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hcc 38  (ATCC)


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    Structured Review

    ATCC hcc 38
    Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and <t>HCC</t> <t>38</t> cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.
    Hcc 38, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 487 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells"

    Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells

    Journal: Translational Oncology

    doi: 10.1016/j.tranon.2026.102779

    Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.
    Figure Legend Snippet: Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

    Techniques Used: CCK-8 Assay, Control, EdU Assay, Fluorescence, Flow Cytometry, Staining



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    Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and <t>HCC</t> <t>38</t> cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.
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    Ptch1 is expressed in breast cancer cell lines. A. PTCH1 mRNA expression (log 2 transformed) in various luminal and HER2 breast cancer cell lines (dark green) and in TNBC cell lines (other colors). TNBC cell lines are depicted according to the “Lehmann TNBC subtype” nomenclature : basal-like 1 (yellow), basal-like 2 (pale green), immunomodulatory (brown), luminal androgen receptor (dark pink), mesenchymal (pale pink) and mesenchymal stem-like (pink). B. PTCH1 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from TNBC cell lines <t>(MDA-MB-231,</t> <t>HCC-38</t> and MDA-MB-468) with antibodies directed against PTCH1. PTCH1 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*).
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    Ptch1 is expressed in breast cancer cell lines. A. PTCH1 mRNA expression (log 2 transformed) in various luminal and HER2 breast cancer cell lines (dark green) and in TNBC cell lines (other colors). TNBC cell lines are depicted according to the “Lehmann TNBC subtype” nomenclature : basal-like 1 (yellow), basal-like 2 (pale green), immunomodulatory (brown), luminal androgen receptor (dark pink), mesenchymal (pale pink) and mesenchymal stem-like (pink). B. PTCH1 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from TNBC cell lines <t>(MDA-MB-231,</t> <t>HCC-38</t> and MDA-MB-468) with antibodies directed against PTCH1. PTCH1 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*).
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    Image Search Results


    Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

    Journal: Translational Oncology

    Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells

    doi: 10.1016/j.tranon.2026.102779

    Figure Lengend Snippet: Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

    Article Snippet: The TNBC cell lines used in this study, including MDA-MB-231, MDA-MB-436, and HCC 38, were obtained from the American Type Culture Collection (ATCC) and maintained in our laboratory.

    Techniques: CCK-8 Assay, Control, EdU Assay, Fluorescence, Flow Cytometry, Staining

    Ptch1 is expressed in breast cancer cell lines. A. PTCH1 mRNA expression (log 2 transformed) in various luminal and HER2 breast cancer cell lines (dark green) and in TNBC cell lines (other colors). TNBC cell lines are depicted according to the “Lehmann TNBC subtype” nomenclature : basal-like 1 (yellow), basal-like 2 (pale green), immunomodulatory (brown), luminal androgen receptor (dark pink), mesenchymal (pale pink) and mesenchymal stem-like (pink). B. PTCH1 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from TNBC cell lines (MDA-MB-231, HCC-38 and MDA-MB-468) with antibodies directed against PTCH1. PTCH1 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*).

    Journal: Translational Oncology

    Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

    doi: 10.1016/j.tranon.2026.102777

    Figure Lengend Snippet: Ptch1 is expressed in breast cancer cell lines. A. PTCH1 mRNA expression (log 2 transformed) in various luminal and HER2 breast cancer cell lines (dark green) and in TNBC cell lines (other colors). TNBC cell lines are depicted according to the “Lehmann TNBC subtype” nomenclature : basal-like 1 (yellow), basal-like 2 (pale green), immunomodulatory (brown), luminal androgen receptor (dark pink), mesenchymal (pale pink) and mesenchymal stem-like (pink). B. PTCH1 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from TNBC cell lines (MDA-MB-231, HCC-38 and MDA-MB-468) with antibodies directed against PTCH1. PTCH1 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*).

    Article Snippet: Human breast cancer cell lines MDA-MB-231, MDA-MB-468 and HCC-38 were purchased from ATCC.

    Techniques: Expressing, Transformation Assay, Western Blot, Software

    PTCH1 drug efflux inhibitor PAH increases the sensitivity of TNBC cells to chemotherapy . Cell viability was measured after 24 h or 48 h treatment with increasing concentration of docetaxel or doxorubicin respectively on MDA-MB-231, MDA-MB-468 and HCC-38 cell lines in the absence or the presence of 15µM PAH. IC 50 values (corresponding to the concentration of chemotherapy inducing 50% of cell death) were calculated. Data reported are the mean ± SEM of at least 3 independent experiments. Significance is attained at P < 0.05 (*).

