human normal colonic epithelial ccd 841 con cell line  (ATCC)

Journal: Molecular Therapy Oncology

Article Title: Tackling cancer heterogeneity with systemically delivered oncolytic adenoviruses transcriptionally targeted with hybrid promoters

doi: 10.1016/j.omton.2025.201073

Figure Lengend Snippet: mRNA and protein expression levels of selected candidates in human CRC cell lines and patients’ samples (A–F) mRNA expression levels of the six selected candidates for inclusion in the hybrid TSP. Quantitative PCR (qPCR) analysis was performed using specific primers for each candidate gene (vWA2, A33, FSCN1, NQO1, PDL1, and AQP5) in four human colorectal cancer cell lines (T84, HCT116, HT29, and LoVo) and in normal human colonic epithelial cells (CCD841). qPCR data are presented as relative quantification (RQ = 2 −ΔΔCt ). Statistical analysis was performed using one-way ANOVA. Data represent the mean of three independent experiments. (G) Immunohistochemical analysis of gpA33 and vWA2 expression was performed on paraffin-embedded primary and metastatic CRC tissue samples. (a and b) Representative images of primary tumor sections stained with an anti-gpA33 antibody and developed as described in the . (c and d) Representative images of primary tumor sections stained with an anti-vWA2 antibody under the same conditions. (e–g) Representative images of uterine, cutaneous, and liver metastases, respectively, stained with the anti-gpA33 antibody. (h–j) Corresponding metastatic tissue sections (uterus, skin, and liver, respectively) stained with an anti-vWA2 antibody. All images were acquired at an original magnification of 200×. Scale bar: 50 μm.

Article Snippet: Human CRC cell lines (LoVo, T84, HCT116, and HT29), normal colon epithelial cells (CCD841), human embryonic kidney cells (HEK293), human fetal lung fibroblasts (WI-38), and human microendothelial cells (HMEC-1) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Quantitative Proteomics, Immunohistochemical staining, Staining

Journal: Molecular Therapy Oncology

Article Title: Tackling cancer heterogeneity with systemically delivered oncolytic adenoviruses transcriptionally targeted with hybrid promoters

doi: 10.1016/j.omton.2025.201073

Figure Lengend Snippet: AR2015 lytic activity in vitro compared to single TSP-driven OAds (A–I) In vitro lytic activity of the OAds AR2015, AV22EL, and AV636, as well as Ad5WT (positive control), in CRC cell lines LoVo, T84, HT29, and HCT116, normal human colonic epithelial cells (CCD841), human fetal lung fibroblasts (WI-38), human microendothelial cells (HMEC-1), and human melanoma cells (A375 and SB2). Cells (1 × 10 4 ) were seeded in 24-well plates and infected 24 h later with increasing multiplicities of infection (MOIs: 0–100). After 6 days, cell viability was assessed using the MTS assay and expressed as mean ± SD ( n = 3), with the viability of uninfected control cells set to 100%. Two-way ANOVA was performed for statistical analysis, followed by Dunnett’s test (vs. Ad(F5)WT). (J) Comparative replication kinetics of AR2015 and AV22EL in CRC cell lines (LoVo, T84, HT29, and HCT116) and normal CCD841 cells. Cells were infected at an MOI of 100, and samples were collected at 5 h (baseline) and 72 h post-infection. Viral replication was quantified by qPCR targeting the adenoviral E4 gene. Data are presented as a fold increase in E4 levels (72 vs. 5 h). (K) Expression of adenoviral E1A protein in LoVo cells at 8 and 24 h post-infection with AV22EL, AR2015, or Ad5WT. Protein levels were assessed by western blot, with β-actin used as a loading control.

Article Snippet: Human CRC cell lines (LoVo, T84, HCT116, and HT29), normal colon epithelial cells (CCD841), human embryonic kidney cells (HEK293), human fetal lung fibroblasts (WI-38), and human microendothelial cells (HMEC-1) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Activity Assay, In Vitro, Positive Control, Infection, MTS Assay, Control, Expressing, Western Blot

Journal: Journal of Gastrointestinal Oncology

Article Title: ISM2 as a prognostic biomarker and mediator of immune infiltration in colorectal cancer: evidence from bioinformatics and experimental analysis

doi: 10.21037/jgo-2025-295

Figure Lengend Snippet: ISM2 promotes the migration and invasion of colon cancer cells. (A) Relative expression of ISM2 in three colon cancer cells in CCLE database. (B) Western blot analysis of ISM2 expression in normal colon epithelial cells and three types of colon cancer cells. (C) Quantitative analysis of the gray value of strip ISM2, mean ± SEM are displayed (n=3). (D) Western blot analysis of ISM2 protein knockdown inefficiency in SW1116 cells transfected with ISM2 SiRNA#1, 2, 3 and NC SiRNA. (E) Quantitative analysis of the gray value of strip ISM2, mean ± SEM are displayed (n=3). (F) Wound healing assay for cell migration in SW1116 cells; the images of wound closure are shown for the indicated number of hours after scratching (0, 36 h) (red lines indicate the wound boundary, magnification ×50). (G) The quantification for wound healing assay. Mean ± SEM are displayed (n=3). (H) CCK8 analysis of SW1116 cell survival (12, 24 and 36 h). (I,J) Transwell migration assay showing the effect of ISM2 knockdown on SW1116 cell migration after 24 hours. Migrated cells were stained with 0.1% crystal violet and counted in at least three random fields (original magnification ×100). Data are presented as mean ± SEM (n=3). ns, no significance; *, P<0.05; **, P<0.01; ***, P<0.001. CCK8, Cell Counting Kit-8; CCLE, Cancer Cell Line Encyclopedia; NC, negative control; OD, optical density; SEM, standard error of the mean; TPM, transcripts per million.

Article Snippet: Human CRC cell lines (SW1116, LOVO, and RKO) and normal human colonic epithelial cells (NCM460) were obtained from the American Type Culture Collection.

Techniques: Migration, Expressing, Western Blot, Stripping Membranes, Knockdown, Transfection, Wound Healing Assay, Transwell Migration Assay, Staining, Cell Counting, Negative Control