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human small cell lung carcinoma line nci h1930  (ATCC)


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    ATCC human small cell lung carcinoma line nci h1930
    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); <t>(c)</t> <t>NCI–H1930</t> (endogenously SLC35D3-expressing).
    Human Small Cell Lung Carcinoma Line Nci H1930, supplied by ATCC, used in various techniques. Bioz Stars score: 92/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human small cell lung carcinoma line nci h1930 - by Bioz Stars, 2026-06
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    1) Product Images from "Integrated transcriptomic and proteomic validation identifies SLC35D3 as a tumor-selective surface antigen for colorectal and neuroendocrine carcinomas"

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

    Journal: Biochemistry and Biophysics Reports

    doi: 10.1016/j.bbrep.2026.102587

    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).
    Figure Legend 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).

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

    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.
    Figure Legend 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.

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



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    ATCC human small cell lung carcinoma line nci h1930
    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); <t>(c)</t> <t>NCI–H1930</t> (endogenously SLC35D3-expressing).
    Human Small Cell Lung Carcinoma Line Nci H1930, supplied by ATCC, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    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); <t>(c)</t> <t>NCI–H1930</t> (endogenously SLC35D3-expressing).
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    Procell Inc a549 human lung carcinoma cell line
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    Korean Cell Line Bank nci h292 human lung mucoepidermoid carcinoma cell line
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    ATCC a549 human lung carcinoma cell line
    Mendelian Randomization Analysis Reveals Causal Relationship Between Phosphatidylcholine and Lung Cancer. A and B show meta-analysis forest plots demonstrating that phosphatidylcholine levels are significantly associated with <t>LUSC</t> risk across multiple studies. The red diamonds represent pooled effect estimates. C presents MR test scatter plots using three different methods (inverse variance weighted, MR-Egger, and weighted median). The consistent regression line slopes across methods indicate a robust causal effect estimate. D compares results from different MR methods, with the blue line showing the primary analysis and scattered points representing alternative approaches. The consistency across methods supports the reliability of findings
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    Image Search Results


    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).

    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

    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.

    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

    Netilmicin sulfate alone and in combination exerted protective effects on an infected A549 cell model (A) Cytotoxic effects of the drugs on A549 cells. (B) Protective effects of different concentrations of NETS on A549 cells. The early interventions on the abscissa reflect the incubation of A549 cells with the drug for 2 h before B. pseudomallei HNBP001 infection. Late intervention was defined as the introduction of the drug to A549 cells 2 h after infection with B. pseudomallei HNBP001 . The ordinate is the survival rate of the infected A549 cells. NC: the blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Bp+30 μM NETS: The infected A549 cells were treated with 30 μM NETS; the other conditions were the same, but different concentrations of NETS were used. (C) Protective effects of several drugs on infected A549 cells; the ordinate is the survival rate of infected A549 cells. NC, blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Other: The infected A549 cells were treated with drugs (including SXT, GM, NETS, CAZ, and NETS+CAZ). (D) Number of intracellular bacteria in infected A549 cells after drug treatment; the ordinate represents the number of bacteria in infected A549 cells. NC is the blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Drug group: 2 × MIC drug was used to treat infected A549 cells. All drugs, including SXT, GM, NETS, CAZ, and NETS+CAZ. (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; ns, no significant difference. Data are represented as mean ± SEM.).

    Journal: iScience

    Article Title: Drug screening to identify compounds to eliminate Burkholderia pseudomallei through Hcp protein

