D) QuSAGE pathway analysis demonstrated enrichment of innate immune and phagocytic signaling pathways in distinct monocyte/macrophage subsets. (E) UMAP showing Mac_C1 signature genes and a heatmap of immune-related gene expression across TAM subclusters ( Z score normalized). (F) Violin plots comparing Nos2 expression levels in Mac_C1 subset between responsive and nonresponsive. (G) Flow cytometry analysis shows the percentage of M1-like (F4/80 + NOS2 + ) and M2-like (F4/80 + CD206 + ) macrophages in tumor tissues of control ( n = 5 mice), nonresponders (with minimal to no response, n = 4 mice), and responders (with a robust therapeutic response, n = 4 mice). (H and I) Comparison of Nos2 expression levels in responders versus nonresponders pre- or post-αOX40 treatment. Bilateral-MC38-bearing mice were treated with αOX40, and tumors from one side were analyzed by RNA-seq prior to (H) or following αOX40 treatment (I). The Nos2 expression was analyzed from RNA-seq data (left) and validated by RT-qPCR (right) ( n = 5 biological replicates). (J) NOS2 expression in tumor biopsies post-treatment determined by RNA-seq. Patients with advanced solid tumors and >1 prior therapy received HFB301001 monotherapy. Tumor biopsy samples were obtained on day 8 of cycle 2 for subsequent RNA-seq analysis. NOS2 expression were compared between patients achieving stable disease (SD, n = 3) and those with progressive disease (PD, n = 3). (K) GO enrichment analysis of upregulated genes in Mac_C1 of responders. (L) Calreticulin expression was quantified by flow cytometry in different response groups following αOX40 treatment ( n = 3 mice per group). (M) NOS2 expression in BMDMs was analyzed by flow cytometry after stimulation with CD8 + T cell supernatant and MC38 lysate, combined with TLR inhibition and IFN-γ blockade ( n = 5 biological replicates). (N) Quantification of Nos2 expression in BMDM by RT-qPCR after 24-h stimulation with MPLA (TLR4 agonist, 100 ng/mL), IFN-γ (20 ng/mL), or both. Data normalized to Gapdh and presented as fold-change relative to unstimulated controls ( n = 4 biological replicates). Data are shown as means ± SD from one of two independent experiments (G, H, I, L, M, and N). Statistical significance was determined using one-way ANOVA with multiple comparisons (G, L, M, and N) or using an unpaired two-tailed t test (H, I, and J). n.s., not significant; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; VST, variance stabilized transformation; sup., supernatant; lys., tumor lysate; inh., inhibitor.

Article Snippet: The mouse colon cancer MC38 cell line (Cat. NO. NM-S13) and the pancreatic cancer KPC cell line (Cat. NO. NM-YD04) were purchased from Shanghai Model Organisms Center, Inc.

Techniques: Expressing, Marker, Protein-Protein interactions, Gene Expression, Flow Cytometry, Control, Clinical Proteomics, Comparison, RNA Sequencing, Quantitative RT-PCR, Inhibition, Two Tailed Test, Transformation Assay

Journal: Cell Reports Medicine

Article Title: Immunogenic tumor cell death and T-cell-derived IFN-γ elicit tumoricidal macrophages to potentiate OX40 immunotherapy

doi: 10.1016/j.xcrm.2026.102699

Figure Lengend Snippet: Rational modulation of tumor microenvironment enhances therapeutic responsiveness to αOX40-based immunotherapy (A–D) OX40-humanized mice bearing subcutaneous MC38 (A), B16 (B), E.G7 (C), or KPC (D) tumors ( n = 5–7 mice per group). Tumor growth curves (numbers indicate complete cures) and Kaplan-Meier survival for each model. Treatments: MPLA+IFN-γ ( i.t. , intratumoral); Combo: MPLA+IFN-γ ( i.t. , intratumoral) + αOX40 ( i.p. , intraperitoneal). (E) Study schema of secondary tumor challenge in MC38 model treated with Combo. (F) Tumor progression and survival outcomes following secondary tumor challenge. Growth kinetics of re-implanted tumors in tumor-cleared mice (previously cured by therapy) versus treatment-naive wild-type controls (left). Kaplan-Meier survival plot (right) ( n = 13 mice per group). (G) Systemic immunity evaluation schema with bilateral MC38 bearing mice were treated with Combo, αOX40, and control. (H) Tumor growth curves and survival plots of (G) ( n = 6–7 mice per group). Data are shown as means ± SD from one of two independent experiments (A–D, F, and H). Statistical significance was determined using log rank test (A–H). n.s., not significant; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: The mouse colon cancer MC38 cell line (Cat. NO. NM-S13) and the pancreatic cancer KPC cell line (Cat. NO. NM-YD04) were purchased from Shanghai Model Organisms Center, Inc.