    Journal: Translational Oncology

    Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

    doi: 10.1016/j.tranon.2026.102777

    Figure Lengend Snippet: PTCH1 drug efflux inhibitor PAH increases the sensitivity of TNBC cells to chemotherapy . Cell viability was measured after 24 h or 48 h treatment with increasing concentration of docetaxel or doxorubicin respectively on MDA-MB-231, MDA-MB-468 and HCC-38 cell lines in the absence or the presence of 15µM PAH. IC 50 values (corresponding to the concentration of chemotherapy inducing 50% of cell death) were calculated. Data reported are the mean ± SEM of at least 3 independent experiments. Significance is attained at P < 0.05 (*).

    Article Snippet: Human breast cancer cell lines MDA-MB-231, MDA-MB-468 and HCC-38 were purchased from ATCC.

    Techniques: Concentration Assay

    Other multidrug transporters are expressed in TNBC cell lines. A. P-gp and ABCG2 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from each TNBC cell line (MDA-MB-231, HCC-38 and MDA-MB-468) with antibodies directed against P-gp or ABCG2 and GAPDH. B. P-gp, ABCG2 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*). ** P < 0.01; *** P < 0.001; ns P > 0.05.

    Journal: Translational Oncology

    Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

    doi: 10.1016/j.tranon.2026.102777

    Figure Lengend Snippet: Other multidrug transporters are expressed in TNBC cell lines. A. P-gp and ABCG2 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from each TNBC cell line (MDA-MB-231, HCC-38 and MDA-MB-468) with antibodies directed against P-gp or ABCG2 and GAPDH. B. P-gp, ABCG2 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*). ** P < 0.01; *** P < 0.001; ns P > 0.05.

    Article Snippet: Human breast cancer cell lines MDA-MB-231, MDA-MB-468 and HCC-38 were purchased from ATCC.

    Techniques: Expressing, Western Blot, Software

    Evaluation of cytotoxicity profiles of SRHC nanoparticles. The dose-response curve illustrates the relationship between the cytotoxicity percentage of SRHC (blue) and conjugated NPs (Polymer-SRHC) (red) on HepG2 cells and the concentration in nmol. The IC 50 values of SRHC and conjugated NPs (Polymer-SRHC) were determined from the curve to be 98.8 nmol and 95.24, respectively.

    Journal: Scientific Reports

    Article Title: Development of an innovative nanopolymer-lncRNA-SRHC complex as therapeutic modalities for targeted hepatocellular carcinoma therapy

    doi: 10.1038/s41598-026-51340-1

    Figure Lengend Snippet: Evaluation of cytotoxicity profiles of SRHC nanoparticles. The dose-response curve illustrates the relationship between the cytotoxicity percentage of SRHC (blue) and conjugated NPs (Polymer-SRHC) (red) on HepG2 cells and the concentration in nmol. The IC 50 values of SRHC and conjugated NPs (Polymer-SRHC) were determined from the curve to be 98.8 nmol and 95.24, respectively.

    Article Snippet: Human HCC HepG2 cells (ATCC HB-8065) were cultured in 25 cm 2 culture flasks.

    Techniques: Polymer, Concentration Assay

    Validation of CD155-TIGIT signaling in SHP-2 recruitment and STAT3 pathway inhibition. (A) Schematic representation of the regulatory mechanism by which tumor cell CD155 modulates the SHP-2/STAT3 axis via TIGIT; (B) WB analysis of CD155 protein expression levels in Hepa1–6 cells; (C) Immunofluorescence staining showing SHP-2 expression and localization in co-cultured NK cells, scale bar: 25 µm; (D) Quantitative analysis of immunofluorescence signal intensity from panel C; (E) Co-IP assay demonstrating the interaction between SHP-2 and STAT3 in TIGIT-overexpressing NK cells; (F) Immunofluorescence colocalization analysis illustrating the distribution of SHP-2 and STAT3 in TIGIT-overexpressing NK cells, scale bar: 25 µm; (G) WB analysis of SHP-2, total STAT3, and its phosphorylated form p-STAT3 (Tyr705) protein levels in TIGIT or SHP-2-overexpressing NK cells. Experiments were conducted in triplicate. * indicates a statistically significant difference between groups, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Frontiers in Immunology

