hcc cell lines snu387 (Procell Inc)
90
Structured Review
Procell Inc
hcc cell lines snu387
Hcc Cell Lines Snu387, supplied by Procell Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hcc cell lines snu387/product/Procell Inc
Average 90 stars, based on 1 article reviews
Hcc Cell Lines Snu387, supplied by Procell Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hcc cell lines snu387/product/Procell Inc
Average 90 stars, based on 1 article reviews
hcc cell lines snu387 - by Bioz Stars,
2026-03
90/100 stars
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1) Product Images from "Cancer Cell‐Derived Exosomal miR‐500a‐3p Modulates Hepatic Stellate Cell Activation and the Immunosuppressive Microenvironment"
Article Title: Cancer Cell‐Derived Exosomal miR‐500a‐3p Modulates Hepatic Stellate Cell Activation and the Immunosuppressive Microenvironment
Journal: Advanced Science
doi: 10.1002/advs.202404089
Figure Legend Snippet: MiR‐500a‐3p facilitated HCC cell proliferation and migration characteristics. A) Determination of miR‐500a‐3p expression in hepatic stellate cells and hepatocellular carcinoma cells using RT‐qPCR (n = 3). B) A lentiviral vector for miR‐500a‐3p‐OV or miR‐500a‐3p‐KD was successfully constructed to transfect SNU387 and Huh‐7, respectively (n = 3). C) The CCK‐8 assay was used to determine the effect of miR‐500a‐3p on the proliferation of SNU387 and Huh‐7 cells (n = 3). D,E) Wound healing assay (D) and transwell assay (E) to detect the effects of miR‐500a‐3p on the migration ability of SNU387 and Huh‐7 cell lines (n = 3). F,G) Representative images (F) and tumor volume of xenograft tumor (G) treated with agomir, agomir‐NC, antagomir‐NC, and antagomir (n = 5 for each group). H) RT‐qPCR was used to determine the miR‐500a‐3p level in each group (n = 3). I) IHC staining determined Ki‐67 positivity in tumors from different groups (bar value = 50 µm). J) Transmission electron microscopy image of HCC‐derived exosomes (n = 3, bar value = 100 nm). K) miR‐500a‐3p expression in hepatic stellate and hepatocellular carcinoma cells and corresponding exosomes (n = 3). L) Exosome markers (CD81, CD9, and Calnexin) in HCC‐derived and HSC‐derived exosomes were detected using Western blot analysis (n = 3). M,N) Nanoparticle tracking analysis of exosomes confirms that more than 95% of the detected particles ranged from 30–150 nm in diameter (n = 3). Data were statistically analyzed using one‐way analysis of variance (A,H,K), unpaired two‐tailed Student's t‐tests (B), or two‐way repeated measures analysis of variance (C, G). Data are presented as the mean ± standard deviation, ns> 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Migration, Expressing, Quantitative RT-PCR, Plasmid Preparation, Construct, CCK-8 Assay, Wound Healing Assay, Transwell Assay, Immunohistochemistry, Transmission Assay, Electron Microscopy, Derivative Assay, Western Blot, Two Tailed Test, Standard Deviation
Figure Legend Snippet: Exosomal miR‐500a‐3p mediates reciprocal activation between HCC cells and HSCs. A) Diagram of LX‐2 cells co‐cultured with HCC cell lines or exosomes. B) Determination of miR‐500a‐3p expression in LX2 and after co‐culture with HCC cells, respectively, using RT‐qPCR (n = 3). C) HCC‐EXO (red) and LX2 cells (green cytoskeleton and blue nuclei) were co‐cultured, and co‐localization was observed using confocal microscopy (bar value = 10 µm). D) Determination of miR‐500a‐3p expression in LX2 cells after co‐culture with HCC exosomes using RT‐qPCR (n = 3). E,F) Effect of HCC exosomes with miR‐500a‐3p‐OV or miR‐500a‐3p‐KD on miR‐500a‐3p expression (E) and hepatic stellate cell activation (F) in LX2 using RT‐qPCR (n = 6). G) Multi‐immunofluorescence staining to determine the effect of SUN387 exosomes on hepatic stellate cell activation (bar value = 50 µm). H–J) Multi‐immunofluorescence staining (H) (bar value = 50 µm), Western blot (I), and RT‐qPCR (J) (n = 3) to detect the effect of miR‐500a‐3p‐OV or miR‐500a‐3p‐KD on LX2 cell activation. K) LX2‐EXO (red) and HCC cells (green cytoskeleton and blue nuclei) were co‐cultured, and co‐localization was observed by confocal microscopy (bar value = 10 µm). L) Wound healing assay to detect the effects of LX2 miR‐500a‐3p‐OV‐ or miR‐500a‐3p‐KD‐derived exosomes on the migration ability of SNU387 cells (n = 3). M) CCK8 assay to detect the effects of LX2 miR‐500a‐3p‐OV‐ or miR‐500a‐3p‐KD‐derived exosomes on the proliferation ability of SNU387 cells (n = 3). Data were statistically analyzed using one‐way analysis of variance or two‐way repeated measures analysis of variance (M). Data are presented as the mean ± standard deviation, ns > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Activation Assay, Cell Culture, Expressing, Co-Culture Assay, Quantitative RT-PCR, Confocal Microscopy, Immunofluorescence, Staining, Western Blot, Wound Healing Assay, Derivative Assay, Migration, CCK-8 Assay, Standard Deviation
Figure Legend Snippet: MiR‐500a‐3p activates HSCs via the SOCS2/JAK3/STAT5A/STAT5B axis. A) RNA‐seq analysis was performed on the three groups of LX2 miR‐500a‐3p‐OV and the NC group, and GO analysis was performed on the differential genes obtained (n = 3). B) Target mRNA with potential binding sites for miR‐500a‐3p as predicted by micro T, miRwalk, Targetscan, and miRDB. C) Putative binding sites of miR‐500a‐3p in SOCS2. D) SOCS2 expression in tumor and normal tissues in the TCGA LIHC cohort. E) Relationship between SOCS2 and overall survival of patients with HCC in the TCGA cohort. F) The scatter diagram indicated that miR‐500a‐3p expression positively correlated with SOCS2 in the TCGA LIHC cohort. G) Luciferase activity of the SOCS2 dual‐luciferase reporter vector (WT or MUT) in HEK293T cells co‐transfected with miR‐500a‐3p (n = 3). H,I) RT‐qPCR and Western blot analyses of the relative levels of SOCS2 expression in LX2 cells after transfection with miR‐500a‐3p mimics (n = 3). J) After a RIP assay had been performed with a SOCS2 plasmid, RT–qPCR indicated significant miR‐500a‐3p enrichment compared to negative controls (n = 3). K,L) Relative levels of SOCS2/JAK3/STAT5A/STAT5B mRNA in LX2 cells after co‐culture with Huh‐7 miR‐500a‐3p‐KD or SNU387 miR‐500a‐3p‐OV‐derived exosomes (n = 6). M–O) RT‐qPCR (M,N) and Western blot (O) analyses of the relative levels of SOCS2/JAK3/STAT5A/STAT5B expression in LX2 cells after transfection with miR‐500a‐3p‐KD or miR‐500a‐3p‐OV (n = 6). Data were statistically analyzed using unpaired two‐tailed Student's t‐tests (J) or one‐way analysis of variance. Data are presented as the mean ± standard deviation, ns > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: RNA Sequencing, Binding Assay, Expressing, Luciferase, Activity Assay, Plasmid Preparation, Transfection, Quantitative RT-PCR, Western Blot, Co-Culture Assay, Derivative Assay, Two Tailed Test, Standard Deviation
Figure Legend Snippet: MiR‐500a‐3p regulates PD‐L1 expression in HSCs and PD‐1 expression in PBMCs. A) RT‐qPCR to determine PD‐L1 expression in LX2 cells or after co‐culture with HCC cells (n = 3). B,C) RT‐qPCR (B) and Western blot (C) analyses of the relative levels of PD‐L1 expression in LX2 cells after transfection with miR‐500a‐3p‐KD or miR‐500a‐3p‐OV (n = 3). D–F) The content of TGF‐β1, IL‐10, and PD‐L1 in the supernatant of hepatic stellate cells transfected with the miR‐500a‐3p‐KD or miR‐500a‐3p‐OV was detected by ELISA (n = 3). G) Diagram of PBMC cells cocultured with HCC cell lines or exosomes. H) HCC‐EXO (red) and PBMC (green cytoskeleton and blue nuclei) were co‐cultured, and co‐localization was observed by confocal microscopy (bar value = 10 µm). I,J) Flow cytometry was used to detect the proportion of CD127 low CD25 high T cells in PBMC after co‐culturing with HCC cells with miR‐500a‐3p‐KD or miR‐500a‐3p‐OV (n = 3). K) RT‐qPCR