Techniques: Control

Journal: Cell Reports Medicine

Article Title: Immunogenic tumor cell death and T-cell-derived IFN-γ elicit tumoricidal macrophages to potentiate OX40 immunotherapy

doi: 10.1016/j.xcrm.2026.102699

Figure Lengend Snippet: The antitumor efficacy of the Combo therapy is contingent upon CD8 + T cells and macrophages (A) UMAP of scRNA-seq data from tumor-infiltrating immune cells in OX40-humanized MC38-bearing mice treated with MPLA, IFN-γ, αOX40, or Combo. Cells are color-coded by annotated cell type. (B) Bubble chart showing the top variable marker genes for identified immune cell types. (C) Pie chart shows the relative abundance of 11 immune cell clusters in control, αOX40, MPLA+IFN-γ, or Combo. (D) Macrophage frequency and absolute count in tumors of MC38-bearing mice after two and three treatment cycles with MPLA, IFN-γ, αOX40, or Combo, analyzed by flow cytometry ( n = 5 mice per group). (E) Schematic of CD8 + T cell depletion assay. (F) Tumor volume and survival were monitored. Kaplan-Meier survival analysis corresponding to the depletion study of CD8 + T cell ( n = 6 mice per group). (G) Schematic of macrophage depletion assay in early and late stage. (H and I) Tumor volume and survival were monitored. Kaplan-Meier survival analysis corresponding to the depletion study in (G) ( n = 6–10 mice per group). Data are shown as means ± SD from one of two independent experiments (D, F, H, and I). Statistical significance was determined using one-way ANOVA with Tukey’s multiple comparisons test (D). Log rank test was used (F, H, and I) for statistical comparison. n.s., not significant; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: The mouse colon cancer MC38 cell line (Cat. NO. NM-S13) and the pancreatic cancer KPC cell line (Cat. NO. NM-YD04) were purchased from Shanghai Model Organisms Center, Inc.

Techniques: Marker, Control, Flow Cytometry, Depletion Assay, Comparison

Journal: Cell Reports Medicine

Article Title: Immunogenic tumor cell death and T-cell-derived IFN-γ elicit tumoricidal macrophages to potentiate OX40 immunotherapy

doi: 10.1016/j.xcrm.2026.102699

Figure Lengend Snippet: NOS2-high macrophages are significantly associated with Combo treatment efficacy (A) UMAP of macrophage subclusters from scRNA-seq data of MC38-bearing mice treated with control, MPLA+IFN-γ, αOX40, or Combo. Cells are color-coded by annotated subtype. (B) Bubble chart showing the top variable marker genes for identified macrophage subclusters. (C) Pie chart shows the relative abundance of four macrophage subclusters in control, αOX40, MPLA+IFN-γ, or Combo. (D) GO pathway analysis identifying significantly enriched signaling pathways in the Mac_S2 subcluster compared to other macrophage subpopulations. (E) Violin plots showing Nos2 expression levels across macrophage subclusters. (F) Violin plots comparing Nos2 and Cd206 expression levels among different treatment groups. (G) Frequency of M1-like, M2-like, or the ratio of M1/M2-like macrophage cells in tumor tissues from control, αOX40, MPLA+IFN-γ, and Combo groups with two time points, as determined by flow cytometry ( n = 5–10 mice per group). (H) Multiple immunofluorescence signal intensities of NOS2 + F4/80 + and CD206 + F4/80 + cells in the TME of control, αOX40, MPLA+IFN-γ, and Combo groups. Scale bars, 20 μm. Data are shown as means ± SD from one of two independent experiments (G and H). Statistical significance was determined using one-way ANOVA with Tukey’s multiple comparisons test (G). n.s., not significant; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: The mouse colon cancer MC38 cell line (Cat. NO. NM-S13) and the pancreatic cancer KPC cell line (Cat. NO. NM-YD04) were purchased from Shanghai Model Organisms Center, Inc.

