human cancer cell lines huh7  (Korean Cell Line Bank)

Journal: bioRxiv

Article Title: B7-H3 Modulates Cell Adhesion and Immune Evasion to Promote Tumor Progression and Natural Killer Cell Resistance in Hepatocellular Carcinoma

doi: 10.64898/2026.03.28.714951

Figure Lengend Snippet: (A) Apoptosis was analyzed by Annexin V and propidium iodide (PI) staining in B7-H3–knockdown Huh7 cells. (B) Quantification of apoptotic Huh7 cells shown in (A). (C) Expression of apoptosis-related proteins in control and B7-H3–knockdown Huh7 cells was analyzed by Western blotting and quantified using ImageJ software. (D) Apoptosis analysis by Annexin V/PI staining in B7-H3–knockdown HepG2 cells. (E) Quantification of apoptotic HepG2 cells shown in (D).

Article Snippet: Human cancer cell lines Huh7 and SNU449 were purchased from the Korean Cell Line Bank (KCLB, Seoul, Korea) and cultured in RPMI-1640 (Biowest, Kansas, MO, USA) medium supplemented with 10% fetal bovine serum (FBS, Corning, Seoul, Korea) and antibiotic-antimycotic solution (AA, Biowest).

Techniques: Staining, Knockdown, Expressing, Control, Western Blot, Software

Journal: bioRxiv

Article Title: B7-H3 Modulates Cell Adhesion and Immune Evasion to Promote Tumor Progression and Natural Killer Cell Resistance in Hepatocellular Carcinoma

doi: 10.64898/2026.03.28.714951

Figure Lengend Snippet: (A, C) Cell adhesion assays of B7-H3–knockdown Huh7 (A) and HepG2 (C) cells on gelatin-coated plates. Adherent cells were visualized by crystal violet staining. (B, D) Quantification of cell adhesion shown in (A) and (C), respectively. Data are presented as relative adhesion (%) compared with control siRNA (siCon)–transfected cells. (E, G) Flow cytometric analysis of cell adhesion molecule expression in B7-H3–knockdown Huh7 (E) and HepG2 (G) cells. (F, H) Quantification of mean fluorescence intensity (MFI) shown in (E) and (G), respectively, expressed as relative MFI (%) compared with siCon cells. *, p < 0.05; **, p < 0.01; ***, p < 0.005.

Article Snippet: Human cancer cell lines Huh7 and SNU449 were purchased from the Korean Cell Line Bank (KCLB, Seoul, Korea) and cultured in RPMI-1640 (Biowest, Kansas, MO, USA) medium supplemented with 10% fetal bovine serum (FBS, Corning, Seoul, Korea) and antibiotic-antimycotic solution (AA, Biowest).

Techniques: Knockdown, Staining, Control, Transfection, Expressing, Fluorescence

Journal: bioRxiv

Article Title: B7-H3 Modulates Cell Adhesion and Immune Evasion to Promote Tumor Progression and Natural Killer Cell Resistance in Hepatocellular Carcinoma

doi: 10.64898/2026.03.28.714951

Figure Lengend Snippet: (A, C) Flow cytometric analysis of PD-L1, PD-L2, CD47, and CD24 expression in B7-H3–knockdown Huh7 (A) and HepG2 (C) cells. (B, D) Quantification of immune checkpoint molecule expression shown in (A) and (C), respectively.

Article Snippet: Human cancer cell lines Huh7 and SNU449 were purchased from the Korean Cell Line Bank (KCLB, Seoul, Korea) and cultured in RPMI-1640 (Biowest, Kansas, MO, USA) medium supplemented with 10% fetal bovine serum (FBS, Corning, Seoul, Korea) and antibiotic-antimycotic solution (AA, Biowest).

Techniques: Expressing, Knockdown

Journal: bioRxiv

Article Title: B7-H3 Modulates Cell Adhesion and Immune Evasion to Promote Tumor Progression and Natural Killer Cell Resistance in Hepatocellular Carcinoma

doi: 10.64898/2026.03.28.714951

Figure Lengend Snippet: (A, B) Western blot analysis of Akt1/2/3, ERK1/2, FAK, MVP, and S6 in B7-H3–knockdown Huh7 and HepG2 cells. Protein levels were quantified using ImageJ software with β-actin as a loading control. (C) Western blot analysis of Akt1/2/3, ERK1/2, and MVP in control and B7-H3 KO SNU449 cells. (D) Western blot analysis of FAK and Src in control and B7-H3 KO SNU449 cells. (E) Western blot analysis of JAK2 and STAT3 in control and B7-H3 KO SNU449 cells. For (C–E), GAPDH was used as a loading control.

