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human lusc cell lines sk mes 1  (ATCC)


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    ATCC human lusc cell lines sk mes 1
    Human Lusc Cell Lines Sk Mes 1, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 651 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+lusc+cell+lines+sk+mes+1/pm40752594-59-16-26?v=ATCC
    Average 96 stars, based on 651 article reviews
    human lusc cell lines sk mes 1 - by Bioz Stars, 2026-07
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    ATCC human lusc cell lines sk mes 1
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    Procell Inc human lung squamous cell carcinoma [lusc] cell line sk-mes-1 #cl-0213
    Human Lung Squamous Cell Carcinoma [Lusc] Cell Line Sk Mes 1 #Cl 0213, 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
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    96
    ATCC human lusc cells lines
    High-throughput library screening identifies the key m6A regulator in <t>LUSC.</t> (A) Mechanism of RNA m6A Modifications. (B) The CNV variation frequency of m6A regulators in TCGA cohort. The height of the column represented the alteration frequency. The amplification frequency, red dot; the deletion frequency, green dot. (C) Differential expression of m6a regulators between normal and LUSC tissues in TCGA cohort. (Normal: blue and LUSC: red). Significant results are indicated as ***p < 0.001, **p < 0.01, and *p < 0.05. (D) The interaction of expression on m6A regulators in LUSC. Different biological functions of m6A regulators were depicted by circles in different colors. The circle size represented the effect of each regulator on the prognosis by P-value. The lines linking regulators showed their interactions, pink represented positive correlation, and blue represented negative correlation. Green dots in the circle showed favorable factors of prognosis. Purple dots in the circle showed risk factors of prognosis. (E–G) Kaplan–Meier survival analysis showed that indicated genes (METTL5, IGF2BP3, and HNRNPC) exhibited prognosis in LUSC patients based on TCGA data. (H) mRNA expression levels of METTL5, IGF2BP3, and HNRNPC were detected using pPCR <t>in</t> <t>SK-MES-1</t> and <t>NCI-H226.</t>
    Human Lusc Cells Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+lusc+cell+lines+sk+mes+1/pmc11864947-32-0-11?v=ATCC
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    96
    ATCC human lusc cell line skmes 1
    High-throughput library screening identifies the key m6A regulator in <t>LUSC.</t> (A) Mechanism of RNA m6A Modifications. (B) The CNV variation frequency of m6A regulators in TCGA cohort. The height of the column represented the alteration frequency. The amplification frequency, red dot; the deletion frequency, green dot. (C) Differential expression of m6a regulators between normal and LUSC tissues in TCGA cohort. (Normal: blue and LUSC: red). Significant results are indicated as ***p < 0.001, **p < 0.01, and *p < 0.05. (D) The interaction of expression on m6A regulators in LUSC. Different biological functions of m6A regulators were depicted by circles in different colors. The circle size represented the effect of each regulator on the prognosis by P-value. The lines linking regulators showed their interactions, pink represented positive correlation, and blue represented negative correlation. Green dots in the circle showed favorable factors of prognosis. Purple dots in the circle showed risk factors of prognosis. (E–G) Kaplan–Meier survival analysis showed that indicated genes (METTL5, IGF2BP3, and HNRNPC) exhibited prognosis in LUSC patients based on TCGA data. (H) mRNA expression levels of METTL5, IGF2BP3, and HNRNPC were detected using pPCR <t>in</t> <t>SK-MES-1</t> and <t>NCI-H226.</t>
    Human Lusc Cell Line Skmes 1, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+lusc+cell+lines+sk+mes+1/pm39169204-278-1-7?v=ATCC
    Average 96 stars, based on 1 article reviews
    human lusc cell line skmes 1 - by Bioz Stars, 2026-07
    96/100 stars
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    96
    ATCC human lusc cell line sk mes 1
    High-throughput library screening identifies the key m6A regulator in <t>LUSC.</t> (A) Mechanism of RNA m6A Modifications. (B) The CNV variation frequency of m6A regulators in TCGA cohort. The height of the column represented the alteration frequency. The amplification frequency, red dot; the deletion frequency, green dot. (C) Differential expression of m6a regulators between normal and LUSC tissues in TCGA cohort. (Normal: blue and LUSC: red). Significant results are indicated as ***p < 0.001, **p < 0.01, and *p < 0.05. (D) The interaction of expression on m6A regulators in LUSC. Different biological functions of m6A regulators were depicted by circles in different colors. The circle size represented the effect of each regulator on the prognosis by P-value. The lines linking regulators showed their interactions, pink represented positive correlation, and blue represented negative correlation. Green dots in the circle showed favorable factors of prognosis. Purple dots in the circle showed risk factors of prognosis. (E–G) Kaplan–Meier survival analysis showed that indicated genes (METTL5, IGF2BP3, and HNRNPC) exhibited prognosis in LUSC patients based on TCGA data. (H) mRNA expression levels of METTL5, IGF2BP3, and HNRNPC were detected using pPCR <t>in</t> <t>SK-MES-1</t> and <t>NCI-H226.</t>
