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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, 2026-07
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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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    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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    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

    Sangyod rice extract demonstrated a reduction in cytotoxicity and ROS levels in OA-induced HepG2 cells. (A) Viability of HepG2 cells exposed to different concentrations of Sangyod rice extract. (B) Viability of Sangyod rice extract treatment after OA-induced HepG2 cells. (C) ROS generation in OA-induced HepG2 cells. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. * p < 0.05 compared to the control group, and # p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract demonstrated a reduction in cytotoxicity and ROS levels in OA-induced HepG2 cells. (A) Viability of HepG2 cells exposed to different concentrations of Sangyod rice extract. (B) Viability of Sangyod rice extract treatment after OA-induced HepG2 cells. (C) ROS generation in OA-induced HepG2 cells. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. * p < 0.05 compared to the control group, and # p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Control

    Sangyod rice extract inhibited apoptosis in OA-induced HepG2 cells by suppressing the Bax and caspase-3 pathway. (A) Representative images of nuclei stained with Hoechst 33342. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of apoptotic cells after treatment with Sangyod rice extract in OA-induced HepG2 cells. (C) Western blot analysis of Bax, Bcl-2, procaspase-3, and cleaved caspase-3. (D) Relative expression of Bax and Bcl-2. (E) Relative expression of procaspase 3, and cleaved caspase 3. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 compared to the control group, and #p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract inhibited apoptosis in OA-induced HepG2 cells by suppressing the Bax and caspase-3 pathway. (A) Representative images of nuclei stained with Hoechst 33342. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of apoptotic cells after treatment with Sangyod rice extract in OA-induced HepG2 cells. (C) Western blot analysis of Bax, Bcl-2, procaspase-3, and cleaved caspase-3. (D) Relative expression of Bax and Bcl-2. (E) Relative expression of procaspase 3, and cleaved caspase 3. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 compared to the control group, and #p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Staining, Western Blot, Expressing, Control

    Sangyod rice extract attenuated inflammation in OA-induced HepG2 cells through inhibition of the NF-κB pathway. (A) TNF-α gene, (B) IL-1β gene, (C) IL-6 gene, (D) IL-10 gene. (E) Western blot analysis of NF-κB. (F) Relative expression of NF-κB protein. Results are presented as the mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract attenuated inflammation in OA-induced HepG2 cells through inhibition of the NF-κB pathway. (A) TNF-α gene, (B) IL-1β gene, (C) IL-6 gene, (D) IL-10 gene. (E) Western blot analysis of NF-κB. (F) Relative expression of NF-κB protein. Results are presented as the mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Inhibition, Western Blot, Expressing, Control

    Sangyod rice extract reduced lipid accumulation in OA-induced HepG2 cells. (A) Oil Red O staining was conducted on HepG2 cells, with red fat droplets indicating lipid accumulation. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of lipid accumulation post Oil Red O extraction. (C) Levels of TG were measured using an assay kit. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract reduced lipid accumulation in OA-induced HepG2 cells. (A) Oil Red O staining was conducted on HepG2 cells, with red fat droplets indicating lipid accumulation. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of lipid accumulation post Oil Red O extraction. (C) Levels of TG were measured using an assay kit. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Staining, Extraction, Control

    Effect of Sangyod rice extract on lipid metabolism in OA-induced HepG2 cells. (A) SREBP-1c gene (B) ACC gene, (C) FASN gene (D) CPT-1 A gene, (E) SCD1 gene, (F) MTTP gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Effect of Sangyod rice extract on lipid metabolism in OA-induced HepG2 cells. (A) SREBP-1c gene (B) ACC gene, (C) FASN gene (D) CPT-1 A gene, (E) SCD1 gene, (F) MTTP gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Control