    Article Title: Targeting the TIGIT/CD155-induced metabolic checkpoint in NK cells restores anti-tumor immunity and suppresses hepatocellular carcinoma growth

    doi: 10.3389/fimmu.2026.1790174

    Figure Lengend Snippet: Validation of CD155-TIGIT signaling in SHP-2 recruitment and STAT3 pathway inhibition. (A) Schematic representation of the regulatory mechanism by which tumor cell CD155 modulates the SHP-2/STAT3 axis via TIGIT; (B) WB analysis of CD155 protein expression levels in Hepa1–6 cells; (C) Immunofluorescence staining showing SHP-2 expression and localization in co-cultured NK cells, scale bar: 25 µm; (D) Quantitative analysis of immunofluorescence signal intensity from panel C; (E) Co-IP assay demonstrating the interaction between SHP-2 and STAT3 in TIGIT-overexpressing NK cells; (F) Immunofluorescence colocalization analysis illustrating the distribution of SHP-2 and STAT3 in TIGIT-overexpressing NK cells, scale bar: 25 µm; (G) WB analysis of SHP-2, total STAT3, and its phosphorylated form p-STAT3 (Tyr705) protein levels in TIGIT or SHP-2-overexpressing NK cells. Experiments were conducted in triplicate. * indicates a statistically significant difference between groups, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: The murine HCC cell line Hepa1-6 (ATCC ® CRL-1830TM) was maintained in high-glucose DMEM supplemented with 10% FBS (Gibco) and 1% penicillin–streptomycin (Gibco) at 37 °C in a humidified incubator containing 5% CO 2 .

    Techniques: Biomarker Discovery, Inhibition, Expressing, Immunofluorescence, Staining, Cell Culture, Co-Immunoprecipitation Assay

    Regulation of NK cell cytotoxicity against tumor cells via the TIGIT/STAT3/GLUT1 pathway. (A) Schematic diagram illustrating the modulation of NK cell anti-tumor activity through interventions on the TIGIT-STAT3-GLUT1 axis; (B, D) flow cytometry combined with CFSE/PI staining to assess the death rate of Hepa1–6 hepatocarcinoma cells, evaluating NK cell cytotoxicity; (C, E) LDH release assay measuring cell lysis levels in co-culture systems. Experiments were repeated three times. ** indicates p < 0.01 compared to the Control group, *** p < 0.001; # indicates p < 0.05 compared to the anti-TIGIT or IL-6+sh-NC groups.

    Journal: Frontiers in Immunology

    Article Title: Targeting the TIGIT/CD155-induced metabolic checkpoint in NK cells restores anti-tumor immunity and suppresses hepatocellular carcinoma growth

    doi: 10.3389/fimmu.2026.1790174

    Figure Lengend Snippet: Regulation of NK cell cytotoxicity against tumor cells via the TIGIT/STAT3/GLUT1 pathway. (A) Schematic diagram illustrating the modulation of NK cell anti-tumor activity through interventions on the TIGIT-STAT3-GLUT1 axis; (B, D) flow cytometry combined with CFSE/PI staining to assess the death rate of Hepa1–6 hepatocarcinoma cells, evaluating NK cell cytotoxicity; (C, E) LDH release assay measuring cell lysis levels in co-culture systems. Experiments were repeated three times. ** indicates p < 0.01 compared to the Control group, *** p < 0.001; # indicates p < 0.05 compared to the anti-TIGIT or IL-6+sh-NC groups.

    Article Snippet: The murine HCC cell line Hepa1-6 (ATCC ® CRL-1830TM) was maintained in high-glucose DMEM supplemented with 10% FBS (Gibco) and 1% penicillin–streptomycin (Gibco) at 37 °C in a humidified incubator containing 5% CO 2 .

    Techniques: Activity Assay, Flow Cytometry, Staining, Lactate Dehydrogenase Assay, Lysis, Co-Culture Assay, Control

    ABHD12 is highly expressed in breast cancer tissues and promotes the proliferative capacity of breast cancer cells. (A and B) WB experiments confirm the expression of ABHD12 protein in breast cancer tissues and adjacent normal breast tissues. (C and D) IHC experiments verify the expression and localization of ABHD12 in breast cancer tissues (cytoplasm). ( E ) RT-qPCR experiments confirm the expression of ABHD12 mRNA in normal breast cells and breast cancer cells. Verification of ABHD12 knockdown and overexpression efficiency at the mRNA level in (F) MDA-MB-231 cell line and ( G ) HCC-1937 cell line. ( H ) Verification of ABHD12 knockdown and overexpression protein efficiency at protein level in MDA-MB-231 and HCC-1937 cell line. ( I ) Colony formation assays and their quantitative analysis in ( J ) MDA-MB-231 and ( K ) HCC-1937 cell lines further validate the impact of ABHD12 on cell proliferation. CCK-8 experiments demonstrate the effects of different ABHD12 expression levels on the proliferative capacity of ( L ) MDA-MB-231 cell line and ( M ) HCC-1937 cell line. * p <0.05, ** p <0.01, *** p <0.001; ns indicates no statistical significance.

