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143b  (ATCC)


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    Structured Review

    ATCC 143b
    FR6 promotes cytosolic and in vivo delivery of fluorous tagged peptides. ( a ) Cellular uptake of unmodified peptide, FPep, FR6/peptide, or FR6/FPep in HeLa cells visualized by confocal microscopy after 6 h incubation. The concentration of peptides was 5 μM. ( b ) Quantification of intracellular delivery efficiency of HeLa cells incubated with FITC FKLA or FR6/ FITC FKLA at different concentrations for 6 h (n = 3). The concentration of FR6 was 5 μM. ( c ) The LDH release of <t>143B</t> cells treated with PBS, FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 2.5 μM. ( d ) The apoptosis of 143B cells treated with FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 5 μM. ( e ) Confocal images of 3D tumor spheroids treated with different peptides for 12 h. The concentration of FITC KLA, FITC FKLA, and FR6 was 5 μM. ( f ) Schematic diagram of the in vivo therapy procedure. ( g ) Tumor progression curves following treatment with PBS, FR6, FKLA, or FR6/FKLA, respectively. Tumor images ( h ) and tumor weights ( i ) of mice treated with different samples.
    143b, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1622 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Fluorous oligoarginines as supra-enhancers for intracellular and transdermal peptide delivery"

    Article Title: Fluorous oligoarginines as supra-enhancers for intracellular and transdermal peptide delivery

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2025.12.027

    FR6 promotes cytosolic and in vivo delivery of fluorous tagged peptides. ( a ) Cellular uptake of unmodified peptide, FPep, FR6/peptide, or FR6/FPep in HeLa cells visualized by confocal microscopy after 6 h incubation. The concentration of peptides was 5 μM. ( b ) Quantification of intracellular delivery efficiency of HeLa cells incubated with FITC FKLA or FR6/ FITC FKLA at different concentrations for 6 h (n = 3). The concentration of FR6 was 5 μM. ( c ) The LDH release of 143B cells treated with PBS, FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 2.5 μM. ( d ) The apoptosis of 143B cells treated with FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 5 μM. ( e ) Confocal images of 3D tumor spheroids treated with different peptides for 12 h. The concentration of FITC KLA, FITC FKLA, and FR6 was 5 μM. ( f ) Schematic diagram of the in vivo therapy procedure. ( g ) Tumor progression curves following treatment with PBS, FR6, FKLA, or FR6/FKLA, respectively. Tumor images ( h ) and tumor weights ( i ) of mice treated with different samples.
    Figure Legend Snippet: FR6 promotes cytosolic and in vivo delivery of fluorous tagged peptides. ( a ) Cellular uptake of unmodified peptide, FPep, FR6/peptide, or FR6/FPep in HeLa cells visualized by confocal microscopy after 6 h incubation. The concentration of peptides was 5 μM. ( b ) Quantification of intracellular delivery efficiency of HeLa cells incubated with FITC FKLA or FR6/ FITC FKLA at different concentrations for 6 h (n = 3). The concentration of FR6 was 5 μM. ( c ) The LDH release of 143B cells treated with PBS, FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 2.5 μM. ( d ) The apoptosis of 143B cells treated with FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 5 μM. ( e ) Confocal images of 3D tumor spheroids treated with different peptides for 12 h. The concentration of FITC KLA, FITC FKLA, and FR6 was 5 μM. ( f ) Schematic diagram of the in vivo therapy procedure. ( g ) Tumor progression curves following treatment with PBS, FR6, FKLA, or FR6/FKLA, respectively. Tumor images ( h ) and tumor weights ( i ) of mice treated with different samples.