    Human Lusc Cell Line Sk Mes 1, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+lusc+cell+lines+sk+mes+1/pmc11339382-280-1-7?v=ATCC
    Average 96 stars, based on 1 article reviews
    human lusc cell line sk mes 1 - by Bioz Stars, 2026-07
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    96
    ATCC human lusc cell lines
    High-throughput library screening identifies the key m6A regulator in <t>LUSC.</t> (A) Mechanism of RNA m6A Modifications. (B) The CNV variation frequency of m6A regulators in TCGA cohort. The height of the column represented the alteration frequency. The amplification frequency, red dot; the deletion frequency, green dot. (C) Differential expression of m6a regulators between normal and LUSC tissues in TCGA cohort. (Normal: blue and LUSC: red). Significant results are indicated as ***p < 0.001, **p < 0.01, and *p < 0.05. (D) The interaction of expression on m6A regulators in LUSC. Different biological functions of m6A regulators were depicted by circles in different colors. The circle size represented the effect of each regulator on the prognosis by P-value. The lines linking regulators showed their interactions, pink represented positive correlation, and blue represented negative correlation. Green dots in the circle showed favorable factors of prognosis. Purple dots in the circle showed risk factors of prognosis. (E–G) Kaplan–Meier survival analysis showed that indicated genes (METTL5, IGF2BP3, and HNRNPC) exhibited prognosis in LUSC patients based on TCGA data. (H) mRNA expression levels of METTL5, IGF2BP3, and HNRNPC were detected using pPCR <t>in</t> <t>SK-MES-1</t> and <t>NCI-H226.</t>
    Human Lusc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+lusc+cell+lines+sk+mes+1/pm37249759-44-30-39?v=ATCC
    Average 96 stars, based on 1 article reviews
    human lusc cell lines - by Bioz Stars, 2026-07
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    ATCC human lusc cell lines skmes 1
    Felodipine suppressed <t>LUSC</t> growth and strengthened tumor immune responses to ICBs. (a–c) Felodipine plus PD1ab inhibited KLN-205 tumor growth in DBA/2 mice ( n = 8). (d) The weight of mice. (e) The survival time of mice receiving felodipine plus PD1ab ( n = 10). (f)–(h) Felodipine plus CTLA4ab inhibited KLN-205 tumor growth in DBA/2 mice ( n = 8). (i) The weight of mice. (j) The survival time of mice receiving felodipine plus CTLA4ab ( n = 10). Data are presented as mean ± SD, n.s. no significance; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Error bars denote s.e.m.
    Human Lusc Cell Lines Skmes 1, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+lusc+cell+lines+sk+mes+1/pmc10518203-33-1-21?v=ATCC
    Average 96 stars, based on 1 article reviews
    human lusc cell lines skmes 1 - by Bioz Stars, 2026-07
    96/100 stars
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    90
    China Center for Type Culture Collection human lusc cell line sk-mes-1
    Felodipine suppressed <t>LUSC</t> growth and strengthened tumor immune responses to ICBs. (a–c) Felodipine plus PD1ab inhibited KLN-205 tumor growth in DBA/2 mice ( n = 8). (d) The weight of mice. (e) The survival time of mice receiving felodipine plus PD1ab ( n = 10). (f)–(h) Felodipine plus CTLA4ab inhibited KLN-205 tumor growth in DBA/2 mice ( n = 8). (i) The weight of mice. (j) The survival time of mice receiving felodipine plus CTLA4ab ( n = 10). Data are presented as mean ± SD, n.s. no significance; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Error bars denote s.e.m.
    Human Lusc Cell Line Sk Mes 1, supplied by China Center for Type Culture Collection, 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/product/human+lusc+cell+lines+sk+mes+1/pm37500615-234-1-28?v=China+Center+for+Type+Culture+Collection
    Average 90 stars, based on 1 article reviews
    human lusc cell line sk-mes-1 - by Bioz Stars, 2026-07
    90/100 stars
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    High-throughput library screening identifies the key m6A regulator in LUSC. (A) Mechanism of RNA m6A Modifications. (B) The CNV variation frequency of m6A regulators in TCGA cohort. The height of the column represented the alteration frequency. The amplification frequency, red dot; the deletion frequency, green dot. (C) Differential expression of m6a regulators between normal and LUSC tissues in TCGA cohort. (Normal: blue and LUSC: red). Significant results are indicated as ***p < 0.001, **p < 0.01, and *p < 0.05. (D) The interaction of expression on m6A regulators in LUSC. Different biological functions of m6A regulators were depicted by circles in different colors. The circle size represented the effect of each regulator on the prognosis by P-value. The lines linking regulators showed their interactions, pink represented positive correlation, and blue represented negative correlation. Green dots in the circle showed favorable factors of prognosis. Purple dots in the circle showed risk factors of prognosis. (E–G) Kaplan–Meier survival analysis showed that indicated genes (METTL5, IGF2BP3, and HNRNPC) exhibited prognosis in LUSC patients based on TCGA data. (H) mRNA expression levels of METTL5, IGF2BP3, and HNRNPC were detected using pPCR in SK-MES-1 and NCI-H226.