    Effect of Sangyod rice extract on the expression of LPL-1, LPL-2, PGC-1α and PPARα in OA-induced HepG2 cells. (A) LPL-1 gene (B) LPL-2 gene, (C) PPARα gene (D) PGC-1α gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Effect of Sangyod rice extract on the expression of LPL-1, LPL-2, PGC-1α and PPARα in OA-induced HepG2 cells. (A) LPL-1 gene (B) LPL-2 gene, (C) PPARα gene (D) PGC-1α gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Expressing, Control

    Sangyod rice extract regulates lipid metabolism through the Akt and MAPK signaling pathways. (A) Western blot analysis of Akt, ERK1/2 amd p38 MAPK, (B) Relative expression of pERK/ERK protein, (C) Relative expression of p-p38/p38 protein, (D) Relative expression of pAkt/Akt protein. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Journal: Food Chemistry: Molecular Sciences

    Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways

    doi: 10.1016/j.fochms.2026.100387

    Figure Lengend Snippet: Sangyod rice extract regulates lipid metabolism through the Akt and MAPK signaling pathways. (A) Western blot analysis of Akt, ERK1/2 amd p38 MAPK, (B) Relative expression of pERK/ERK protein, (C) Relative expression of p-p38/p38 protein, (D) Relative expression of pAkt/Akt protein. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.

    Article Snippet: The HepG2 human hepatocellular carcinoma cell line was procured from the American Type Culture Collection (Manassas, VA, USA) and nurtured in Dulbecco's modified Eagle's medium (Gibco, Waltham, MA, USA) enriched with 10% fetal bovine serum (Gibco, Waltham, MA, USA), 1% penicillin/streptomycin (Gibco, Waltham, MA, USA), and 1% l -glutamine (Gibco, Waltham, MA, USA).

    Techniques: Protein-Protein interactions, Western Blot, Expressing, Control

    Rationale for selecting CDKN1A /p21 as a therapeutic target in bladder cancer and validation of p21 mRNA expression. (A) Pan‐cancer analysis of CDKN1A alteration frequencies based on TCGA datasets. The analysis was performed using the TIMER3 web server. (B) CDKN1A mRNA expression in bladder cancer and normal bladder tissues, shown as log2(TPM + 1), where TPM denotes transcripts per million. Data were analyzed using the TIMER3 web server. (C) Representative p21 immunohistochemical staining images from a bladder cancer tissue microarray stratified by pathological stage (Tis, T1, T2, T3, and T4). Scale bars, 200 μm. (D) Quantification of p21 H‐scores in Tis, T1, T2, T3, and T4 lesions. Compared with Tis lesions, T1, T2, T3, and T4 tumors showed significantly lower p21 H‐scores. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01 (one‐way ANOVA). (E) Western blot analysis of basal and p21 mRNA‐induced p21 protein expression in T24 and J82 bladder cancer cells. Basal p21 protein levels were very low in both cell lines, whereas transfection of p21 mRNA led to robust p21 expression. For p21 blots, both short‐exposure (se) and long‐exposure (le) images are shown. β‐Actin serves as a loading control. (F) Immunofluorescence analysis of EGFP‐HA and p21‐HA expression in T24 and J82 cells using an anti‐HA antibody. Nuclei were stained with DAPI. The p21‐HA signal was predominantly localized to the nucleus, whereas EGFP showed diffuse cytoplasmic distribution. Scale bars, 20 μm.

    Journal: The FASEB Journal

    Article Title: Intravesical Delivery of P21 mRNA –Loaded Lipid Nanoparticles as a Tumor Suppressor Replacement Therapy for Bladder Cancer