    Techniques Used: In Vivo, Confocal Microscopy, Incubation, Concentration Assay



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    143b  (ATCC)
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    FR6 promotes cytosolic and in vivo delivery of fluorous tagged peptides. ( a ) Cellular uptake of unmodified peptide, FPep, FR6/peptide, or FR6/FPep in HeLa cells visualized by confocal microscopy after 6 h incubation. The concentration of peptides was 5 μM. ( b ) Quantification of intracellular delivery efficiency of HeLa cells incubated with FITC FKLA or FR6/ FITC FKLA at different concentrations for 6 h (n = 3). The concentration of FR6 was 5 μM. ( c ) The LDH release of <t>143B</t> cells treated with PBS, FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 2.5 μM. ( d ) The apoptosis of 143B cells treated with FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 5 μM. ( e ) Confocal images of 3D tumor spheroids treated with different peptides for 12 h. The concentration of FITC KLA, FITC FKLA, and FR6 was 5 μM. ( f ) Schematic diagram of the in vivo therapy procedure. ( g ) Tumor progression curves following treatment with PBS, FR6, FKLA, or FR6/FKLA, respectively. Tumor images ( h ) and tumor weights ( i ) of mice treated with different samples.
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    Identification of active compounds and target prediction in YHD. (A) Venn diagram of the target of YHD and the target of <t>osteosarcoma.</t> (B – D) Gene Ontology (GO) enrichment analysis results. (E, F) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis results. (G) The component-target-pathway-disease network implicated in the mechanism of YHD in osteosarcoma treatment. The triangles represent osteosarcoma, the diamonds represent pathways, the circles represent key genes, and the squares represent the active ingredients of YHD. (H) Heatmap of molecular docking score. A binding energy heatmap with a bluer color indicates a more stable binding. (I) Molecular docking visualization between the active components of YHD and key targets.
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    Identification of active compounds and target prediction in YHD. (A) Venn diagram of the target of YHD and the target of <t>osteosarcoma.</t> (B – D) Gene Ontology (GO) enrichment analysis results. (E, F) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis results. (G) The component-target-pathway-disease network implicated in the mechanism of YHD in osteosarcoma treatment. The triangles represent osteosarcoma, the diamonds represent pathways, the circles represent key genes, and the squares represent the active ingredients of YHD. (H) Heatmap of molecular docking score. A binding energy heatmap with a bluer color indicates a more stable binding. (I) Molecular docking visualization between the active components of YHD and key targets.
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    Identification of active compounds and target prediction in YHD. (A) Venn diagram of the target of YHD and the target of <t>osteosarcoma.</t> (B – D) Gene Ontology (GO) enrichment analysis results. (E, F) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis results. (G) The component-target-pathway-disease network implicated in the mechanism of YHD in osteosarcoma treatment. The triangles represent osteosarcoma, the diamonds represent pathways, the circles represent key genes, and the squares represent the active ingredients of YHD. (H) Heatmap of molecular docking score. A binding energy heatmap with a bluer color indicates a more stable binding. (I) Molecular docking visualization between the active components of YHD and key targets.
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    Identification of active compounds and target prediction in YHD. (A) Venn diagram of the target of YHD and the target of <t>osteosarcoma.</t> (B – D) Gene Ontology (GO) enrichment analysis results. (E, F) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis results. (G) The component-target-pathway-disease network implicated in the mechanism of YHD in osteosarcoma treatment. The triangles represent osteosarcoma, the diamonds represent pathways, the circles represent key genes, and the squares represent the active ingredients of YHD. (H) Heatmap of molecular docking score. A binding energy heatmap with a bluer color indicates a more stable binding. (I) Molecular docking visualization between the active components of YHD and key targets.
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    Identification of active compounds and target prediction in YHD. (A) Venn diagram of the target of YHD and the target of <t>osteosarcoma.</t> (B – D) Gene Ontology (GO) enrichment analysis results. (E, F) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis results. (G) The component-target-pathway-disease network implicated in the mechanism of YHD in osteosarcoma treatment. The triangles represent osteosarcoma, the diamonds represent pathways, the circles represent key genes, and the squares represent the active ingredients of YHD. (H) Heatmap of molecular docking score. A binding energy heatmap with a bluer color indicates a more stable binding. (I) Molecular docking visualization between the active components of YHD and key targets.
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    Image Search Results


    FR6 promotes cytosolic and in vivo delivery of fluorous tagged peptides. ( a ) Cellular uptake of unmodified peptide, FPep, FR6/peptide, or FR6/FPep in HeLa cells visualized by confocal microscopy after 6 h incubation. The concentration of peptides was 5 μM. ( b ) Quantification of intracellular delivery efficiency of HeLa cells incubated with FITC FKLA or FR6/ FITC FKLA at different concentrations for 6 h (n = 3). The concentration of FR6 was 5 μM. ( c ) The LDH release of 143B cells treated with PBS, FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 2.5 μM. ( d ) The apoptosis of 143B cells treated with FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 5 μM. ( e ) Confocal images of 3D tumor spheroids treated with different peptides for 12 h. The concentration of FITC KLA, FITC FKLA, and FR6 was 5 μM. ( f ) Schematic diagram of the in vivo therapy procedure. ( g ) Tumor progression curves following treatment with PBS, FR6, FKLA, or FR6/FKLA, respectively. Tumor images ( h ) and tumor weights ( i ) of mice treated with different samples.