Techniques: Control, Marker, Protein-Protein interactions, Expressing, Flow Cytometry, Immunofluorescence

Journal: Cell Reports Medicine

Article Title: Immunogenic tumor cell death and T-cell-derived IFN-γ elicit tumoricidal macrophages to potentiate OX40 immunotherapy

doi: 10.1016/j.xcrm.2026.102699

Figure Lengend Snippet: NOS2-dependent direct tumor cell killing by macrophages in Combo therapy (A) Schematic of co-culture using CFSE-labeled MC38 cells with tumor- or spleen-derived macrophages, with/without NIL treatment. (B) Flow cytometry quantification of 7-AAD + MC38 cells after 48 h co-culture with tumor-(right) or spleen (left)-derived macrophages ( n = 3 biological replicates). (C) Quantification of 7-AAD + MC38 cells after 48 h in vitro co-culture with or without NIL treatment ( n = 3 biological replicates). (D) Treatment schedule for MC38- or B16-tumor-bearing Nos2 KOor WT mice treated with Combo ( n = 6 mice per group). (E and F) Survival curves of MC38-bearing (E) and B16-bearing mice (F) were analyzed using the log rank test. (G) Flow cytometry analysis of 7-AAD + MC38 cells after 48-h co-culture with CFSE-labeled MC38 cells and BMDMs from Nos2 KO mice ( n = 5 biological replicates). (H) Phagocytosis rate of MC38 cells engulfed by BMDMs was assessed by flow cytometry ( n = 3 biological replicates). (I) Surface expression of CRT on MC38 cells was assessed by flow cytometry after co-culture with MPLA- and IFN-γ-polarized BMDMs in vitro ( n = 3 biological replicates). (J) Analysis of CALR + MC38 cells from MC38-tumor-bearing mice following final treatment with control or Combo, assessed by flow cytometry ( n = 5 biological replicates). Data are shown as means ± SD from one of two independent experiments (B, C, E, F, G, H, I, and J). Statistical significance was determined using one-way ANOVA with Tukey’s multiple comparisons (B, C, and I) or using unpaired Student’s t test (G, H, and J). Log rank tests (E and F) were also used for statistical analysis. n.s., not significant; ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. Combo, MPLA, and IFN-γ combined with αOX86 (E and F).

Article Snippet: The mouse colon cancer MC38 cell line (Cat. NO. NM-S13) and the pancreatic cancer KPC cell line (Cat. NO. NM-YD04) were purchased from Shanghai Model Organisms Center, Inc.

Techniques: Co-Culture Assay, Labeling, Derivative Assay, Flow Cytometry, In Vitro, Expressing, Control

Journal: Cell Reports Medicine

Article Title: Immunogenic tumor cell death and T-cell-derived IFN-γ elicit tumoricidal macrophages to potentiate OX40 immunotherapy