    doi: 10.1096/fj.202600049R

    Figure Lengend Snippet: Rationale for selecting CDKN1A /p21 as a therapeutic target in bladder cancer and validation of p21 mRNA expression. (A) Pan‐cancer analysis of CDKN1A alteration frequencies based on TCGA datasets. The analysis was performed using the TIMER3 web server. (B) CDKN1A mRNA expression in bladder cancer and normal bladder tissues, shown as log2(TPM + 1), where TPM denotes transcripts per million. Data were analyzed using the TIMER3 web server. (C) Representative p21 immunohistochemical staining images from a bladder cancer tissue microarray stratified by pathological stage (Tis, T1, T2, T3, and T4). Scale bars, 200 μm. (D) Quantification of p21 H‐scores in Tis, T1, T2, T3, and T4 lesions. Compared with Tis lesions, T1, T2, T3, and T4 tumors showed significantly lower p21 H‐scores. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01 (one‐way ANOVA). (E) Western blot analysis of basal and p21 mRNA‐induced p21 protein expression in T24 and J82 bladder cancer cells. Basal p21 protein levels were very low in both cell lines, whereas transfection of p21 mRNA led to robust p21 expression. For p21 blots, both short‐exposure (se) and long‐exposure (le) images are shown. β‐Actin serves as a loading control. (F) Immunofluorescence analysis of EGFP‐HA and p21‐HA expression in T24 and J82 cells using an anti‐HA antibody. Nuclei were stained with DAPI. The p21‐HA signal was predominantly localized to the nucleus, whereas EGFP showed diffuse cytoplasmic distribution. Scale bars, 20 μm.

    Article Snippet: The human bladder carcinoma cell line J82 and the human embryonic kidney cell line HEK293T were purchased from the American Type Culture Collection (ATCC).

    Techniques: Biomarker Discovery, Expressing, Immunohistochemical staining, Staining, Microarray, Western Blot, Transfection, Control, Immunofluorescence

    10-HDA inhibited CRC cell growth and gap closure and increased intracellular ROS. ( A ) MTT analysis of HCT 116 and HT-29 cell viability after 48 h exposure to 10-HDA. ( B ) Colony formation of HCT 116 cells following 14 d treatment with 10-HDA. ( C ) Scratch assay analysis of HCT 116 gap closure after 24 h incubation with 10-HDA. ( D ) Flow cytometric analysis of HCT 116 intracellular ROS levels following 3 h exposure to 10-HDA. ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, no statistical significance. Control, vehicle-treated cells.

    Journal: Foods

    Article Title: 10-Hydroxy-2-decenoic Acid Suppresses Colorectal Cancer Progression by Inhibiting Wnt/β-Catenin Signaling and Promoting Apoptosis

    doi: 10.3390/foods15091608

    Figure Lengend Snippet: 10-HDA inhibited CRC cell growth and gap closure and increased intracellular ROS. ( A ) MTT analysis of HCT 116 and HT-29 cell viability after 48 h exposure to 10-HDA. ( B ) Colony formation of HCT 116 cells following 14 d treatment with 10-HDA. ( C ) Scratch assay analysis of HCT 116 gap closure after 24 h incubation with 10-HDA. ( D ) Flow cytometric analysis of HCT 116 intracellular ROS levels following 3 h exposure to 10-HDA. ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, no statistical significance. Control, vehicle-treated cells.

    Article Snippet: Human colorectal carcinoma cell lines HCT 116 (ATCC; CCL-247) and HT-29 (ATCC; HTB-38) were purchased from Zhong Qiao Xin Zhou Biotechnology Co., Ltd. (Shanghai, China).

    Techniques: Wound Healing Assay, Incubation, Control

    10-HDA inhibited tumor growth and modified the histopathological features of HCT 116 xenografts in vivo. ( A ) Schematic overview of HCT 116 xenograft establishment and 10-HDA administration. ( B ) Representative images of xenograft tumors from saline-treated control mice and 10-HDA-treated mice, with corresponding tumor volume quantification. Control, blue; 100 mg/kg 10-HDA, orange; 200 mg/kg 10-HDA, purple. ( C ) H&E-stained sections of xenograft tumors. Red arrows indicate tumor cells; yellow arrows denote necrotic regions; blue arrows indicate atypical (pathological) mitotic figures; and green arrows indicate inflammatory cell infiltration. ( D ) Ki-67 immunohistochemical staining of xenograft tumors from control and 10-HDA-treated mice. n = 6; * p < 0.05, ** p < 0.01, **** p < 0.0001; ns, no statistical significance. Control, saline-treated tumor-bearing mice.