    Journal: Bioactive Materials

    Article Title: Fluorous oligoarginines as supra-enhancers for intracellular and transdermal peptide delivery

    doi: 10.1016/j.bioactmat.2025.12.027

    Figure Lengend Snippet: FR6 promotes cytosolic and in vivo delivery of fluorous tagged peptides. ( a ) Cellular uptake of unmodified peptide, FPep, FR6/peptide, or FR6/FPep in HeLa cells visualized by confocal microscopy after 6 h incubation. The concentration of peptides was 5 μM. ( b ) Quantification of intracellular delivery efficiency of HeLa cells incubated with FITC FKLA or FR6/ FITC FKLA at different concentrations for 6 h (n = 3). The concentration of FR6 was 5 μM. ( c ) The LDH release of 143B cells treated with PBS, FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 2.5 μM. ( d ) The apoptosis of 143B cells treated with FR6, KLA, FKLA, FR6/KLA, or FR6/FKLA for 24 h, respectively. The concentration of KLA, FKLA, and FR6 was 5 μM. ( e ) Confocal images of 3D tumor spheroids treated with different peptides for 12 h. The concentration of FITC KLA, FITC FKLA, and FR6 was 5 μM. ( f ) Schematic diagram of the in vivo therapy procedure. ( g ) Tumor progression curves following treatment with PBS, FR6, FKLA, or FR6/FKLA, respectively. Tumor images ( h ) and tumor weights ( i ) of mice treated with different samples.

    Article Snippet: HeLa, 143B, HEK293, RAW264.7, and NIH3T3 were sourced from ATCC.

    Techniques: In Vivo, Confocal Microscopy, Incubation, Concentration Assay

    Identification of active compounds and target prediction in YHD. (A) Venn diagram of the target of YHD and the target of osteosarcoma. (B – D) Gene Ontology (GO) enrichment analysis results. (E, F) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis results. (G) The component-target-pathway-disease network implicated in the mechanism of YHD in osteosarcoma treatment. The triangles represent osteosarcoma, the diamonds represent pathways, the circles represent key genes, and the squares represent the active ingredients of YHD. (H) Heatmap of molecular docking score. A binding energy heatmap with a bluer color indicates a more stable binding. (I) Molecular docking visualization between the active components of YHD and key targets.

    Journal: Genes & Diseases

    Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

    doi: 10.1016/j.gendis.2025.101862

    Figure Lengend Snippet: Identification of active compounds and target prediction in YHD. (A) Venn diagram of the target of YHD and the target of osteosarcoma. (B – D) Gene Ontology (GO) enrichment analysis results. (E, F) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis results. (G) The component-target-pathway-disease network implicated in the mechanism of YHD in osteosarcoma treatment. The triangles represent osteosarcoma, the diamonds represent pathways, the circles represent key genes, and the squares represent the active ingredients of YHD. (H) Heatmap of molecular docking score. A binding energy heatmap with a bluer color indicates a more stable binding. (I) Molecular docking visualization between the active components of YHD and key targets.

    Article Snippet: Human osteosarcoma cell lines (HOS, 143B), human bone marrow stromal cells (HS-5), human proximal renal tubular epithelial cells (HK-2), and human normal liver cells (LO2) were all purchased from the American Type Culture Collection (ATCC).

