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The overexpression of Sohlh2 inhibited the proliferation and the proportion of cells in the S phase, promoting apoptosis in HCC cells. (A-B) <t>CCK8</t> for cell proliferation. Flow cytometry was applied for cell cycle analysis in HepG2(C, E) and Hep3B (D, F). Flow cytometry was used to detect apoptosis in HepG2 (G) and Hep3B cells (H). Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N = 3.
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The overexpression of Sohlh2 inhibited the proliferation and the proportion of cells in the S phase, promoting apoptosis in HCC cells. (A-B) <t>CCK8</t> for cell proliferation. Flow cytometry was applied for cell cycle analysis in HepG2(C, E) and Hep3B (D, F). Flow cytometry was used to detect apoptosis in HepG2 (G) and Hep3B cells (H). Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N = 3.
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The overexpression of Sohlh2 inhibited the proliferation and the proportion of cells in the S phase, promoting apoptosis in HCC cells. (A-B) <t>CCK8</t> for cell proliferation. Flow cytometry was applied for cell cycle analysis in HepG2(C, E) and Hep3B (D, F). Flow cytometry was used to detect apoptosis in HepG2 (G) and Hep3B cells (H). Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N = 3.
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The overexpression of Sohlh2 inhibited the proliferation and the proportion of cells in the S phase, promoting apoptosis in HCC cells. (A-B) <t>CCK8</t> for cell proliferation. Flow cytometry was applied for cell cycle analysis in HepG2(C, E) and Hep3B (D, F). Flow cytometry was used to detect apoptosis in HepG2 (G) and Hep3B cells (H). Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N = 3.
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The overexpression of Sohlh2 inhibited the proliferation and the proportion of cells in the S phase, promoting apoptosis in HCC cells. (A-B) <t>CCK8</t> for cell proliferation. Flow cytometry was applied for cell cycle analysis in HepG2(C, E) and Hep3B (D, F). Flow cytometry was used to detect apoptosis in HepG2 (G) and Hep3B cells (H). Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N = 3.
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The overexpression of Sohlh2 inhibited the proliferation and the proportion of cells in the S phase, promoting apoptosis in HCC cells. (A-B) <t>CCK8</t> for cell proliferation. Flow cytometry was applied for cell cycle analysis in HepG2(C, E) and Hep3B (D, F). Flow cytometry was used to detect apoptosis in HepG2 (G) and Hep3B cells (H). Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N = 3.
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The effect of AFP on the expression of MMP9 and MICA/B shedding on the membrane of HCC cells. (A) Western blotting experiment was performed to detect the expression levels of MMP9; (B) Grey scale values of MMP9 expression were calculated using Image J software and then statistically analysed and plotted; (C) qRT‐PCR experiment was used to check MMP9 mRNA expression levels; (D) Western blotting was performed to detect the expression levels of sMICA/B in HLE, HLE‐NC, HLE‐AFP cells; (E) Western blotting was performed to detect the expression levels of sMICA/B in HuH‐7, HuH‐7‐NC, HuH‐7‐shAFP cells; (F) ELISA were performed to detect the content of sMICA/B in HCC cell supernatants; (G) <t>CCK‐8</t> experiments were performed to detect the IC50 of GM6001 and TAPI‐1; (H) Detection of MICA/B expression in HCC cells while treated with GM6001 and TAPI‐1 by flow cytometry; (I) Prism GraphPad(10.0) for statistical analysis and graphing of flow cytometry results; (J) Detection of sMICA/B in HCC cells supernatants while treated with GM6001 and TAPI‐1 by ELISA; (K) Western blotting experiment was performed to detect the expression levels of PI3K, AKT, p‐AKT and MMP9; (L) Grey scale values of protein expression were calculated using Image J software and then statistically analysed and plotted. ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001. The picture represents at least three repetitions of the experiment. AKT, protein kinase B; GM6001 and TAPI‐1, MMP9 inhibitors; MMP9, matrix metallopeptidase 9; p‐AKT, phospho‐protein kinase B; PI3K, phosphatidylinositol‐3‐kinase; sMICA/B, soluble major histocompatibility complex class I chain‐related proteins A and B.
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The effect of AFP on the expression of MMP9 and MICA/B shedding on the membrane of HCC cells. (A) Western blotting experiment was performed to detect the expression levels of MMP9; (B) Grey scale values of MMP9 expression were calculated using Image J software and then statistically analysed and plotted; (C) qRT‐PCR experiment was used to check MMP9 mRNA expression levels; (D) Western blotting was performed to detect the expression levels of sMICA/B in HLE, HLE‐NC, HLE‐AFP cells; (E) Western blotting was performed to detect the expression levels of sMICA/B in HuH‐7, HuH‐7‐NC, HuH‐7‐shAFP cells; (F) ELISA were performed to detect the content of sMICA/B in HCC cell supernatants; (G) <t>CCK‐8</t> experiments were performed to detect the IC50 of GM6001 and TAPI‐1; (H) Detection of MICA/B expression in HCC cells while treated with GM6001 and TAPI‐1 by flow cytometry; (I) Prism GraphPad(10.0) for statistical analysis and graphing of flow cytometry results; (J) Detection of sMICA/B in HCC cells supernatants while treated with GM6001 and TAPI‐1 by ELISA; (K) Western blotting experiment was performed to detect the expression levels of PI3K, AKT, p‐AKT and MMP9; (L) Grey scale values of protein expression were calculated using Image J software and then statistically analysed and plotted. ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001. The picture represents at least three repetitions of the experiment. AKT, protein kinase B; GM6001 and TAPI‐1, MMP9 inhibitors; MMP9, matrix metallopeptidase 9; p‐AKT, phospho‐protein kinase B; PI3K, phosphatidylinositol‐3‐kinase; sMICA/B, soluble major histocompatibility complex class I chain‐related proteins A and B.
V V Cck8 Reagent Cat No Ck04 Lot No Wu732 Dojindo Kumamoto Japan, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The overexpression of Sohlh2 inhibited the proliferation and the proportion of cells in the S phase, promoting apoptosis in HCC cells. (A-B) CCK8 for cell proliferation. Flow cytometry was applied for cell cycle analysis in HepG2(C, E) and Hep3B (D, F). Flow cytometry was used to detect apoptosis in HepG2 (G) and Hep3B cells (H). Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N = 3.