    Journal: Breast Cancer : Targets and Therapy

    Article Title: Multi-Omics Characterization of ABHD12 Across Pan-Cancer and Validation of Its Role in Promoting Proliferation and Metastasis in Breast Cancer

    doi: 10.2147/BCTT.S554836

    Figure Lengend Snippet: ABHD12 is highly expressed in breast cancer tissues and promotes the proliferative capacity of breast cancer cells. (A and B) WB experiments confirm the expression of ABHD12 protein in breast cancer tissues and adjacent normal breast tissues. (C and D) IHC experiments verify the expression and localization of ABHD12 in breast cancer tissues (cytoplasm). ( E ) RT-qPCR experiments confirm the expression of ABHD12 mRNA in normal breast cells and breast cancer cells. Verification of ABHD12 knockdown and overexpression efficiency at the mRNA level in (F) MDA-MB-231 cell line and ( G ) HCC-1937 cell line. ( H ) Verification of ABHD12 knockdown and overexpression protein efficiency at protein level in MDA-MB-231 and HCC-1937 cell line. ( I ) Colony formation assays and their quantitative analysis in ( J ) MDA-MB-231 and ( K ) HCC-1937 cell lines further validate the impact of ABHD12 on cell proliferation. CCK-8 experiments demonstrate the effects of different ABHD12 expression levels on the proliferative capacity of ( L ) MDA-MB-231 cell line and ( M ) HCC-1937 cell line. * p <0.05, ** p <0.01, *** p <0.001; ns indicates no statistical significance.

    Article Snippet: HCC-1937 cells were cultured in HCC-1937 cell-specific medium (CM-0093, Procell, China) supplemented with RPMI-1640, 10% FBS, and 1% penicillin-streptomycin solution (dual antibiotics).

    Techniques: Expressing, Quantitative RT-PCR, Knockdown, Over Expression, CCK-8 Assay

    Overexpression of ABHD12 in breast cancer cell lines enhances the invasive and migratory capabilities of breast cancer cells and promotes tumor formation in mice. Scratch assays demonstrate the differential effects of varying ABHD12 expression levels on the migratory capacity of (A and B) MDA-MB-231 cell line and (C and D) HCC-1937 cell line. Transwell invasion and migration assays validate the impact of ABHD12 knockdown and overexpression on the invasive and migratory properties of ( E–G ) MDA-MB-231 cell line and ( H–J ) HCC-1937 cell line. ( K–N ) Animal experiments assess the effects of ABHD12 knockdown and overexpression on body weight and tumor mass/volume in NCG mice. * p <0.05, ** p <0.01, *** p <0.001.

    Journal: Breast Cancer : Targets and Therapy

    Article Title: Multi-Omics Characterization of ABHD12 Across Pan-Cancer and Validation of Its Role in Promoting Proliferation and Metastasis in Breast Cancer

    doi: 10.2147/BCTT.S554836

    Figure Lengend Snippet: Overexpression of ABHD12 in breast cancer cell lines enhances the invasive and migratory capabilities of breast cancer cells and promotes tumor formation in mice. Scratch assays demonstrate the differential effects of varying ABHD12 expression levels on the migratory capacity of (A and B) MDA-MB-231 cell line and (C and D) HCC-1937 cell line. Transwell invasion and migration assays validate the impact of ABHD12 knockdown and overexpression on the invasive and migratory properties of ( E–G ) MDA-MB-231 cell line and ( H–J ) HCC-1937 cell line. ( K–N ) Animal experiments assess the effects of ABHD12 knockdown and overexpression on body weight and tumor mass/volume in NCG mice. * p <0.05, ** p <0.01, *** p <0.001.

    Article Snippet: HCC-1937 cells were cultured in HCC-1937 cell-specific medium (CM-0093, Procell, China) supplemented with RPMI-1640, 10% FBS, and 1% penicillin-streptomycin solution (dual antibiotics).

    Techniques: Over Expression, Expressing, Migration, Knockdown

    ABHD12 is highly expressed in breast cancer tissues and promotes the proliferative capacity of breast cancer cells. (A and B) WB experiments confirm the expression of ABHD12 protein in breast cancer tissues and adjacent normal breast tissues. (C and D) IHC experiments verify the expression and localization of ABHD12 in breast cancer tissues (cytoplasm). ( E ) RT-qPCR experiments confirm the expression of ABHD12 mRNA in normal breast cells and breast cancer cells. Verification of ABHD12 knockdown and overexpression efficiency at the mRNA level in (F) MDA-MB-231 cell line and ( G ) HCC-1937 cell line. ( H ) Verification of ABHD12 knockdown and overexpression protein efficiency at protein level in MDA-MB-231 and HCC-1937 cell line. ( I ) Colony formation assays and their quantitative analysis in ( J ) MDA-MB-231 and ( K ) HCC-1937 cell lines further validate the impact of ABHD12 on cell proliferation. CCK-8 experiments demonstrate the effects of different ABHD12 expression levels on the proliferative capacity of ( L ) MDA-MB-231 cell line and ( M ) HCC-1937 cell line. * p <0.05, ** p <0.01, *** p <0.001; ns indicates no statistical significance.