Article Snippet: Human cancer cell lines Huh7 and SNU449 were purchased from the Korean Cell Line Bank (KCLB, Seoul, Korea) and cultured in RPMI-1640 (Biowest, Kansas, MO, USA) medium supplemented with 10% fetal bovine serum (FBS, Corning, Seoul, Korea) and antibiotic-antimycotic solution (AA, Biowest).

Techniques: Western Blot, Knockdown, Software, Control

Journal: Analytical Cellular Pathology (Amsterdam)

Article Title: SLC1A4 Promotes Malignant Transformation of Hepatocellular Carcinoma by Activating the AKT Signaling

doi: 10.1155/ancp/1115184

Figure Lengend Snippet: Regulatory mechanism of SLC1A4 on AKT signaling. (a and b) qRT-PCR for mRNA levels of SLC1A4, c-Myc, and EpCAM in Huh7 and HepG2 cells. Cells were stably infected with lentivirus for silencing SLC1A4 expression. (c) Western blot for the levels of β -catenin, p-AKT, AKT, EpCAM, c-Myc, and SLC1A4 in Huh7 and HepG2 cells. Cells were stably infected with lentivirus for silencing SLC1A4 expression. (d) Western blot for EpCAM, c-Myc, and Flag levels in Huh7 cells. The stably infected Huh7 cells with lentivirus for silencing SLC1A4 expression were further transfected with Flag-AKT plasmid or control Flag-vector for 48 h. (e) Immunofluorescence staining for protein level of β -catenin in nuclei of Huh7 cells with SLC1A4 knockdown. Scale bar, 10 μm. (f and g) Co-IP for K63-dependent ubiquitin level of AKT protein in Huh7 (f) and HepG2 (g) cells with the knockdown of SLC1A4. The stably infected Huh7 cells with lentivirus for silencing SLC1A4 expression were further transfected with pHA-Ub (K63O) for 48 h, and cell lysates were immunoprecipitated with an anti-AKT antibody and examined for HA levels. Data were analyzed by Student's two-sided t -test and are presented as mean ± SD with three biological replicates. ⁣ ∗ p < 0.05, ⁣ ∗∗ p < 0.01, and ⁣ ∗∗∗ p < 0.001.

Article Snippet: The human hepatic cancer cell line Huh7 (RRID: CVCL_0336) was obtained from JCRB Cell Bank (Tokyo, Japan), the human hepatic cancer cell line HepG2 (RRID: CVCL_0027) was obtained from ATCC (Manassas, VA, USA), and the human embryonic kidney fibroblast line HEK293T (RRID: CVCL_0063) was also obtained from ATCC.

Techniques: Quantitative RT-PCR, Stable Transfection, Infection, Expressing, Western Blot, Transfection, Plasmid Preparation, Control, Immunofluorescence, Staining, Knockdown, Co-Immunoprecipitation Assay, Ubiquitin Proteomics, Immunoprecipitation

Journal: Analytical Cellular Pathology (Amsterdam)

Article Title: SLC1A4 Promotes Malignant Transformation of Hepatocellular Carcinoma by Activating the AKT Signaling

doi: 10.1155/ancp/1115184

Figure Lengend Snippet: The regulatory effect of SLC1A4 and AKT on transcriptional activity of c-Myc and EpCAM promoters. (a and b) Fold change of luciferase expression of pGL-c-Myc (a) and pGL-EpCAM (b) plasmids in Huh7 cells with the knockdown of SLC1A4. (c and d) Fold change of luciferase expression of pGL-c-Myc (c) and pGL-EpCAM (d) plasmids in Huh7 cells. The stably infected Huh7 cells with lentivirus for silencing SLC1A4 expression were further transfected with Flag-AKT plasmid for 36 h. Data were analyzed by Student's two-sided t -test or one-way ANOVA and are presented as mean ± SD with three biological replicates. ⁣ ∗ p < 0.05, ⁣ ∗∗ p < 0.01, and ⁣ ∗∗∗ p < 0.001.

Article Snippet: The human hepatic cancer cell line Huh7 (RRID: CVCL_0336) was obtained from JCRB Cell Bank (Tokyo, Japan), the human hepatic cancer cell line HepG2 (RRID: CVCL_0027) was obtained from ATCC (Manassas, VA, USA), and the human embryonic kidney fibroblast line HEK293T (RRID: CVCL_0063) was also obtained from ATCC.