    Journal: Foods

    Article Title: 10-Hydroxy-2-decenoic Acid Suppresses Colorectal Cancer Progression by Inhibiting Wnt/β-Catenin Signaling and Promoting Apoptosis

    doi: 10.3390/foods15091608

    Figure Lengend Snippet: 10-HDA inhibited tumor growth and modified the histopathological features of HCT 116 xenografts in vivo. ( A ) Schematic overview of HCT 116 xenograft establishment and 10-HDA administration. ( B ) Representative images of xenograft tumors from saline-treated control mice and 10-HDA-treated mice, with corresponding tumor volume quantification. Control, blue; 100 mg/kg 10-HDA, orange; 200 mg/kg 10-HDA, purple. ( C ) H&E-stained sections of xenograft tumors. Red arrows indicate tumor cells; yellow arrows denote necrotic regions; blue arrows indicate atypical (pathological) mitotic figures; and green arrows indicate inflammatory cell infiltration. ( D ) Ki-67 immunohistochemical staining of xenograft tumors from control and 10-HDA-treated mice. n = 6; * p < 0.05, ** p < 0.01, **** p < 0.0001; ns, no statistical significance. Control, saline-treated tumor-bearing mice.

    Article Snippet: Human colorectal carcinoma cell lines HCT 116 (ATCC; CCL-247) and HT-29 (ATCC; HTB-38) were purchased from Zhong Qiao Xin Zhou Biotechnology Co., Ltd. (Shanghai, China).

    Techniques: Modification, In Vivo, Saline, Control, Staining, Immunohistochemical staining

    Evaluation of the safety profile of 10-HDA treatment. ( A ) Mice weight changes compared with normal mice. Normal, red; model, blue; 100 mg/kg 10-HDA, orange; 200 mg/kg 10-HDA, purple. ( B ) Serum levels of liver function markers (AST, ALT, and ALP). ( C ) Representative H&E-stained histopathological sections of the heart, liver, spleen, lung and kidney. All analyses were performed on samples from healthy mice (normal control), and saline (model)- and 10-HDA-treated mice bearing HCT 116 xenograft tumors. n = 6; * p < 0.05, ** p < 0.01; ns, no statistical significance.

    Journal: Foods

    Article Title: 10-Hydroxy-2-decenoic Acid Suppresses Colorectal Cancer Progression by Inhibiting Wnt/β-Catenin Signaling and Promoting Apoptosis

    doi: 10.3390/foods15091608

    Figure Lengend Snippet: Evaluation of the safety profile of 10-HDA treatment. ( A ) Mice weight changes compared with normal mice. Normal, red; model, blue; 100 mg/kg 10-HDA, orange; 200 mg/kg 10-HDA, purple. ( B ) Serum levels of liver function markers (AST, ALT, and ALP). ( C ) Representative H&E-stained histopathological sections of the heart, liver, spleen, lung and kidney. All analyses were performed on samples from healthy mice (normal control), and saline (model)- and 10-HDA-treated mice bearing HCT 116 xenograft tumors. n = 6; * p < 0.05, ** p < 0.01; ns, no statistical significance.

    Article Snippet: Human colorectal carcinoma cell lines HCT 116 (ATCC; CCL-247) and HT-29 (ATCC; HTB-38) were purchased from Zhong Qiao Xin Zhou Biotechnology Co., Ltd. (Shanghai, China).

