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culture medium  (Celprogen Inc)


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    Celprogen Inc culture medium
    Culture Medium, supplied by Celprogen Inc, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/culture medium/product/Celprogen Inc
    Average 93 stars, based on 4 article reviews
    culture medium - by Bioz Stars, 2026-02
    93/100 stars

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    PB2 inhibited viability and promoted apoptosis of OSCC cells. (a) The chemical structure of PB2. (b) The viability of oral mucosa <t>epithelial</t> cell (OMEC) treated with PB2 was detected by CCK-8 assay. (c) The viability of human OSCC cell line (SCC-25) treated with PB2 was detected by CCK-8 assay. (d) The apoptosis of SCC-25 cells treated with PB2 was analyzed by Tunel assay. (e) The expression of apoptosis related proteins in SCC-25 cells treated with PB2 was determined by Western blot. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. PB2 (0 μM) group.
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    miR-214 and ULK1 detection by PCR. (a) Detection of miR-214 in normal oral <t>epithelial</t> cells and CAL-27. (b) Changes of miR-214 level after chemotherapy. (c) Detection of ULK1 in normal oral epithelial cells and CAL-27. (d) Changes of ULK1 level after chemotherapy. ∗∗ P < 0.01.
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    Celprogen Inc human oral epithelial cell medium
    Initial <t>cell</t> attachment of <t>human</t> <t>oral</t> <t>epithelial</t> cells cultured on untreated control and UV-treated titanium surfaces. ( a ) Cells cultured on the untreated control and UV-treated titanium surfaces were stained for actin with rhodamine-phalloidin (red) and observed by using fluorescence microscope after 3 and 24 h of culture. Scale bar = 200 µm. ( b ) Cell number was quantified with a colorimetric-based WST-1 assay (* P < 0.05). ( c ) Cell coverage area as a percentage on the untreated control and UV-treated titanium surfaces (* P < 0.05).
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    Image Search Results


    WNT7B promotes the migration and invasion of OSCC cells. ( A - D ) Wound-healing assay, the migration and invasion assay analyses of changes in migratory capacity as WNT7B is overexpressed in HN6/HN30 cells. Bars, 500 μm. ( E - H ) Western blot analysis that detected epithelial to mesenchymal transition marker E-cadherin protein levels decreased and the N-cadherin protein increased in HN6 and HN30 cells after WNT7B overexpressed. GAPDH served as a normalization control for WB. n = 3 independent experiments; error bars, mean ± SD; ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001; t-test

    Journal: BMC Oral Health

    Article Title: WNT7B promotes cancer progression via WNT/β-catenin signaling pathway and predicts a poor prognosis in oral squamous cell carcinoma

    doi: 10.1186/s12903-024-05113-9

    Figure Lengend Snippet: WNT7B promotes the migration and invasion of OSCC cells. ( A - D ) Wound-healing assay, the migration and invasion assay analyses of changes in migratory capacity as WNT7B is overexpressed in HN6/HN30 cells. Bars, 500 μm. ( E - H ) Western blot analysis that detected epithelial to mesenchymal transition marker E-cadherin protein levels decreased and the N-cadherin protein increased in HN6 and HN30 cells after WNT7B overexpressed. GAPDH served as a normalization control for WB. n = 3 independent experiments; error bars, mean ± SD; ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001; t-test

    Article Snippet: Human oral epithelial cells, H203, were purchased from Procell Life Science & Technology Co., Ltd. (Procell, Wuhan, #CP-H203) and maintained in a complete culture medium for human oral epithelial cells (Procell, Wuhan, #CM-H203).