Techniques: Activity Assay, Luciferase, Expressing, Knockdown, Stable Transfection, Infection, Transfection, Plasmid Preparation

Journal: Analytical Cellular Pathology (Amsterdam)

Article Title: SLC1A4 Promotes Malignant Transformation of Hepatocellular Carcinoma by Activating the AKT Signaling

doi: 10.1155/ancp/1115184

Figure Lengend Snippet: Influence of SLC1A4 on D-serine uptake and mTOR activation in hepatic cancer cells. (a) Uptake of D-serine into Huh7 cells with different levels of SLC1A4 was measured over a period of 60 min. D-serine at a final concentration of 50 μM and L-glutamine at a final concentration of 100 μM were used to incubate with Huh7 cells. (b) Western blot for p-AKT, p-mTOR, mTOR, and SLC1A4 levels in Huh7 cell lysates. The stably infected cells with lentivirus were cultivated in a medium with or without 50 μM D-serine for 24 h. Data were analyzed by Student's two-sided t -test are presented as mean ± SD with five biological replicates. ⁣ ∗∗∗ p < 0.001.

Article Snippet: The human hepatic cancer cell line Huh7 (RRID: CVCL_0336) was obtained from JCRB Cell Bank (Tokyo, Japan), the human hepatic cancer cell line HepG2 (RRID: CVCL_0027) was obtained from ATCC (Manassas, VA, USA), and the human embryonic kidney fibroblast line HEK293T (RRID: CVCL_0063) was also obtained from ATCC.

Techniques: Activation Assay, Concentration Assay, Western Blot, Stable Transfection, Infection

Journal: Analytical Cellular Pathology (Amsterdam)

Article Title: SLC1A4 Promotes Malignant Transformation of Hepatocellular Carcinoma by Activating the AKT Signaling

doi: 10.1155/ancp/1115184

Figure Lengend Snippet: Regulatory effect of SLC1A4 on phenotypes of hepatic cancer cells. (a and b) Proliferation of Huh7 (a) and HepG2 (b) cells with the knockdown of SLC1A4. (c and d) Images (c) and statistical analysis (d) of migrated Huh7 cells with the knockdown of SLC1A4. Scale bar, 100 μm. (e and f) Images (e) and statistical analysis (f) of cancer stem spheres formed by Huh7 cells with the knockdown of SLC1A4. Scale bar, 1 mm. Data were analyzed by one-way ANOVA and are presented as mean ± SD with three biological replicates. ⁣ ∗ p < 0.05, ⁣ ∗∗ p < 0.01, and ⁣ ∗∗∗ p < 0.001.

Article Snippet: The human hepatic cancer cell line Huh7 (RRID: CVCL_0336) was obtained from JCRB Cell Bank (Tokyo, Japan), the human hepatic cancer cell line HepG2 (RRID: CVCL_0027) was obtained from ATCC (Manassas, VA, USA), and the human embryonic kidney fibroblast line HEK293T (RRID: CVCL_0063) was also obtained from ATCC.

Techniques: Knockdown

Journal: Analytical Cellular Pathology (Amsterdam)

Article Title: SLC1A4 Promotes Malignant Transformation of Hepatocellular Carcinoma by Activating the AKT Signaling

doi: 10.1155/ancp/1115184

Figure Lengend Snippet: Influence of SLC1A4 on cytoskeletal remodeling and cancer metastasis. (a) Immunofluorescence staining for F-actin using phalloidin in Huh7 cells with SLC1A4 knockdown. Nuclei were stained with DAPI. Scale bar, 10 μm. (b) Statistical analysis of GFP fluorescence in NCG mice on 30 days post tail vein injection of Huh7 cells. Huh7 cells were stably infected with lentivirus for silencing SLC1A4 expression. (c and d) Image (c) and statistical analysis (d) of formed lung metastatic nodules in NCG mice on 30 days post tail vein injection of Huh7 cells. The red arrows in (c) present the lung metastatic nodules. Huh7 cells were stably infected with lentivirus for silencing SLC1A4 expression. Data were analyzed by Student's two-sided t -test and are presented as mean ± SD with three biological replicates. ⁣ ∗ p < 0.05 and ⁣ ∗∗ p < 0.01.

Article Snippet: The human hepatic cancer cell line Huh7 (RRID: CVCL_0336) was obtained from JCRB Cell Bank (Tokyo, Japan), the human hepatic cancer cell line HepG2 (RRID: CVCL_0027) was obtained from ATCC (Manassas, VA, USA), and the human embryonic kidney fibroblast line HEK293T (RRID: CVCL_0063) was also obtained from ATCC.

Techniques: Immunofluorescence, Staining, Knockdown, Fluorescence, Injection, Stable Transfection, Infection, Expressing