    doi: 10.1016/j.isci.2026.115367

    Figure Lengend Snippet: Netilmicin sulfate alone and in combination exerted protective effects on an infected A549 cell model (A) Cytotoxic effects of the drugs on A549 cells. (B) Protective effects of different concentrations of NETS on A549 cells. The early interventions on the abscissa reflect the incubation of A549 cells with the drug for 2 h before B. pseudomallei HNBP001 infection. Late intervention was defined as the introduction of the drug to A549 cells 2 h after infection with B. pseudomallei HNBP001 . The ordinate is the survival rate of the infected A549 cells. NC: the blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Bp+30 μM NETS: The infected A549 cells were treated with 30 μM NETS; the other conditions were the same, but different concentrations of NETS were used. (C) Protective effects of several drugs on infected A549 cells; the ordinate is the survival rate of infected A549 cells. NC, blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Other: The infected A549 cells were treated with drugs (including SXT, GM, NETS, CAZ, and NETS+CAZ). (D) Number of intracellular bacteria in infected A549 cells after drug treatment; the ordinate represents the number of bacteria in infected A549 cells. NC is the blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Drug group: 2 × MIC drug was used to treat infected A549 cells. All drugs, including SXT, GM, NETS, CAZ, and NETS+CAZ. (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; ns, no significant difference. Data are represented as mean ± SEM.).

    Article Snippet: The A549 human lung carcinoma epithelial cell line was purchased from Procell (Wuhan, China; Cat# CL-0016).

    Techniques: Infection, Incubation, Negative Control, Bacteria

    Netilmicin sulfate alone and in combination exerted protective effects on an infected A549 cell model (A) Cytotoxic effects of the drugs on A549 cells. (B) Protective effects of different concentrations of NETS on A549 cells. The early interventions on the abscissa reflect the incubation of A549 cells with the drug for 2 h before B. pseudomallei HNBP001 infection. Late intervention was defined as the introduction of the drug to A549 cells 2 h after infection with B. pseudomallei HNBP001 . The ordinate is the survival rate of the infected A549 cells. NC: the blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Bp+30 μM NETS: The infected A549 cells were treated with 30 μM NETS; the other conditions were the same, but different concentrations of NETS were used. (C) Protective effects of several drugs on infected A549 cells; the ordinate is the survival rate of infected A549 cells. NC, blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Other: The infected A549 cells were treated with drugs (including SXT, GM, NETS, CAZ, and NETS+CAZ). (D) Number of intracellular bacteria in infected A549 cells after drug treatment; the ordinate represents the number of bacteria in infected A549 cells. NC is the blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Drug group: 2 × MIC drug was used to treat infected A549 cells. All drugs, including SXT, GM, NETS, CAZ, and NETS+CAZ. (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; ns, no significant difference. Data are represented as mean ± SEM.).

    Journal: iScience

    Article Title: Drug screening to identify compounds to eliminate Burkholderia pseudomallei through Hcp protein

    doi: 10.1016/j.isci.2026.115367

    Figure Lengend Snippet: Netilmicin sulfate alone and in combination exerted protective effects on an infected A549 cell model (A) Cytotoxic effects of the drugs on A549 cells. (B) Protective effects of different concentrations of NETS on A549 cells. The early interventions on the abscissa reflect the incubation of A549 cells with the drug for 2 h before B. pseudomallei HNBP001 infection. Late intervention was defined as the introduction of the drug to A549 cells 2 h after infection with B. pseudomallei HNBP001 . The ordinate is the survival rate of the infected A549 cells. NC: the blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Bp+30 μM NETS: The infected A549 cells were treated with 30 μM NETS; the other conditions were the same, but different concentrations of NETS were used. (C) Protective effects of several drugs on infected A549 cells; the ordinate is the survival rate of infected A549 cells. NC, blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Other: The infected A549 cells were treated with drugs (including SXT, GM, NETS, CAZ, and NETS+CAZ). (D) Number of intracellular bacteria in infected A549 cells after drug treatment; the ordinate represents the number of bacteria in infected A549 cells. NC is the blank negative control group of fresh 10% DMEM. Bp: infected A549 cell group. Drug group: 2 × MIC drug was used to treat infected A549 cells. All drugs, including SXT, GM, NETS, CAZ, and NETS+CAZ. (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; ns, no significant difference. Data are represented as mean ± SEM.).