    Techniques: Migration, Wound Healing Assay, Invasion Assay, Western Blot, Marker, Control

    WNT7B inhibited epithelial to mesenchymal transition in OSCC cells. ( A - D ) Wound-healing assay, the migration and invasion assay analyses of changes in migratory capacity as WNT7B was knockdown in HN6/HN30 cells. Bars, 500 μm. ( E - H ) Western blot analysis detecting epithelial to mesenchymal transition marker E-cadherin protein levels increased and N-cadherin protein levels decreased in HN6/HN30 cells after WNT7B knockdown. GAPDH served as a normalization control for WB. Error bars, mean ± SD; n = 3 independent experiments; error bars, mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001; t-test

    Journal: BMC Oral Health

    Article Title: WNT7B promotes cancer progression via WNT/β-catenin signaling pathway and predicts a poor prognosis in oral squamous cell carcinoma

    doi: 10.1186/s12903-024-05113-9

    Figure Lengend Snippet: WNT7B inhibited epithelial to mesenchymal transition in OSCC cells. ( A - D ) Wound-healing assay, the migration and invasion assay analyses of changes in migratory capacity as WNT7B was knockdown in HN6/HN30 cells. Bars, 500 μm. ( E - H ) Western blot analysis detecting epithelial to mesenchymal transition marker E-cadherin protein levels increased and N-cadherin protein levels decreased in HN6/HN30 cells after WNT7B knockdown. GAPDH served as a normalization control for WB. Error bars, mean ± SD; n = 3 independent experiments; error bars, mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001; t-test

    Article Snippet: Human oral epithelial cells, H203, were purchased from Procell Life Science & Technology Co., Ltd. (Procell, Wuhan, #CP-H203) and maintained in a complete culture medium for human oral epithelial cells (Procell, Wuhan, #CM-H203).

    Techniques: Wound Healing Assay, Migration, Invasion Assay, Knockdown, Western Blot, Marker, Control

    PB2 inhibited viability and promoted apoptosis of OSCC cells. (a) The chemical structure of PB2. (b) The viability of oral mucosa epithelial cell (OMEC) treated with PB2 was detected by CCK-8 assay. (c) The viability of human OSCC cell line (SCC-25) treated with PB2 was detected by CCK-8 assay. (d) The apoptosis of SCC-25 cells treated with PB2 was analyzed by Tunel assay. (e) The expression of apoptosis related proteins in SCC-25 cells treated with PB2 was determined by Western blot. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. PB2 (0 μM) group.

    Journal: Bioengineered

    Article Title: Procyanidin B2 inhibits angiogenesis and cell growth in oral squamous cell carcinoma cells through the vascular endothelial growth factor (VEGF)/VEGF receptor 2 (VEGFR2) pathway

    doi: 10.1080/21655979.2022.2033013

    Figure Lengend Snippet: PB2 inhibited viability and promoted apoptosis of OSCC cells. (a) The chemical structure of PB2. (b) The viability of oral mucosa epithelial cell (OMEC) treated with PB2 was detected by CCK-8 assay. (c) The viability of human OSCC cell line (SCC-25) treated with PB2 was detected by CCK-8 assay. (d) The apoptosis of SCC-25 cells treated with PB2 was analyzed by Tunel assay. (e) The expression of apoptosis related proteins in SCC-25 cells treated with PB2 was determined by Western blot. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. PB2 (0 μM) group.

    Article Snippet: OMEC was cultured in the completed culture medium for human oral epithelial cells (Procell).

    Techniques: CCK-8 Assay, TUNEL Assay, Expressing, Western Blot

    PB2 inhibited invasion, migration and epithelial-mesenchymal transition (EMT) of OSCC cells. The migration (a) and invasion (b) of SCC-25 cells treated with PB2 were detected by wound healing assay and transwell assay. The expression of metastasis associated proteins (c) and EMT related proteins (d) was analyzed by Western blot. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. PB2 (0 μM) group.

    Journal: Bioengineered

    Article Title: Procyanidin B2 inhibits angiogenesis and cell growth in oral squamous cell carcinoma cells through the vascular endothelial growth factor (VEGF)/VEGF receptor 2 (VEGFR2) pathway

    doi: 10.1080/21655979.2022.2033013

    Figure Lengend Snippet: PB2 inhibited invasion, migration and epithelial-mesenchymal transition (EMT) of OSCC cells. The migration (a) and invasion (b) of SCC-25 cells treated with PB2 were detected by wound healing assay and transwell assay. The expression of metastasis associated proteins (c) and EMT related proteins (d) was analyzed by Western blot. *P < 0.05, **P < 0.01 and ***P < 0.001 vs. PB2 (0 μM) group.

    Article Snippet: OMEC was cultured in the completed culture medium for human oral epithelial cells (Procell).

