human small cell lung carcinoma line nci h1930  (ATCC)

Journal: Biochemistry and Biophysics Reports

Article Title: Integrated transcriptomic and proteomic validation identifies SLC35D3 as a tumor-selective surface antigen for colorectal and neuroendocrine carcinomas

doi: 10.1016/j.bbrep.2026.102587

Figure Lengend Snippet: Immunohistochemical analysis of SLC35D3 expression in human tumors, normal tissues, and positive-control samples. (A) SLC35D3 staining in human tumors: (a) primary colon tumor; (b) corresponding lymph-node metastasis; (c) normal adjacent tissue (NAT) of a; (d) primary rectal tumor; (e) corresponding lymph-node metastasis; (f) NAT of d; (g–h) small-cell lung carcinoma (SCLC); (i) pancreatic neuroendocrine neoplasm; (j) pancreatic islet tumor. (B) SLC35D3 staining in human normal tissues: (a) cerebrum; (b) bone marrow; (c) lung; (d) heart; (e) liver; (f) kidney; (g) eye; (h) colon; (i) adrenal gland; (j) pancreas; (k) hypophysis; (l) stomach; (m) small intestine; (n) prostate. Arrowheads indicate SLC35D3-positive cells. (C) SLC35D3 staining of negative and positive control cell lines: (a) HCT 116-mock (negative control); (b) HCT 116-hSLC35D3 (engineered overexpression); (c) NCI–H1930 (endogenously SLC35D3-expressing).

Article Snippet: The human pancreatic islet cell carcinoma line QGP-1 (Japanese Collection of Research Bioresources Cell Bank, Osaka, Japan; Cat. No. JCRB0183), human small-cell lung carcinoma line NCI–H1930 (American Type Culture Collection (ATCC), Manassas, VA, USA; Cat. No. CRL-5906), human colorectal carcinoma line LoVo (ATCC; Cat. No. CCL-229), human gastric carcinoma line SNU-16 (ATCC; Cat. No. CRL-5974), and human colorectal carcinoma line HCT 116 (ATCC; Cat. No. CCL-247) were used.

Techniques: Immunohistochemical staining, Expressing, Positive Control, Staining, Negative Control, Over Expression

Journal: Biochemistry and Biophysics Reports

Article Title: Integrated transcriptomic and proteomic validation identifies SLC35D3 as a tumor-selective surface antigen for colorectal and neuroendocrine carcinomas

doi: 10.1016/j.bbrep.2026.102587

Figure Lengend Snippet: Validation of cell-surface SLC35D3 expression in cancer cell lines by flow cytometry and comparison with CCLE transcriptomic data. Flow cytometry histograms of cell-surface SLC35D3 staining in human cancer cell lines (HCT 116, LoVo, QGP-1, NCI–H1930, and SNU-16). For each cell line, the MFI ratio (anti-SLC35D3/isotype) and the corresponding mRNA expression level (log2[TPM+1]) from the CCLE are indicated below the histogram. HCT 116 served as a negative control and showed minimal surface staining, consistent with a CCLE value of log2[TPM+1] = 0.0.

Article Snippet: The human pancreatic islet cell carcinoma line QGP-1 (Japanese Collection of Research Bioresources Cell Bank, Osaka, Japan; Cat. No. JCRB0183), human small-cell lung carcinoma line NCI–H1930 (American Type Culture Collection (ATCC), Manassas, VA, USA; Cat. No. CRL-5906), human colorectal carcinoma line LoVo (ATCC; Cat. No. CCL-229), human gastric carcinoma line SNU-16 (ATCC; Cat. No. CRL-5974), and human colorectal carcinoma line HCT 116 (ATCC; Cat. No. CCL-247) were used.

Techniques: Biomarker Discovery, Expressing, Flow Cytometry, Comparison, Staining, Negative Control

Journal: Frontiers in Immunology

Article Title: STAT6 inhibition of M2 macrophages suppresses tumor growth by modulating the tumor microenvironment in colon cancer model

doi: 10.3389/fimmu.2026.1733991

Figure Lengend Snippet: TAMpep-IP suppresses tumor growth in the colon cancer model. (A) BALB/c mice were subcutaneously inoculated with CT26 colon carcinoma cells (3 × 10 5 cells per mouse). Starting on day 7 post-inoculation, TAMpep-IP (400 nmol/kg) was administered subcutaneously every three days for a total of seven doses. (B) Representative images of tumors excised at the experimental endpoint (day 25) showed visibly reduced tumor size in the TAMpep-IP–treated group compared to control. (C) Tumor volumes were measured every 3 days following tumor implantation. Mice treated with TAMpep-IP exhibited significantly reduced tumor growth relative to the control group (control: n = 6; TAMpep-IP: n = 6). (D) Tumor proliferation was evaluated by immunohistochemical staining of Ki-67 in tumor sections. Quantitative analysis showed a significantly lower proportion of Ki-67 + proliferating cells in TAMpep-IP–treated tumors. Representative immunohistochemistry images were acquired at ×100 magnification. Scale bar = 1000 μm. All data are presented as mean ± SEM. *p<0.05, ***p<0.001.