    Journal: Frontiers in Oncology

    Article Title: The human 18S rRNA m6A methyltransferase METTL5 promotes tumorigenesis via DEPDC1 in lung squamous cell carcinoma

    doi: 10.3389/fonc.2025.1522157

    Figure Lengend Snippet: High-throughput library screening identifies the key m6A regulator in LUSC. (A) Mechanism of RNA m6A Modifications. (B) The CNV variation frequency of m6A regulators in TCGA cohort. The height of the column represented the alteration frequency. The amplification frequency, red dot; the deletion frequency, green dot. (C) Differential expression of m6a regulators between normal and LUSC tissues in TCGA cohort. (Normal: blue and LUSC: red). Significant results are indicated as ***p < 0.001, **p < 0.01, and *p < 0.05. (D) The interaction of expression on m6A regulators in LUSC. Different biological functions of m6A regulators were depicted by circles in different colors. The circle size represented the effect of each regulator on the prognosis by P-value. The lines linking regulators showed their interactions, pink represented positive correlation, and blue represented negative correlation. Green dots in the circle showed favorable factors of prognosis. Purple dots in the circle showed risk factors of prognosis. (E–G) Kaplan–Meier survival analysis showed that indicated genes (METTL5, IGF2BP3, and HNRNPC) exhibited prognosis in LUSC patients based on TCGA data. (H) mRNA expression levels of METTL5, IGF2BP3, and HNRNPC were detected using pPCR in SK-MES-1 and NCI-H226.

    Article Snippet: Human LUSC cells lines (SK-MES-1 and NCI-H226) were obtained from the American Type Culture Collection and cultured in L-15 medium containing 10% fetal bovine serum (Gibco) at 5% CO2 and 37°C.