to determine the expression of miR‐500a‐3p in PBMC or after co‐culturing with HCC cells. L,M) RT‐qPCR to determine the expression of miR‐500a‐3p (L) and PD‐1 (M) in PBMC or after co‐culturing with HCC‐derived exosomes (n = 3). N,O) RT‐qPCR to determine the expression of miR‐500a‐3p (N) and PD‐1 (O) in PBMC after co‐culturing with HCC cells with miR‐500a‐3p‐KD or miR‐500a‐3p‐OV (n = 3). Data were statistically analyzed using a one‐way analysis of variance. Data are presented as the mean ± standard deviation, ns >0.05, * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Expressing, Quantitative RT-PCR, Co-Culture Assay, Western Blot, Transfection, Enzyme-linked Immunosorbent Assay, Cell Culture, Confocal Microscopy, Flow Cytometry, Derivative Assay, Standard Deviation
Figure Legend Snippet: MiR‐500a‐3p promotes HCC growth and HSC activation via the SOCS2/STAT5/PD‐L1 axis in mouse models. A) Diagram of the procedure to establish PB‐YAP‐HDI orthotopic HCC models and the agomir miR‐500a‐3p, agomir‐NC, antagomir‐NC, and antagomir miR‐500a‐3p treatments. B) Growth curves for mouse weight were measured twice a week after every injection of PB‐YAP in ICR mice. C) IVIS imaging to detect the growth of in situ liver tumors at 24 and 48 days in the four groups (n = 6 for each group). D) Representative images of orthotopic liver tumor treated with agomir, agomir‐NC, antagomir‐NC, and antagomir (n = 6 for each group). E) The morphology of primary HSCs extracted from ICR mice was visualized by white light and immunofluorescence microscopy (bar value = 100 µm). F) RT‐qPCR to determine the levels of miR‐500a‐3p, HSC activation indicators (α‐SMA, FAP, and vimentin), and PD‐L1 in the four groups (n = 3). G–I) Tumor area (G), tumor foci (H), and HE staining images (bar value = 2.5 mm) (I) in the four groups. The data for the tumor area are shared with Figure . J) RT‐qPCR to determine the levels of miR‐500a‐3p and STAT5A/STAT5B expression in the four groups (n = 3). K) Western blotting to determine the levels of SOCS2/STAT5A/STAT5B expression, HSC activation indicators (α‐SMA and FAP), and PD‐L1 in the four groups (n = 3). L) Representative images of IHC staining of mouse tumors revealed the effects of miR‐500a‐3p from HSCs on the SOCS2/ STAT5A/STAT5B axis, the activation of α‐SMA and FAP, the proliferation index Ki‐67, and PD‐L1 markers (bar value = 50 µm). Data were statistically analyzed using one‐way analysis of variance or two‐way repeated measures analysis of variance (B). Data are presented as the mean ± standard deviation, * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Activation Assay, Injection, Imaging, In Situ, Immunofluorescence, Microscopy, Quantitative RT-PCR, Staining, Expressing, Western Blot, Immunohistochemistry, Standard Deviation
![A Basal expression levels of miR-423-5p and MALAT-1 across seven HCC cell lines (SNU449, HepG2, SNU475, Hep3B, SKHep1, <t>SNU387,</t> and SNU389) assessed by qRT-PCR. Expression values were normalized to endogenous controls and used to guide selection of models for functional assays. B Generation of stable miR-423-5p-overexpressing clones in HepG2, Hep3B, and SNU387 cells using lentiviral vectors expressing GFP. Puromycin selection was applied to enrich successfully transduced cells. qRT-PCR confirmed persistent miR-423-5p upregulation. C Stable overexpression of miR-423-5p led to a consistent downregulation of MALAT-1 levels compared to vector-only controls in all three cell models. D – E Establishment of stable MALAT-1-overexpressing clones in SNU387 and Hep3B cells via lentiviral transduction. Overexpression was confirmed by qRT-PCR. In the selected clones (SNU387 clone 1 and Hep3B clone 2), MALAT-1 upregulation was associated with reduced miR-423-5p levels, confirming a reciprocal regulatory relationship. * \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p < 0.05$$\end{document} p < 0.05 , ** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.01$$\end{document} < 0.01 , *** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.001$$\end{document} < 0.001 , **** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.0001$$\end{document} < 0.0001](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_7375/pmc12487375/pmc12487375__13046_2025_3524_Fig2_HTML.jpg)