Journal: Translational Oncology

Article Title: Sohlh2 inhibited the angiogenesis of hepatocellular carcinoma through the HIF-1α/VEGFA pathway

doi: 10.1016/j.tranon.2026.102718

Figure Lengend Snippet: The overexpression of Sohlh2 inhibited the proliferation and the proportion of cells in the S phase, promoting apoptosis in HCC cells. (A-B) CCK8 for cell proliferation. Flow cytometry was applied for cell cycle analysis in HepG2(C, E) and Hep3B (D, F). Flow cytometry was used to detect apoptosis in HepG2 (G) and Hep3B cells (H). Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N = 3.

Article Snippet: After 48 h of culture, 10 μL of CCK8 reagent (CK04, Dojindo, JPN) was added to each well, followed by incubation at 37 °C for 2 h. Optical density (OD) at 450 nm was measured using a microplate reader (1681130, Bio-Rad, USA).

Techniques: Over Expression, Flow Cytometry, Cell Cycle Assay, Standard Deviation

Overexpression Sohlh2 inhibited cell proliferation and angiogenesis of HCC through the downregulation of the HIF-1α/VEGF pathway. (A-B) CCK8 assay of HepG2 and Hep3B cells. (C-D) Angiogenesis was evaluated using tube formation assay. Immunofluorescence experiments detected the expression of HIF-1α (E-F) and CD31 (G-H) in HepG2 and Hep3B cells. Western blot was used to determine the HIF-1α and VEGFA proteins in HepG2 (I) and Hep3B (J) cells. The protein bands were analyzed by Image J software. Magnification: 200 ×; Scale bar: 50 μm. Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N=3.

Journal: Translational Oncology

Article Title: Sohlh2 inhibited the angiogenesis of hepatocellular carcinoma through the HIF-1α/VEGFA pathway

doi: 10.1016/j.tranon.2026.102718

Figure Lengend Snippet: Overexpression Sohlh2 inhibited cell proliferation and angiogenesis of HCC through the downregulation of the HIF-1α/VEGF pathway. (A-B) CCK8 assay of HepG2 and Hep3B cells. (C-D) Angiogenesis was evaluated using tube formation assay. Immunofluorescence experiments detected the expression of HIF-1α (E-F) and CD31 (G-H) in HepG2 and Hep3B cells. Western blot was used to determine the HIF-1α and VEGFA proteins in HepG2 (I) and Hep3B (J) cells. The protein bands were analyzed by Image J software. Magnification: 200 ×; Scale bar: 50 μm. Data were presented as the mean ± standard deviation, and differences between groups were analyzed using one-way analysis of variance, N=3.