    Techniques: Staining, Control, Saline

    Transcriptomic analysis of ectopic xenograft tumor tissues derived from HCT 116 cells in 10-HDA- and saline-treated (control) mice. ( A ) Volcano plot of DEGs. Each dot represents one gene; red indicates significantly upregulated genes and green indicates significantly downregulated genes (FDR < 0.05 and |log2FoldChange| > 1). ( B ) Heatmap of representative DEGs related to tumor progression. Colors indicate relative expression (red, upregulation; blue, downregulation). ( C ) GO enrichment of DEGs showing top terms in biological process (BP, red), cellular component (CC, green), and molecular function (MF, blue). ( D ) Top 20 enriched KEGG pathways of DEGs. The x-axis shows the number of DEGs in each pathway; bar color represents statistical significance (adjusted p -value). ( E ) Relative mRNA expression levels of ANO1 , MKi67 , LTBP1 , FGF19 , NECTIN4 , PLD1 , and SKA1 in HCT 116 cells treated with 10-HDA or vehicle (control). Control, dark blue; 1.0 mM 10-HDA, blue; 1.5 mM 10-HDA, light blue; 2.0 mM 10-HDA, green. ( F ) Relative mRNA expression levels of ANO1 , MKi67 , LTBP1 , FGF19 , NECTIN4 , PLD1 , and SKA1 in xenograft tumors from 10-HDA- or saline-treated (control) mice. Control, green; 100 mg/kg 10-HDA, blue; 200 mg/kg 10-HDA, yellow. * p < 0.05, ** p < 0.01, **** p < 0.0001; ns, no statistical significance.

    Journal: Foods

    Article Title: 10-Hydroxy-2-decenoic Acid Suppresses Colorectal Cancer Progression by Inhibiting Wnt/β-Catenin Signaling and Promoting Apoptosis

    doi: 10.3390/foods15091608

    Figure Lengend Snippet: Transcriptomic analysis of ectopic xenograft tumor tissues derived from HCT 116 cells in 10-HDA- and saline-treated (control) mice. ( A ) Volcano plot of DEGs. Each dot represents one gene; red indicates significantly upregulated genes and green indicates significantly downregulated genes (FDR < 0.05 and |log2FoldChange| > 1). ( B ) Heatmap of representative DEGs related to tumor progression. Colors indicate relative expression (red, upregulation; blue, downregulation). ( C ) GO enrichment of DEGs showing top terms in biological process (BP, red), cellular component (CC, green), and molecular function (MF, blue). ( D ) Top 20 enriched KEGG pathways of DEGs. The x-axis shows the number of DEGs in each pathway; bar color represents statistical significance (adjusted p -value). ( E ) Relative mRNA expression levels of ANO1 , MKi67 , LTBP1 , FGF19 , NECTIN4 , PLD1 , and SKA1 in HCT 116 cells treated with 10-HDA or vehicle (control). Control, dark blue; 1.0 mM 10-HDA, blue; 1.5 mM 10-HDA, light blue; 2.0 mM 10-HDA, green. ( F ) Relative mRNA expression levels of ANO1 , MKi67 , LTBP1 , FGF19 , NECTIN4 , PLD1 , and SKA1 in xenograft tumors from 10-HDA- or saline-treated (control) mice. Control, green; 100 mg/kg 10-HDA, blue; 200 mg/kg 10-HDA, yellow. * p < 0.05, ** p < 0.01, **** p < 0.0001; ns, no statistical significance.

    Article Snippet: Human colorectal carcinoma cell lines HCT 116 (ATCC; CCL-247) and HT-29 (ATCC; HTB-38) were purchased from Zhong Qiao Xin Zhou Biotechnology Co., Ltd. (Shanghai, China).