    Article Snippet: A549 human lung carcinoma cell line , Procell , Cat#CL-0016.

    Techniques: Infection, Incubation, Negative Control, Bacteria

    Mendelian Randomization Analysis Reveals Causal Relationship Between Phosphatidylcholine and Lung Cancer. A and B show meta-analysis forest plots demonstrating that phosphatidylcholine levels are significantly associated with LUSC risk across multiple studies. The red diamonds represent pooled effect estimates. C presents MR test scatter plots using three different methods (inverse variance weighted, MR-Egger, and weighted median). The consistent regression line slopes across methods indicate a robust causal effect estimate. D compares results from different MR methods, with the blue line showing the primary analysis and scattered points representing alternative approaches. The consistency across methods supports the reliability of findings

    Journal: Discover Oncology

    Article Title: Comprehensive multi omics profiling and Mendelian randomization assessment of lipid metabolites in lung cancer prognosis

    doi: 10.1007/s12672-026-04893-6

    Figure Lengend Snippet: Mendelian Randomization Analysis Reveals Causal Relationship Between Phosphatidylcholine and Lung Cancer. A and B show meta-analysis forest plots demonstrating that phosphatidylcholine levels are significantly associated with LUSC risk across multiple studies. The red diamonds represent pooled effect estimates. C presents MR test scatter plots using three different methods (inverse variance weighted, MR-Egger, and weighted median). The consistent regression line slopes across methods indicate a robust causal effect estimate. D compares results from different MR methods, with the blue line showing the primary analysis and scattered points representing alternative approaches. The consistency across methods supports the reliability of findings

    Article Snippet: ATCC-procured H520 and SW900 human lung squamous cell carcinoma (LUSC) cell lines, alongside BEAS-2B normal bronchial epithelial cells, were utilized.

    Techniques:

    Mendelian Randomization Analysis Reveals Associations between LUSC and Metabolites. The charts present Mendelian randomization findings exploring the link between lung cancer and metabolites. A and B illustrate the associations, while C and D confirm consistency. The analysis suggests significant relations between certain metabolites and lung cancer risk, offering new insights for research

    Journal: Discover Oncology

    Article Title: Comprehensive multi omics profiling and Mendelian randomization assessment of lipid metabolites in lung cancer prognosis

    doi: 10.1007/s12672-026-04893-6

    Figure Lengend Snippet: Mendelian Randomization Analysis Reveals Associations between LUSC and Metabolites. The charts present Mendelian randomization findings exploring the link between lung cancer and metabolites. A and B illustrate the associations, while C and D confirm consistency. The analysis suggests significant relations between certain metabolites and lung cancer risk, offering new insights for research

    Article Snippet: ATCC-procured H520 and SW900 human lung squamous cell carcinoma (LUSC) cell lines, alongside BEAS-2B normal bronchial epithelial cells, were utilized.

    Techniques:

    RT-qPCR Validation of Prognostic Genes. Relative mRNA expression of CD44, OR51E2, KRT5, and S100A9 in H520 and SW900 lung squamous cell carcinoma (LUSC) cell lines vs. BEAS-2B controls. *** P < 0.001, **** P < 0.0001

    Journal: Discover Oncology

    Article Title: Comprehensive multi omics profiling and Mendelian randomization assessment of lipid metabolites in lung cancer prognosis

    doi: 10.1007/s12672-026-04893-6

    Figure Lengend Snippet: RT-qPCR Validation of Prognostic Genes. Relative mRNA expression of CD44, OR51E2, KRT5, and S100A9 in H520 and SW900 lung squamous cell carcinoma (LUSC) cell lines vs. BEAS-2B controls. *** P < 0.001, **** P < 0.0001

    Article Snippet: ATCC-procured H520 and SW900 human lung squamous cell carcinoma (LUSC) cell lines, alongside BEAS-2B normal bronchial epithelial cells, were utilized.

    Techniques: Quantitative RT-PCR, Biomarker Discovery, Expressing