    Journal: Breast Cancer : Targets and Therapy

    Article Title: Multi-Omics Characterization of ABHD12 Across Pan-Cancer and Validation of Its Role in Promoting Proliferation and Metastasis in Breast Cancer

    doi: 10.2147/BCTT.S554836

    Figure Lengend Snippet: ABHD12 is highly expressed in breast cancer tissues and promotes the proliferative capacity of breast cancer cells. (A and B) WB experiments confirm the expression of ABHD12 protein in breast cancer tissues and adjacent normal breast tissues. (C and D) IHC experiments verify the expression and localization of ABHD12 in breast cancer tissues (cytoplasm). ( E ) RT-qPCR experiments confirm the expression of ABHD12 mRNA in normal breast cells and breast cancer cells. Verification of ABHD12 knockdown and overexpression efficiency at the mRNA level in (F) MDA-MB-231 cell line and ( G ) HCC-1937 cell line. ( H ) Verification of ABHD12 knockdown and overexpression protein efficiency at protein level in MDA-MB-231 and HCC-1937 cell line. ( I ) Colony formation assays and their quantitative analysis in ( J ) MDA-MB-231 and ( K ) HCC-1937 cell lines further validate the impact of ABHD12 on cell proliferation. CCK-8 experiments demonstrate the effects of different ABHD12 expression levels on the proliferative capacity of ( L ) MDA-MB-231 cell line and ( M ) HCC-1937 cell line. * p <0.05, ** p <0.01, *** p <0.001; ns indicates no statistical significance.

    Article Snippet: BRCA cell lines HCC-1937, MCF-10A, MCF-7, BT474, SK-BR-3, MDA-MB-468, BT-549, and MDA-MB-231 were purchased from Procell Life Science & Technology Co., Ltd., Wuhan, China.

    Techniques: Expressing, Quantitative RT-PCR, Knockdown, Over Expression, CCK-8 Assay

    Overexpression of ABHD12 in breast cancer cell lines enhances the invasive and migratory capabilities of breast cancer cells and promotes tumor formation in mice. Scratch assays demonstrate the differential effects of varying ABHD12 expression levels on the migratory capacity of (A and B) MDA-MB-231 cell line and (C and D) HCC-1937 cell line. Transwell invasion and migration assays validate the impact of ABHD12 knockdown and overexpression on the invasive and migratory properties of ( E–G ) MDA-MB-231 cell line and ( H–J ) HCC-1937 cell line. ( K–N ) Animal experiments assess the effects of ABHD12 knockdown and overexpression on body weight and tumor mass/volume in NCG mice. * p <0.05, ** p <0.01, *** p <0.001.

    Journal: Breast Cancer : Targets and Therapy

    Article Title: Multi-Omics Characterization of ABHD12 Across Pan-Cancer and Validation of Its Role in Promoting Proliferation and Metastasis in Breast Cancer

    doi: 10.2147/BCTT.S554836

    Figure Lengend Snippet: Overexpression of ABHD12 in breast cancer cell lines enhances the invasive and migratory capabilities of breast cancer cells and promotes tumor formation in mice. Scratch assays demonstrate the differential effects of varying ABHD12 expression levels on the migratory capacity of (A and B) MDA-MB-231 cell line and (C and D) HCC-1937 cell line. Transwell invasion and migration assays validate the impact of ABHD12 knockdown and overexpression on the invasive and migratory properties of ( E–G ) MDA-MB-231 cell line and ( H–J ) HCC-1937 cell line. ( K–N ) Animal experiments assess the effects of ABHD12 knockdown and overexpression on body weight and tumor mass/volume in NCG mice. * p <0.05, ** p <0.01, *** p <0.001.

    Article Snippet: BRCA cell lines HCC-1937, MCF-10A, MCF-7, BT474, SK-BR-3, MDA-MB-468, BT-549, and MDA-MB-231 were purchased from Procell Life Science & Technology Co., Ltd., Wuhan, China.

    Techniques: Over Expression, Expressing, Migration, Knockdown