    Techniques: High Throughput Screening Assay, Library Screening, Amplification, Quantitative Proteomics, Expressing

    METTL5 promotes tumor progression in LUSC. (A–D) Transfection knockdown or overexpression efficiencies was validated by western blot and qPCR, respectively. (E, F) Colony formation assay and CCK-8 was used to analyze the proliferation viability of METTL5 in LUSC cell. All the data are presented as the mean ± standard deviation (n = 3). *P < 0.05, **P < 0.01, compared with the control group. (G–I) Transwell migration assay and wound healing assay was used to analyze the migration viability of METTL5 in LUSC cell. All the data are presented as the mean ± standard deviation (n = 3). *P < 0.05, **P < 0.01, compared with the control group. (J) The image of mice bearing subcutaneous tumors derived from SK-MES-1 cells treated with different treatment (shNC, shMETTL5#1, or shMETTL5#2) at the indicated times. (K) The xenograft growth curves for the shMETTL5#1, shMETTL5#2, and shNC groups were plotted by measuring the tumor size (width2 × length × π/6) with a Vernier caliper every 7 days. (L) Nude mice were sacrificed, and xenografts were harvested and weighed.

    Journal: Frontiers in Oncology

    Article Title: The human 18S rRNA m6A methyltransferase METTL5 promotes tumorigenesis via DEPDC1 in lung squamous cell carcinoma

    doi: 10.3389/fonc.2025.1522157

    Figure Lengend Snippet: METTL5 promotes tumor progression in LUSC. (A–D) Transfection knockdown or overexpression efficiencies was validated by western blot and qPCR, respectively. (E, F) Colony formation assay and CCK-8 was used to analyze the proliferation viability of METTL5 in LUSC cell. All the data are presented as the mean ± standard deviation (n = 3). *P < 0.05, **P < 0.01, compared with the control group. (G–I) Transwell migration assay and wound healing assay was used to analyze the migration viability of METTL5 in LUSC cell. All the data are presented as the mean ± standard deviation (n = 3). *P < 0.05, **P < 0.01, compared with the control group. (J) The image of mice bearing subcutaneous tumors derived from SK-MES-1 cells treated with different treatment (shNC, shMETTL5#1, or shMETTL5#2) at the indicated times. (K) The xenograft growth curves for the shMETTL5#1, shMETTL5#2, and shNC groups were plotted by measuring the tumor size (width2 × length × π/6) with a Vernier caliper every 7 days. (L) Nude mice were sacrificed, and xenografts were harvested and weighed.

    Article Snippet: Human LUSC cells lines (SK-MES-1 and NCI-H226) were obtained from the American Type Culture Collection and cultured in L-15 medium containing 10% fetal bovine serum (Gibco) at 5% CO2 and 37°C.

    Techniques: Transfection, Knockdown, Over Expression, Western Blot, Colony Assay, CCK-8 Assay, Standard Deviation, Control, Transwell Migration Assay, Wound Healing Assay, Migration, Derivative Assay

    METTL5 promoted DEP domain containing 1 (DEPDC1) translation via 18S rRNA methyltransferase. (A) The Venn plot showed DEPDC1 was identified based on the intersection analysis. (B, C) The expression of DEPDC1 between normal and tumor tissues. (D) The survival analysis of LUSC patients with low and high DEPDC1 expression. (E, F) Relative DEPDC1 mRNA and protein expression levels in LUSC cells transected with METTL5 knockdown or overexpression. (G, H) The polysomes of METTL5‐WT and METTL5‐KD cells were extracted and subjected to a 10% to 50% sucrose gradient ultracentrifugation. The mRNA expression level in each fraction was determined by qRT‐PCR (upper) and visualized by DNA agarose gel (lower). (I, J) LC/MS was performed with an m6A antibody. (K, L) Polysome profiling by sucrose density gradient showing decreased polysomes and accumulated 80S monosomes. (M) Western blotting analysis of DEPDC1 protein levels in LUSC cells subjected to different treatments. (N) m6A DNA methylation assay detected alterations in m6dA of genomic DNA in METTL5-WT and METTL5-KD cells. (O) Dual luciferase reporter assay results indicated that METTL5 exhibits no regulatory effect on DNA methylation. n = 3 independent experiments, ns means no significant difference. Data are mean ± SEM. NS, non-significant, **p < 0.01, and ***p < 0.001. Two-tailed unpaired Student’s t test (E–G, I, M–O) .