    Techniques: Derivative Assay, Saline, Control, Expressing

    10-HDA induced apoptosis in HCT 116 cells and subcutaneous HCT 116 xenograft tumors. ( A ) Relative mRNA expression levels of Bcl-2 , BAX , BINP2 , and caspase-3 in HCT 116 cells treated with 10-HDA or vehicle (control). Control, dark blue, 1.0 mM 10-HDA, blue; 1.5 mM 10-HDA, light blue; 2.0 mM 10-HDA, green. ( B ) Relative mRNA expression levels of Bcl-2 , BAX , BINP2 , and caspase-3 in xenograft tumors from 10-HDA- or saline-treated (control) mice. Control, green; 100 mg/kg 10-HDA, blue; 200 mg/kg 10-HDA, yellow. ( C ) Western blotting analysis of caspase-3, Bcl-2, BAX, and cleaved caspase-3 protein levels, as well as the calculated cleaved caspase-3/caspase-3 and Bcl-2/BAX ratios in HCT 116 cells treated with 10-HDA or vehicle (control). ( D ) Immunohistochemical staining of Bcl-2 and BAX in xenograft tumors from 10-HDA- or saline-treated (control) mice. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, no statistical significance.

    Journal: Foods

    Article Title: 10-Hydroxy-2-decenoic Acid Suppresses Colorectal Cancer Progression by Inhibiting Wnt/β-Catenin Signaling and Promoting Apoptosis

    doi: 10.3390/foods15091608

    Figure Lengend Snippet: 10-HDA induced apoptosis in HCT 116 cells and subcutaneous HCT 116 xenograft tumors. ( A ) Relative mRNA expression levels of Bcl-2 , BAX , BINP2 , and caspase-3 in HCT 116 cells treated with 10-HDA or vehicle (control). Control, dark blue, 1.0 mM 10-HDA, blue; 1.5 mM 10-HDA, light blue; 2.0 mM 10-HDA, green. ( B ) Relative mRNA expression levels of Bcl-2 , BAX , BINP2 , and caspase-3 in xenograft tumors from 10-HDA- or saline-treated (control) mice. Control, green; 100 mg/kg 10-HDA, blue; 200 mg/kg 10-HDA, yellow. ( C ) Western blotting analysis of caspase-3, Bcl-2, BAX, and cleaved caspase-3 protein levels, as well as the calculated cleaved caspase-3/caspase-3 and Bcl-2/BAX ratios in HCT 116 cells treated with 10-HDA or vehicle (control). ( D ) Immunohistochemical staining of Bcl-2 and BAX in xenograft tumors from 10-HDA- or saline-treated (control) mice. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, no statistical significance.

    Article Snippet: Human colorectal carcinoma cell lines HCT 116 (ATCC; CCL-247) and HT-29 (ATCC; HTB-38) were purchased from Zhong Qiao Xin Zhou Biotechnology Co., Ltd. (Shanghai, China).

    Techniques: Expressing, Control, Saline, Western Blot, Immunohistochemical staining, Staining

    Involvement of Wnt/β-Catenin signaling in the anti-CRC effects of 10-HDA. ( A ) Relative mRNA expression levels of WNT11 , RNF43 , FRAT1 , β-catenin , and MMP7 in HCT 116 cells treated with 10-HDA or vehicle (control). Control, dark blue; 1.0 mM 10-HDA, blue, 1.5 mM 10-HDA, light blue; 2.0 mM 10-HDA, green. ( B ) Relative mRNA expression levels of WNT11 , RNF43 , FRAT1 , β-catenin , and MMP7 in xenograft tumors from 10-HDA- or saline-treated (control) mice. Control, green; 100 mg/kg 10-HDA, blue; 200 mg/kg 10-HDA, yellow. ( C ) Western blotting analysis of β-catenin expression in HCT 116 cells treated with 10-HDA or vehicle (control). ( D ) Western blotting analysis of β-catenin, p-GSK3β and GSK3β in xenograft tumor tissues from 10-HDA- and saline-treated (control) mice. ( E ) Immunohistochemical staining of β-catenin in xenograft tumors. ( F ) Western blotting analysis and densitometric quantification of the nuclear and cytoplasmic β-catenin in HCT 116 cells after 10-HDA or vehicle (control) treatment. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, no statistical significance.