Article Snippet: The murine colon carcinoma cell line CT26 (KCLB 80009; Korean Cell Line Bank, Seoul, Korea) was cultured in Dulbecco’s modified Eagle’s medium (DMEM) (D5671; Welgene, Gyeongsangbuk, Korea) supplemented with 10% heat-inactivated FBS, 100 U/mL penicillin, and 1% penicillin–streptomycin.

Techniques: Control, Tumor Implantation, Immunohistochemical staining, Staining, Immunohistochemistry

Journal: Frontiers in Immunology

Article Title: STAT6 inhibition of M2 macrophages suppresses tumor growth by modulating the tumor microenvironment in colon cancer model

doi: 10.3389/fimmu.2026.1733991

Figure Lengend Snippet: TAMpep-IP reduces M2 macrophages in tumor tissues of colon cancer model. (A) Tumor-infiltrating immune cells were isolated from CT26 tumors in control and TAMpep-IP–treated mice. Flow cytometry was used to identify CD206 + F4/80 + macrophages within the CD45 + CD11b + population. TAMpep-IP significantly decreased the proportion of M2-like tumor-associated macrophages. (B) Quantitative RT-PCR analysis of tumor tissues revealed that TGF-β mRNA expression, a key M2-associated cytokine, was significantly reduced in TAMpep-IP–treated tumors compared to controls. (C) Western blot analysis of tumor showed a marked decrease in CD206 protein levels following TAMpep-IP, indicating effective suppression of M2 macrophage markers. (D) CD206 + macrophages were further visualized by immunohistochemical staining of tumor sections. ImageJ-based quantification confirmed a significant reduction in CD206 + area in TAMpep-IP–treated tumors. Representative immunohistochemistry images were acquired at ×100 magnification. Scale bar = 1000 μm. All data are presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001.

Article Snippet: The murine colon carcinoma cell line CT26 (KCLB 80009; Korean Cell Line Bank, Seoul, Korea) was cultured in Dulbecco’s modified Eagle’s medium (DMEM) (D5671; Welgene, Gyeongsangbuk, Korea) supplemented with 10% heat-inactivated FBS, 100 U/mL penicillin, and 1% penicillin–streptomycin.

Techniques: Isolation, Control, Flow Cytometry, Quantitative RT-PCR, Expressing, Western Blot, Immunohistochemical staining, Staining, Immunohistochemistry

Journal: Frontiers in Immunology

Article Title: STAT6 inhibition of M2 macrophages suppresses tumor growth by modulating the tumor microenvironment in colon cancer model

doi: 10.3389/fimmu.2026.1733991

Figure Lengend Snippet: TAMpep-IP enhances inflammatory cytokine expression and activated CD8 + T cells in tumor tissues of colon cancer model. (A) Flow cytometry was used to evaluate CD8 + T cell function in CT26 tumor tissues from control and TAMpep-IP-treated mice. TAMpep-IP significantly increased the proportion of activated Granzyme B + CD8 + T cells, while reducing the frequency of exhausted Tim-3 + CD8 + T cells, indicating enhanced cytotoxic T cell activity. (B, C) Confocal immunofluorescence analysis was performed on tumor sections stained with DAPI (nuclei), anti-CD8 (green), anti-Granzyme B (red), and anti-PD-1 (red). Activated CD8 + T cells were identified by co-localization of CD8 and Granzyme B, whereas exhausted CD8 + T cells were identified by co-localization of CD8 and PD-1. Quantification revealed a significant increase in intertumoral CD8 + Granzyme B + T cells and a concomitant decrease in CD8 + PD-1 + exhausted T cells following TAMpep-IP. Representative confocal images were acquired using a 40× objective lens. Scale bar = 20 μm. (D) Quantitative RT-PCR analysis of CT26 tumor tissues showed significantly elevated mRNA levels of pro-inflammatory cytokines TNF-α, IL-1β, and IL-12 in TAMpep-IP–treated mice compared to controls, indicating induction of a pro-inflammatory tumor microenvironment. All data are presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001, ****p < 0.0001.