doi: 10.1016/j.xcrm.2026.102699

Figure Lengend Snippet: Foxp3 + Treg depletion and macrophage reprogramming are involved in the anti-tumor effect of Combo (A) Flow cytometry analysis of TME. MC38-tumor-bearing mice were treated with control, αOX40, MPLA+IFN-γ, or Combo for two and three doses, and tumors were analyzed by flow cytometry. (B) Frequency and absolute count of CD25 + FOXP3 + cells in tumor tissues from control, αOX40, MPLA+IFN-γ, and Combo groups with two time points, as determined by flow cytometry ( n = 5 mice per group). (C) Treatment schedule for MC38-tumor-bearing Fcer1g KO or FcγRIIb KO mice. Mice were treated with Control, αOX40, MPLA+IFN-γ, and Combo every 3 days for a total of four doses. (D and E) Survival curves of Fcgr1g KO (D) and FcgrIIb KO (E) mice following treatment ( n = 5–6 mice per group) were monitored. (F) Treatment schedule. MC38-tumor-bearing mice were treated with MPLA and IFN-γ in combination with either OX40-mIgG2a or OX40-hIgG1 agonist antibodies (top), and the corresponding survival curves are shown (bottom) ( n = 5–7 mice per group). (G) Schematic of the co-culture experiment involving BMDMs and Tregs at a ratio of 1:4 (BMDM:Treg); Nos2 expression was measured by RT-qPCR. (H) Relative expression of Nos2 following the co-culture ( n = 4 biological replicates). (I) Multiple immunofluorescence (mIF) staining of MC38 tumors from mice treated with control, αOX40, MPLA+IFN-γ, or Combo, showing FOXP3 and NOS2 expression in border or intra-tumoral. Scale bars, 50 μm. (J) Analysis of cell numbers of FOXP3 and NOS2 expression at the border and intra-tumoral. Representative images from five randomly chosen fields were quantified with ImageJ. Data are shown as means ± SD from one of two independent experiments (B, D, E, F, H, and I). Statistical significance was determined using one-way ANOVA with Tukey’s multiple comparisons (B and H). Log rank test was also used (D–F). n.s., not significant; ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. Combo, MPLA, and IFN-γ combined with αOX86 (C–E).

Article Snippet: The mouse colon cancer MC38 cell line (Cat. NO. NM-S13) and the pancreatic cancer KPC cell line (Cat. NO. NM-YD04) were purchased from Shanghai Model Organisms Center, Inc.

Techniques: Flow Cytometry, Control, Co-Culture Assay, Expressing, Quantitative RT-PCR, Immunofluorescence, Staining

Journal: Iranian Journal of Pharmaceutical Research : IJPR

Article Title: Gamabufotalin Suppresses Colorectal Cancer Growth via Oxidative Stress-Induced Apoptosis and DNA Synthesis Inhibition

doi: 10.5812/ijpr-169859

Figure Lengend Snippet: In vitro experiments demonstrated that gamabufotalin (GA) has a dose-dependent inhibitory effect on colorectal cancer (CRC) cells. A, the chemical formula of GA; B, SW480, HCT-116, HT-29, NCM460, and 293T cells were treated with 0-20000 nM GA for 48 hours, and viability was initially determined using the CCK-8 kit. Each concentration point was repeated six times (n = 6). C, CRC SW480, HCT-116, and HT-29 cells were co-incubated with GA at concentrations ranging from 0 to 200 nM for 48 hours, and the relative cell viability of each experimental group was evaluated using the CCK-8 kit. D, the cell viability of SW480, HCT-116, HT-29, NCM460, and 293T cells was measured using the CCK-8 kit at a GA concentration of 50 nM. E, the cell viability of CRC SW480 and HCT-116 cells was measured under a serum concentration of 1% in the culture condition. F, SW480 cells were treated with GA for 48 hours, and the morphological changes in SW480 cells caused by GA were photographed using an inverted microscope. G, SW480 cells were treated with different concentrations of GA for 24 hours, and the width of the scratch was measured, and the cell scratch closure rate was calculated. Post hoc analysis using LSD was performed after one-way ANOVA to evaluate significance, ** P < 0.01.

Article Snippet: SW480, HCT-116, NCM460, and 293T human colon cancer cell lines were procured from the American Type Culture Collection (ATCC).

Techniques: In Vitro, CCK-8 Assay, Concentration Assay, Incubation, Inverted Microscopy

Journal: Archiv Der Pharmazie

Article Title: Synthesis and Characterization of Sulfonamide‐Schiff Bases, and Investigation of Cytotoxic, Antioxidant, HDAC, and Apoptotic Activities in Human Colon Cancer Cells (DLD‐1 and HT‐29)

doi: 10.1002/ardp.70235

Figure Lengend Snippet: (a) Cell viability (%) and half‐maximal inhibitory concentration (LogIC₅₀) for compound 1 and 3a–d in DLD‐1 cells (MTT assay); (b) one‐way ANOVA (Dunnett's multiple comparisons) of percentage viability for each compound (dose: 100 µM), shown as bar graphs relative to control (cells + medium) (n: 3).

Article Snippet: Colon cancer cell lines DLD‐1 (ATCC:CCL‐221), HT‐29 (ATTC:HTB‐38), and normal cell line CCD‐18Co (ATCC:CRL‐1459) used in this study were obtained from Gebze Technical University and SAP Institute (Türkiye).