    Journal: Foods

    Article Title: 10-Hydroxy-2-decenoic Acid Suppresses Colorectal Cancer Progression by Inhibiting Wnt/β-Catenin Signaling and Promoting Apoptosis

    doi: 10.3390/foods15091608

    Figure Lengend Snippet: Involvement of Wnt/β-Catenin signaling in the anti-CRC effects of 10-HDA. ( A ) Relative mRNA expression levels of WNT11 , RNF43 , FRAT1 , β-catenin , and MMP7 in HCT 116 cells treated with 10-HDA or vehicle (control). Control, dark blue; 1.0 mM 10-HDA, blue, 1.5 mM 10-HDA, light blue; 2.0 mM 10-HDA, green. ( B ) Relative mRNA expression levels of WNT11 , RNF43 , FRAT1 , β-catenin , and MMP7 in xenograft tumors from 10-HDA- or saline-treated (control) mice. Control, green; 100 mg/kg 10-HDA, blue; 200 mg/kg 10-HDA, yellow. ( C ) Western blotting analysis of β-catenin expression in HCT 116 cells treated with 10-HDA or vehicle (control). ( D ) Western blotting analysis of β-catenin, p-GSK3β and GSK3β in xenograft tumor tissues from 10-HDA- and saline-treated (control) mice. ( E ) Immunohistochemical staining of β-catenin in xenograft tumors. ( F ) Western blotting analysis and densitometric quantification of the nuclear and cytoplasmic β-catenin in HCT 116 cells after 10-HDA or vehicle (control) treatment. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, no statistical significance.

    Article Snippet: Human colorectal carcinoma cell lines HCT 116 (ATCC; CCL-247) and HT-29 (ATCC; HTB-38) were purchased from Zhong Qiao Xin Zhou Biotechnology Co., Ltd. (Shanghai, China).

    Techniques: Expressing, Control, Saline, Western Blot, Immunohistochemical staining, Staining

    The cytotoxicity of Caco-2 cells ( A ) and HT-29 cells ( B ) after treatment with co-fermented mature tea leaves samples for 72 h. Different lowercase letters indicate significant differences among fermentation times within the same treatment ( p < 0.05).

    Journal: Foods

    Article Title: Valorization and Functional Enhancement of Mature Assam Tea Leaves Through Indigenous Filamentous Fungi-Based Fermentation for Functional Drink Development

    doi: 10.3390/foods15091562

    Figure Lengend Snippet: The cytotoxicity of Caco-2 cells ( A ) and HT-29 cells ( B ) after treatment with co-fermented mature tea leaves samples for 72 h. Different lowercase letters indicate significant differences among fermentation times within the same treatment ( p < 0.05).

    Article Snippet: Human colon carcinoma cell line (Caco-2) and Human colon adenocarcinoma cell line (HT-29) obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA) were used to carry out the cell cytotoxicity test.

    Techniques:

    Inhibitory activity of prodigiosin pigment and cisplatin against viability of HepG2 and MCF-7 cells. Values are presented as mean ± SD ( n = 3). One-way ANOVA showed significant differences in cell viability among treatments ( p < 0.001)

    Journal: World Journal of Microbiology & Biotechnology

    Article Title: Bioproduction, characterization, and evaluation of the biological activities of prodigiosin from Serratia marcescens HMS

    doi: 10.1007/s11274-026-04936-8

    Figure Lengend Snippet: Inhibitory activity of prodigiosin pigment and cisplatin against viability of HepG2 and MCF-7 cells. Values are presented as mean ± SD ( n = 3). One-way ANOVA showed significant differences in cell viability among treatments ( p < 0.001)

    Article Snippet: Cell lines: Human breast adenocarcinoma (MCF-7) and human hepatocellular carcinoma (HepG2) cell lines were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

    Techniques: Activity Assay