![miR-423-5p overexpression reduces proliferation in HCC cell lines ( A - C ), while MALAT-1 overexpression alone does not affect growth ( D - E ). Live-cell monitoring of cell confluence using the IncuCyte system in Hep3B and SNU387 models seeded at two different densities ( F – H ). miR-423-5p-overexpressing cells exhibited markedly reduced confluence compared to control cells over time. * \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p < 0.05$$\end{document} p < 0.05 , ** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.01$$\end{document} < 0.01 , *** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.001$$\end{document} < 0.001 , **** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.0001$$\end{document} < 0.0001](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_7375/pmc12487375/pmc12487375__13046_2025_3524_Fig3_HTML.jpg)
![A Wound healing assay performed in HepG2, Hep3B, and SNU387 cell lines stably overexpressing miR-423-5p vs empty vector (Left side). Wound healing assay performed in Hep3B, and SNU387 cell lines stably overexpressing MALAT-1 vs empty vector (Right side). B Transwell migration and invasion assay using Cultrex BME-coated inserts. miR-423-5p overexpression significantly decreased the number of migrating and invading cells after 48 hours compared to control cells (Left Side). MALAT-1 overexpression is remarkably boosting migrating and invasive capability of HEP3B and SNU387 (Right side). C Colony formation assay under low-density and semi-starved conditions for 14 days revealed impaired clonogenicity in all miR-423-5p-overexpressing HCC cell models compared to respective controls. * \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p < 0.05$$\end{document} p < 0.05 , ** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.01$$\end{document} < 0.01 , *** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.001$$\end{document} < 0.001 , **** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.0001$$\end{document} < 0.0001](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_7375/pmc12487375/pmc12487375__13046_2025_3524_Fig4_HTML.jpg)
![A Representative fluorescence microscopy images of mitochondria in SNU387 clones expressing either miR-423-5p or MALAT-1, transfected with MTS-mCherry-GFP1-10 plasmid. miR-423-5p-overexpressing cells showed fewer and smaller mitochondria with a rounded morphology, whereas MALAT-1-overexpressing cells displayed increased mitochondrial number and size. B qRT-PCR analysis of mitochondrial-related gene expression in SNU387 clones. Genes encoded by both mitochondrial and nuclear DNA involved in mitochondrial respiration and activity were significantly downregulated in miR-423-5p-overexpressing cells and upregulated in MALAT-1-overexpressing clones. C Seahorse Mito Stress Test performed in miR-423-5p-overexpressing SNU387 and Hep3B cells revealed reduced mitochondrial function, including decreased basal respiration, maximal respiration, ATP production, proton leak, and spare respiratory capacity, compared to control cells. * \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p < 0.05$$\end{document} p < 0.05 , ** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.01$$\end{document} < 0.01 , *** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.001$$\end{document} < 0.001 , **** p -value \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$< 0.0001$$\end{document} < 0.0001 .](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_7375/pmc12487375/pmc12487375__13046_2025_3524_Fig6_HTML.jpg)