Article Snippet: The murine colon carcinoma cell line CT26 (KCLB 80009; Korean Cell Line Bank, Seoul, Korea) was cultured in Dulbecco’s modified Eagle’s medium (DMEM) (D5671; Welgene, Gyeongsangbuk, Korea) supplemented with 10% heat-inactivated FBS, 100 U/mL penicillin, and 1% penicillin–streptomycin.

Techniques: Expressing, Flow Cytometry, Cell Function Assay, Control, Activity Assay, Immunofluorescence, Staining, Quantitative RT-PCR

Journal: Oncology Letters

Article Title: BUD23 is associated with malignancy and correlates with immune infiltration in NSCLC

doi: 10.3892/ol.2026.15608

Figure Lengend Snippet: BUD23 knockdown suppresses the proliferative and migration of NSCLC cells. (A) RT-qPCR was used to quantify BUD23 mRNA levels in HBE cells and a panel of NSCLC cell lines. Validation of BUD23 knockdown efficiency in (B) A549 and (C) H1299 cells by RT-qPCR. Assessment of cell viability in (D) A549 and (E) H1299 cells via CCK-8 assay and cell migration in (F) A549 and (G) H1299 cells by wound healing assay (magnification, ×10). CCK-8 assays of (H) A549 and (I) H1299 cells 24 h after BUD23 knockdown with or without subsequent co-culture with Jurkat T cells for 48 h in Transwell chambers. (J) Quantification of apoptosis in A549 and H1299 cells via Annexin V/PI flow cytometry. **P<0.01 and ***P<0.001 vs. HBE, NC, Con or as indicated. NSCLC, non-small cell lung cancer; RT-qPCR, reverse transcription-quantitative PCR; HBE, human bronchial epithelial; CCK-8, Cell Counting Kit-8; NC, negative control; Con, control; Si1/2, small interfering RNA targeting BUD23.

Article Snippet: The HBE [full name: HBE4-E6/E7 (Human Bronchial Epithelial Cells; cat. no. CRL-2078)] cell line, A549 lung adenocarcinoma cell line (cat. no. CCL-185), H1299 lung large cell carcinoma cell line (cat. no. CRL-5803), H460 lung large cell carcinoma cell line (cat. no. HTB-177) and Jurkat T cells (cat. no. TIB-152; a childhood T acute lymphoblastic leukemia T-cell line), were purchased from the American Type Culture Collection.

Techniques: Knockdown, Migration, Quantitative RT-PCR, Biomarker Discovery, CCK-8 Assay, Wound Healing Assay, Co-Culture Assay, Flow Cytometry, Reverse Transcription, Real-time Polymerase Chain Reaction, Cell Counting, Negative Control, Control, Small Interfering RNA

Journal: Oncology Letters

Article Title: BUD23 is associated with malignancy and correlates with immune infiltration in NSCLC

doi: 10.3892/ol.2026.15608

Figure Lengend Snippet: BUD23 knockdown significantly downregulates POLR2J expression in non-small cell lung cancer. (A) Venn diagram showing the intersection between LUAD GSEA core enrichment genes (key genes driving Hallmark DNA repair pathway enrichment) and LUSC GSEA core enrichment genes within the Hallmark DNA repair gene set, identifying 49 common genes. (B) Venn diagram showing the intersection between BUD23-correlated genes (correlation index >0.3) derived from the TCGA-LUAD cohort and BUD23-correlated genes (correlation index >0.3) derived from the TCGA-LUSC cohort via multi-gene correlation analysis, yielding 79 overlapping genes. (C) Venn diagram showing the secondary intersection between the 49 overlapping GSEA core enrichment genes (from panel A) and the 79 overlapping BUD23-correlated genes (from panel B), identifying 4 shared common genes: TAF6, POLR2J, RFC2 and VPS37D. (D) Validation of TAF6, POLR2J, RFC2 and VPS37D mRNA expression following BUD23 knockdown in A549 cells via reverse transcription-quantitative PCR. Cell-cycle analysis in (E) A549 and (F) H1299 cells following BUD23 knockdown. ***P<0.001 vs. Con. POLR2J, RNA polymerase II subunit J; LUAD, lung adenocarcinoma; GSEA, gene set enrichment analysis; LUSC, lung squamous cell carcinoma; TCGA, The Cancer Genome Atlas; TAF6, TATA-box binding protein associated factor 6; RFC2, replication factor C subunit 2; VPS37D, vacuolar protein sorting-associated protein 37D; Con, control; Si1, small interfering RNA targeting BUD23.