Techniques: Concentration Assay, MTT Assay, Control

Journal: Archiv Der Pharmazie

Article Title: Synthesis and Characterization of Sulfonamide‐Schiff Bases, and Investigation of Cytotoxic, Antioxidant, HDAC, and Apoptotic Activities in Human Colon Cancer Cells (DLD‐1 and HT‐29)

doi: 10.1002/ardp.70235

Figure Lengend Snippet: (a) Cell viability (%) and half‐maximal inhibitory concentration (LogIC₅₀) for compound 1 and 3a–d in DLD‐1 cells by WST‐8 assay; (b) cell viability (%) and LogIC₅₀ for compound 1 and 3a–d in HT‐29 cells by WST‐8 assay (Control: cells with medium only) (n: 3).

Article Snippet: Colon cancer cell lines DLD‐1 (ATCC:CCL‐221), HT‐29 (ATTC:HTB‐38), and normal cell line CCD‐18Co (ATCC:CRL‐1459) used in this study were obtained from Gebze Technical University and SAP Institute (Türkiye).

Techniques: Concentration Assay, Control

Journal: Archiv Der Pharmazie

Article Title: Synthesis and Characterization of Sulfonamide‐Schiff Bases, and Investigation of Cytotoxic, Antioxidant, HDAC, and Apoptotic Activities in Human Colon Cancer Cells (DLD‐1 and HT‐29)

doi: 10.1002/ardp.70235

Figure Lengend Snippet: (a) ELISA‐based induction of total antioxidant capacity for compound 1 and 3a–d in DLD‐1 cells; (b) ELISA‐based induction for compound 1 and 3a–d in HT‐29 cells (Blank: ddH₂O; Positive control: Trolox; Control: cells + medium).

Article Snippet: Colon cancer cell lines DLD‐1 (ATCC:CCL‐221), HT‐29 (ATTC:HTB‐38), and normal cell line CCD‐18Co (ATCC:CRL‐1459) used in this study were obtained from Gebze Technical University and SAP Institute (Türkiye).

Techniques: Enzyme-linked Immunosorbent Assay, Positive Control, Control

Journal: Archiv Der Pharmazie

Article Title: Synthesis and Characterization of Sulfonamide‐Schiff Bases, and Investigation of Cytotoxic, Antioxidant, HDAC, and Apoptotic Activities in Human Colon Cancer Cells (DLD‐1 and HT‐29)

doi: 10.1002/ardp.70235

Figure Lengend Snippet: (a) ELISA‐based induction of HDAC activity for compound 1 and 3a–d in DLD‐1 cells; (b) ELISA‐based induction of HDAC activity for compound 1 and 3a–d in HT‐29 cells (Blank: ddH₂O; Positive control: HeLa nuclear extract; Control: cells + medium).

Article Snippet: Colon cancer cell lines DLD‐1 (ATCC:CCL‐221), HT‐29 (ATTC:HTB‐38), and normal cell line CCD‐18Co (ATCC:CRL‐1459) used in this study were obtained from Gebze Technical University and SAP Institute (Türkiye).

Techniques: Enzyme-linked Immunosorbent Assay, Activity Assay, Positive Control, Control

Journal: Archiv Der Pharmazie

Article Title: Synthesis and Characterization of Sulfonamide‐Schiff Bases, and Investigation of Cytotoxic, Antioxidant, HDAC, and Apoptotic Activities in Human Colon Cancer Cells (DLD‐1 and HT‐29)

doi: 10.1002/ardp.70235

Figure Lengend Snippet: (a) Western blot analysis of p38/MAPK and ERK1 protein levels in DLD‐1 cells treated with compound 1 and 3a–d ; (b) corresponding analysis in HT‐29 cells (Housekeeping: β‐actin; Control: cells + medium).

Article Snippet: Colon cancer cell lines DLD‐1 (ATCC:CCL‐221), HT‐29 (ATTC:HTB‐38), and normal cell line CCD‐18Co (ATCC:CRL‐1459) used in this study were obtained from Gebze Technical University and SAP Institute (Türkiye).

Techniques: Western Blot, Control