    Techniques: Migration, Wound Healing Assay, Transwell Assay, Expressing, Western Blot

    miR-214 and ULK1 detection by PCR. (a) Detection of miR-214 in normal oral epithelial cells and CAL-27. (b) Changes of miR-214 level after chemotherapy. (c) Detection of ULK1 in normal oral epithelial cells and CAL-27. (d) Changes of ULK1 level after chemotherapy. ∗∗ P < 0.01.

    Journal: Journal of Immunology Research

    Article Title: miR-214 Modulates the Growth and Migration of Oral Cancer before and after Chemotherapy through Mediating ULK1

    doi: 10.1155/2022/4589182

    Figure Lengend Snippet: miR-214 and ULK1 detection by PCR. (a) Detection of miR-214 in normal oral epithelial cells and CAL-27. (b) Changes of miR-214 level after chemotherapy. (c) Detection of ULK1 in normal oral epithelial cells and CAL-27. (d) Changes of ULK1 level after chemotherapy. ∗∗ P < 0.01.

    Article Snippet: In a 37°C cell incubator (51032124, Thermo Fisher Scientific, USA) with 5% CO 2 , CAL-27 was cultured in CAL-27 cell-specific medium (CM-0265, Procell) and human oral epithelial cells in human oral epithelial cell complete medium (CM-h203, Procell), both for 24 h. The cultured CAL-27 cells were assigned to control group and chemotherapy group, among which, cisplatin (10 μ g/mL, 100 μ L) [ ] and paclitaxel (8 μ g/mL, 100 μ L) [ ] were added to the culture medium of chemotherapy group.

    Techniques:

    Initial cell attachment of human oral epithelial cells cultured on untreated control and UV-treated titanium surfaces. ( a ) Cells cultured on the untreated control and UV-treated titanium surfaces were stained for actin with rhodamine-phalloidin (red) and observed by using fluorescence microscope after 3 and 24 h of culture. Scale bar = 200 µm. ( b ) Cell number was quantified with a colorimetric-based WST-1 assay (* P < 0.05). ( c ) Cell coverage area as a percentage on the untreated control and UV-treated titanium surfaces (* P < 0.05).

    Journal: Materials

    Article Title: Ultraviolet Light Treatment of Titanium Enhances Attachment, Adhesion, and Retention of Human Oral Epithelial Cells via Decarbonization

    doi: 10.3390/ma14010151

    Figure Lengend Snippet: Initial cell attachment of human oral epithelial cells cultured on untreated control and UV-treated titanium surfaces. ( a ) Cells cultured on the untreated control and UV-treated titanium surfaces were stained for actin with rhodamine-phalloidin (red) and observed by using fluorescence microscope after 3 and 24 h of culture. Scale bar = 200 µm. ( b ) Cell number was quantified with a colorimetric-based WST-1 assay (* P < 0.05). ( c ) Cell coverage area as a percentage on the untreated control and UV-treated titanium surfaces (* P < 0.05).

    Article Snippet: Cells were cultured in culture dishes (Falcon, Glendale, AZ, USA) with commercial human oral epithelial cell medium containing serum (Celprogen Inc.).

    Techniques: Cell Attachment Assay, Cell Culture, Staining, Fluorescence, Microscopy, WST-1 Assay

    Initial cell attachment of human oral epithelial cells cultured on untreated control, human laminin-5 coated, and UV-treated titanium surfaces. Cell number was quantified with a colorimetric-based WST-1 assay (* P < 0.05).

    Journal: Materials

    Article Title: Ultraviolet Light Treatment of Titanium Enhances Attachment, Adhesion, and Retention of Human Oral Epithelial Cells via Decarbonization

    doi: 10.3390/ma14010151

    Figure Lengend Snippet: Initial cell attachment of human oral epithelial cells cultured on untreated control, human laminin-5 coated, and UV-treated titanium surfaces. Cell number was quantified with a colorimetric-based WST-1 assay (* P < 0.05).

    Article Snippet: Cells were cultured in culture dishes (Falcon, Glendale, AZ, USA) with commercial human oral epithelial cell medium containing serum (Celprogen Inc.).

    Techniques: Cell Attachment Assay, Cell Culture, WST-1 Assay