Article Snippet: After 48 h of culture, 10 μL of CCK8 reagent (CK04, Dojindo, JPN) was added to each well, followed by incubation at 37 °C for 2 h. Optical density (OD) at 450 nm was measured using a microplate reader (1681130, Bio-Rad, USA).

Techniques: Over Expression, CCK-8 Assay, Tube Formation Assay, Immunofluorescence, Expressing, Western Blot, Software, Standard Deviation

The effect of AFP on the expression of MMP9 and MICA/B shedding on the membrane of HCC cells. (A) Western blotting experiment was performed to detect the expression levels of MMP9; (B) Grey scale values of MMP9 expression were calculated using Image J software and then statistically analysed and plotted; (C) qRT‐PCR experiment was used to check MMP9 mRNA expression levels; (D) Western blotting was performed to detect the expression levels of sMICA/B in HLE, HLE‐NC, HLE‐AFP cells; (E) Western blotting was performed to detect the expression levels of sMICA/B in HuH‐7, HuH‐7‐NC, HuH‐7‐shAFP cells; (F) ELISA were performed to detect the content of sMICA/B in HCC cell supernatants; (G) CCK‐8 experiments were performed to detect the IC50 of GM6001 and TAPI‐1; (H) Detection of MICA/B expression in HCC cells while treated with GM6001 and TAPI‐1 by flow cytometry; (I) Prism GraphPad(10.0) for statistical analysis and graphing of flow cytometry results; (J) Detection of sMICA/B in HCC cells supernatants while treated with GM6001 and TAPI‐1 by ELISA; (K) Western blotting experiment was performed to detect the expression levels of PI3K, AKT, p‐AKT and MMP9; (L) Grey scale values of protein expression were calculated using Image J software and then statistically analysed and plotted. ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001. The picture represents at least three repetitions of the experiment. AKT, protein kinase B; GM6001 and TAPI‐1, MMP9 inhibitors; MMP9, matrix metallopeptidase 9; p‐AKT, phospho‐protein kinase B; PI3K, phosphatidylinositol‐3‐kinase; sMICA/B, soluble major histocompatibility complex class I chain‐related proteins A and B.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Alpha‐Fetoprotein Stimulates Cleavage of Membranal MICA /B on Liver Cancer Cell Lead to Escape Immune Surveillance of Natural Killer Cells

doi: 10.1111/jcmm.71076

Figure Lengend Snippet: The effect of AFP on the expression of MMP9 and MICA/B shedding on the membrane of HCC cells. (A) Western blotting experiment was performed to detect the expression levels of MMP9; (B) Grey scale values of MMP9 expression were calculated using Image J software and then statistically analysed and plotted; (C) qRT‐PCR experiment was used to check MMP9 mRNA expression levels; (D) Western blotting was performed to detect the expression levels of sMICA/B in HLE, HLE‐NC, HLE‐AFP cells; (E) Western blotting was performed to detect the expression levels of sMICA/B in HuH‐7, HuH‐7‐NC, HuH‐7‐shAFP cells; (F) ELISA were performed to detect the content of sMICA/B in HCC cell supernatants; (G) CCK‐8 experiments were performed to detect the IC50 of GM6001 and TAPI‐1; (H) Detection of MICA/B expression in HCC cells while treated with GM6001 and TAPI‐1 by flow cytometry; (I) Prism GraphPad(10.0) for statistical analysis and graphing of flow cytometry results; (J) Detection of sMICA/B in HCC cells supernatants while treated with GM6001 and TAPI‐1 by ELISA; (K) Western blotting experiment was performed to detect the expression levels of PI3K, AKT, p‐AKT and MMP9; (L) Grey scale values of protein expression were calculated using Image J software and then statistically analysed and plotted. ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001. The picture represents at least three repetitions of the experiment. AKT, protein kinase B; GM6001 and TAPI‐1, MMP9 inhibitors; MMP9, matrix metallopeptidase 9; p‐AKT, phospho‐protein kinase B; PI3K, phosphatidylinositol‐3‐kinase; sMICA/B, soluble major histocompatibility complex class I chain‐related proteins A and B.

Article Snippet: The cells were cultured in an incubator for 24 h, after which the medium was discarded, fresh serum‐free medium (100 μL per well) was added, and CCK8 detection reagent (Cat #CK04, DOJINDO, Japan) was added (10 μL per well).

Techniques: Expressing, Membrane, Western Blot, Software, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Flow Cytometry, Immunopeptidomics