Article Snippet: The HBE [full name: HBE4-E6/E7 (Human Bronchial Epithelial Cells; cat. no. CRL-2078)] cell line, A549 lung adenocarcinoma cell line (cat. no. CCL-185), H1299 lung large cell carcinoma cell line (cat. no. CRL-5803), H460 lung large cell carcinoma cell line (cat. no. HTB-177) and Jurkat T cells (cat. no. TIB-152; a childhood T acute lymphoblastic leukemia T-cell line), were purchased from the American Type Culture Collection.

Techniques: Knockdown, Expressing, Derivative Assay, Biomarker Discovery, Reverse Transcription, Real-time Polymerase Chain Reaction, Cell Cycle Assay, Binding Assay, Control, Small Interfering RNA

Journal: Oncology Reports

Article Title: NF-κB-driven LUZP1 promotes metastasis and chemoresistance in head and neck squamous cell carcinoma

doi: 10.3892/or.2026.9115

Figure Lengend Snippet: NF-κB signaling activation promotes LUZP1 expression in HNSCC cells. (A) The expression of LUZP1 in FaDu, OECM-1 and SAS cells treated with SB431542 (10 µM), LY294002 (10 µM), Rapamycin (10 µM), BAY 11–7085 (5 µM) or YC-1 (30 µM) was determined by western blot assay. Signal quantification was measured using ImageJ 1.54 g software (National Institutes of Health) and the relative intensity was normalized to untreated control. The red dashed line represents the normalized value as 1. (B) The expression of LUZP1 in FaDu, OECM-1 and SAS cells with or without BAY 11–7085 was validated by western blot assay. (C) Spearman's monotonic correlation between LUZP1 and NFKB1 or NFKB2 expression in HNSCC was analyzed using The Cancer Genome Atlas RNA-Sequencing database on the GEPIA server. (D) Protein expression of NF-κB p65 and LUZP1 in OECM-1 and SAS cells with NF-κB p65 knockdown (+) or control shRNA -), as determined by western blot analysis. β-actin, loading control. (E) IC 50 values of docetaxel in OECM-1 and SAS cells with or without NF-κB p65 knockdown. (F) IC 50 values of cisplatin in OECM-1 and SAS cells with or without NF-κB p65 knockdown. The expression of LUZP1 in different HNSCC cells treated with (G) IL-1β (3 ng/ml) or (H) TNFα (10 ng/ml) for the indicated times was determined by western blot assay. β-actin, loading control. (I) Transwell cell migration assay was conducted using OECM-1 cells with or without LUZP1 knockdown in the presence or absence of TNFα (10 ng/ml) treatment. Signal quantification using crystal violet extract was measured by colorimetric analysis at 570 nm, and the relative signal intensities were normalized to untreated shControl (shLUZP1, -; TNFα, -) (n=3). (J) Genomic visualization of the human LUZP1 locus (GRCh38/hg38) showing RefSeq-curated exon annotations, NF-κB RelA ChIP-seq binding signals in FaDu cells (ReMap), layered H3K27ac ChIP-seq profiles from ENCODE cell lines, and GeneHancer regulatory element annotations. Red boxes denote promoter regions and gray boxes indicate putative enhancers. Blue vertical bars mark the locations of ChIP-qPCR primer sets designed for experimental validation. (K) ChIP-qPCR analysis showing increased NF-κB (RelA) occupancy at the LUZP1 promoter in response to TNF-α treatment. For statistical analyses, (E and F) a 2-tailed unpaired Student's t -test; (I) a factorial two-way ANOVA, followed by Tukey's Honestly Significant Difference post hoc test. **P<0.01. TPM, transcripts per million; ChIP-seq, chromatin immunoprecipitation sequencing; LUZP1, leucine zipper protein 1; sh, short hairpin.

Article Snippet: The human pharyngeal squamous cell carcinoma cell line FaDu (cat. no. HTB-43) was obtained from the American Type Culture Collection.

Techniques: Activation Assay, Expressing, Western Blot, Software, Control, RNA Sequencing, Knockdown, shRNA, Cell Migration Assay, ChIP-sequencing, Binding Assay, ChIP-qPCR, Biomarker Discovery