    Journal: Frontiers in Oncology

    Article Title: The human 18S rRNA m6A methyltransferase METTL5 promotes tumorigenesis via DEPDC1 in lung squamous cell carcinoma

    doi: 10.3389/fonc.2025.1522157

    Figure Lengend Snippet: METTL5 promoted DEP domain containing 1 (DEPDC1) translation via 18S rRNA methyltransferase. (A) The Venn plot showed DEPDC1 was identified based on the intersection analysis. (B, C) The expression of DEPDC1 between normal and tumor tissues. (D) The survival analysis of LUSC patients with low and high DEPDC1 expression. (E, F) Relative DEPDC1 mRNA and protein expression levels in LUSC cells transected with METTL5 knockdown or overexpression. (G, H) The polysomes of METTL5‐WT and METTL5‐KD cells were extracted and subjected to a 10% to 50% sucrose gradient ultracentrifugation. The mRNA expression level in each fraction was determined by qRT‐PCR (upper) and visualized by DNA agarose gel (lower). (I, J) LC/MS was performed with an m6A antibody. (K, L) Polysome profiling by sucrose density gradient showing decreased polysomes and accumulated 80S monosomes. (M) Western blotting analysis of DEPDC1 protein levels in LUSC cells subjected to different treatments. (N) m6A DNA methylation assay detected alterations in m6dA of genomic DNA in METTL5-WT and METTL5-KD cells. (O) Dual luciferase reporter assay results indicated that METTL5 exhibits no regulatory effect on DNA methylation. n = 3 independent experiments, ns means no significant difference. Data are mean ± SEM. NS, non-significant, **p < 0.01, and ***p < 0.001. Two-tailed unpaired Student’s t test (E–G, I, M–O) .

    Article Snippet: Human LUSC cells lines (SK-MES-1 and NCI-H226) were obtained from the American Type Culture Collection and cultured in L-15 medium containing 10% fetal bovine serum (Gibco) at 5% CO2 and 37°C.

    Techniques: Expressing, Knockdown, Over Expression, Quantitative RT-PCR, Agarose Gel Electrophoresis, Liquid Chromatography with Mass Spectroscopy, Western Blot, DNA Methylation Assay, Luciferase, Reporter Assay, Two Tailed Test

    METTL5 promotes LUSC progression through DEPDC1 expression. (A) Cell viability was measured in METTL5 silencing cells with or without overexpression of DEPDC1. (B) Colony formation assay indicated the rescue effect of DEPDC1 on METTL5 silencing. (C, D) Transwell migration assays and wound healing assays were performed in METTL5-deficient cells with or without overexpression of DEPDC1. All the data are presented as the mean ± standard deviation (n=3). **P<0.01, compared with the control group. (E) The image of mice bearing subcutaneous tumors derived from SK-MES-1 cells treated with different treatment (Ctrl, METTL5 overexpression, or METTL5 overexpression+DEPDC1 knockdown) at the indicated times. (F) The xenograft growth curves for the METTL5 overexpression, METTL5 overexpression+ DEPDC1 knockdown, and Ctrl groups were plotted by measuring the tumor size (width2 × length × π/6) with a Vernier caliper every 7 days. (G) Nude mice were sacrificed, and xenografts were harvested and weighed.

    Journal: Frontiers in Oncology

    Article Title: The human 18S rRNA m6A methyltransferase METTL5 promotes tumorigenesis via DEPDC1 in lung squamous cell carcinoma

    doi: 10.3389/fonc.2025.1522157

    Figure Lengend Snippet: METTL5 promotes LUSC progression through DEPDC1 expression. (A) Cell viability was measured in METTL5 silencing cells with or without overexpression of DEPDC1. (B) Colony formation assay indicated the rescue effect of DEPDC1 on METTL5 silencing. (C, D) Transwell migration assays and wound healing assays were performed in METTL5-deficient cells with or without overexpression of DEPDC1. All the data are presented as the mean ± standard deviation (n=3). **P<0.01, compared with the control group. (E) The image of mice bearing subcutaneous tumors derived from SK-MES-1 cells treated with different treatment (Ctrl, METTL5 overexpression, or METTL5 overexpression+DEPDC1 knockdown) at the indicated times. (F) The xenograft growth curves for the METTL5 overexpression, METTL5 overexpression+ DEPDC1 knockdown, and Ctrl groups were plotted by measuring the tumor size (width2 × length × π/6) with a Vernier caliper every 7 days. (G) Nude mice were sacrificed, and xenografts were harvested and weighed.

    Article Snippet: Human LUSC cells lines (SK-MES-1 and NCI-H226) were obtained from the American Type Culture Collection and cultured in L-15 medium containing 10% fetal bovine serum (Gibco) at 5% CO2 and 37°C.

    Techniques: Expressing, Over Expression, Colony Assay, Migration, Standard Deviation, Control, Derivative Assay, Knockdown

    Felodipine suppressed LUSC growth and strengthened tumor immune responses to ICBs. (a–c) Felodipine plus PD1ab inhibited KLN-205 tumor growth in DBA/2 mice ( n = 8). (d) The weight of mice. (e) The survival time of mice receiving felodipine plus PD1ab ( n = 10). (f)–(h) Felodipine plus CTLA4ab inhibited KLN-205 tumor growth in DBA/2 mice ( n = 8). (i) The weight of mice. (j) The survival time of mice receiving felodipine plus CTLA4ab ( n = 10). Data are presented as mean ± SD, n.s. no significance; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Error bars denote s.e.m.

    Journal: Open Medicine

    Article Title: The antihypertensive felodipine shows synergistic activity with immune checkpoint blockade and inhibits tumor growth via NFAT1 in LUSC

    doi: 10.1515/med-2023-0801

    Figure Lengend Snippet: Felodipine suppressed LUSC growth and strengthened tumor immune responses to ICBs. (a–c) Felodipine plus PD1ab inhibited KLN-205 tumor growth in DBA/2 mice ( n = 8). (d) The weight of mice. (e) The survival time of mice receiving felodipine plus PD1ab ( n = 10). (f)–(h) Felodipine plus CTLA4ab inhibited KLN-205 tumor growth in DBA/2 mice ( n = 8). (i) The weight of mice. (j) The survival time of mice receiving felodipine plus CTLA4ab ( n = 10). Data are presented as mean ± SD, n.s. no significance; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Error bars denote s.e.m.

    Article Snippet: The human LUSC cell lines SKMES-1 and NCIH226 were procured from Pricella, Wuhan, China (Cat # CL-0213, Cat # CL-0396) and American Type Culture Collection, respectively.

    Techniques:

    Felodipine inhibited human LUSC proliferation and migration. (a) CCK-8 assay analyzing SKMES-1 proliferation after felodipine (0, 10, 50 μM) treatment. (b) CCK-8 assay investigating NCIH226 proliferation after felodipine (0, 10, 50 μM) treatment. (c and d) Colony formation assay evaluating SKMES-1 proliferation after felodipine (10 μM) treatment. (e and f) Wound healing assay examining SKMES-1 migration after felodipine (10 μM) treatment; scale bars, 200 μm. (g) – (i) Subcutaneous tumor model in nude mice ( n = 8) evaluating SKMES-1 growth following felodipine treatment (20 mg/kg); data are expressed as mean ± SD, n.s. no significance; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Error bars denote s.e.m.

    Journal: Open Medicine

    Article Title: The antihypertensive felodipine shows synergistic activity with immune checkpoint blockade and inhibits tumor growth via NFAT1 in LUSC

    doi: 10.1515/med-2023-0801

    Figure Lengend Snippet: Felodipine inhibited human LUSC proliferation and migration. (a) CCK-8 assay analyzing SKMES-1 proliferation after felodipine (0, 10, 50 μM) treatment. (b) CCK-8 assay investigating NCIH226 proliferation after felodipine (0, 10, 50 μM) treatment. (c and d) Colony formation assay evaluating SKMES-1 proliferation after felodipine (10 μM) treatment. (e and f) Wound healing assay examining SKMES-1 migration after felodipine (10 μM) treatment; scale bars, 200 μm. (g) – (i) Subcutaneous tumor model in nude mice ( n = 8) evaluating SKMES-1 growth following felodipine treatment (20 mg/kg); data are expressed as mean ± SD, n.s. no significance; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Error bars denote s.e.m.

    Article Snippet: The human LUSC cell lines SKMES-1 and NCIH226 were procured from Pricella, Wuhan, China (Cat # CL-0213, Cat # CL-0396) and American Type Culture Collection, respectively.

    Techniques: Migration, CCK-8 Assay, Colony Assay, Wound Healing Assay

    Felodipine suppressed human LUSC progression via NFAT1. (a and b) Data from the TCGA database were used to explore the relationship between OS, DFS, and NFAT1 expression in LUSC patients, respectively. (c) qPCR detection of NFAT1 after felodipine (10, 50, 100 μM) treatment in SKMES-1. (d) qPCR detection of NFAT1 after felodipine (10, 50, 100 μM) treatment in NCH226. (e) CCK-8 assay examining SKMES-1 proliferation after felodipine treatment and NFAT1 knockdown. (f) CCK-8 assay examining NCH226 proliferation after felodipine treatment and NFAT1 knockdown. Data are presented as mean ± SD, n.s. no significance; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Error bars denote s.e.m.

    Journal: Open Medicine

    Article Title: The antihypertensive felodipine shows synergistic activity with immune checkpoint blockade and inhibits tumor growth via NFAT1 in LUSC

    doi: 10.1515/med-2023-0801

    Figure Lengend Snippet: Felodipine suppressed human LUSC progression via NFAT1. (a and b) Data from the TCGA database were used to explore the relationship between OS, DFS, and NFAT1 expression in LUSC patients, respectively. (c) qPCR detection of NFAT1 after felodipine (10, 50, 100 μM) treatment in SKMES-1. (d) qPCR detection of NFAT1 after felodipine (10, 50, 100 μM) treatment in NCH226. (e) CCK-8 assay examining SKMES-1 proliferation after felodipine treatment and NFAT1 knockdown. (f) CCK-8 assay examining NCH226 proliferation after felodipine treatment and NFAT1 knockdown. Data are presented as mean ± SD, n.s. no significance; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Error bars denote s.e.m.

    Article Snippet: The human LUSC cell lines SKMES-1 and NCIH226 were procured from Pricella, Wuhan, China (Cat # CL-0213, Cat # CL-0396) and American Type Culture Collection, respectively.

    Techniques: Expressing, CCK-8 Assay, Knockdown

    A schematic diagram illustrating felodipine exhibited synergistic activity with ICB and inhibited tumor growth by mediating NFAT1 expression in LUSC.

    Journal: Open Medicine

    Article Title: The antihypertensive felodipine shows synergistic activity with immune checkpoint blockade and inhibits tumor growth via NFAT1 in LUSC

    doi: 10.1515/med-2023-0801

    Figure Lengend Snippet: A schematic diagram illustrating felodipine exhibited synergistic activity with ICB and inhibited tumor growth by mediating NFAT1 expression in LUSC.

    Article Snippet: The human LUSC cell lines SKMES-1 and NCIH226 were procured from Pricella, Wuhan, China (Cat # CL-0213, Cat # CL-0396) and American Type Culture Collection, respectively.

    Techniques: Activity Assay, Expressing