    Techniques: Binding Assay

    YHD selectively inhibits osteosarcoma (OS) cells without affecting the viability or apoptosis of normal human cells. (A, B) CCK8 assay detected the effect of YHD on the viability of OS cells at 24 h and 48 h. (C, D) Colony formation assay detected the effect of YHD on the colony-forming ability of OS cells. (E – G) Flow cytometry was used to detect the effect of YHD on the cell cycle of OS cells. (H – J) Western blot analysis detected the effect of YHD on the levels of proliferation-related proteins in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Journal: Genes & Diseases

    Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

    doi: 10.1016/j.gendis.2025.101862

    Figure Lengend Snippet: YHD selectively inhibits osteosarcoma (OS) cells without affecting the viability or apoptosis of normal human cells. (A, B) CCK8 assay detected the effect of YHD on the viability of OS cells at 24 h and 48 h. (C, D) Colony formation assay detected the effect of YHD on the colony-forming ability of OS cells. (E – G) Flow cytometry was used to detect the effect of YHD on the cell cycle of OS cells. (H – J) Western blot analysis detected the effect of YHD on the levels of proliferation-related proteins in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Article Snippet: Human osteosarcoma cell lines (HOS, 143B), human bone marrow stromal cells (HS-5), human proximal renal tubular epithelial cells (HK-2), and human normal liver cells (LO2) were all purchased from the American Type Culture Collection (ATCC).

    Techniques: CCK-8 Assay, Colony Assay, Flow Cytometry, Western Blot, Standard Deviation

    YHD can inhibit the migration and invasion of osteosarcoma (OS) cells, and promote their apoptosis. (A, B) Scratch healing assay showed that YHD inhibited the migration of OS cells. (C, D) Transwell assay showed that YHD inhibited the invasion of OS cells. (E – G) Western blot analysis detected the effect of YHD on the levels of proteins related to migration and invasion in OS cells. (H–K) Flow cytometry was used to detect the effect of YHD on apoptosis in OS cells. (L – N) Western blot analysis detected the effect of YHD on the levels of apoptosis-related proteins in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Journal: Genes & Diseases

    Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

    doi: 10.1016/j.gendis.2025.101862

    Figure Lengend Snippet: YHD can inhibit the migration and invasion of osteosarcoma (OS) cells, and promote their apoptosis. (A, B) Scratch healing assay showed that YHD inhibited the migration of OS cells. (C, D) Transwell assay showed that YHD inhibited the invasion of OS cells. (E – G) Western blot analysis detected the effect of YHD on the levels of proteins related to migration and invasion in OS cells. (H–K) Flow cytometry was used to detect the effect of YHD on apoptosis in OS cells. (L – N) Western blot analysis detected the effect of YHD on the levels of apoptosis-related proteins in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Article Snippet: Human osteosarcoma cell lines (HOS, 143B), human bone marrow stromal cells (HS-5), human proximal renal tubular epithelial cells (HK-2), and human normal liver cells (LO2) were all purchased from the American Type Culture Collection (ATCC).

    Techniques: Migration, Transwell Assay, Western Blot, Flow Cytometry, Standard Deviation

    YHD induces osteosarcoma (OS) cell death by increasing ROS levels. (A) The effect of YHD on ROS levels in OS cells was detected using the DCFH probe method. (B) After N-acetylcysteine (NAC) treatment, the effect of YHD on ROS levels in OS cells was detected using the DCFH probe method. (C) After NAC treatment, CCK8 assay detected the effect of YHD on the viability of OS cells at 24 h and 48 h. (D, E) After NAC treatment, scratch healing assay showed that YHD inhibited the migration of OS cells. (F, G) After NAC treatment, Transwell assay showed that YHD inhibited the invasion of OS cells. (H, I) After NAC treatment, flow cytometry was used to detect the effect of YHD on the apoptosis of OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Journal: Genes & Diseases

    Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

    doi: 10.1016/j.gendis.2025.101862

    Figure Lengend Snippet: YHD induces osteosarcoma (OS) cell death by increasing ROS levels. (A) The effect of YHD on ROS levels in OS cells was detected using the DCFH probe method. (B) After N-acetylcysteine (NAC) treatment, the effect of YHD on ROS levels in OS cells was detected using the DCFH probe method. (C) After NAC treatment, CCK8 assay detected the effect of YHD on the viability of OS cells at 24 h and 48 h. (D, E) After NAC treatment, scratch healing assay showed that YHD inhibited the migration of OS cells. (F, G) After NAC treatment, Transwell assay showed that YHD inhibited the invasion of OS cells. (H, I) After NAC treatment, flow cytometry was used to detect the effect of YHD on the apoptosis of OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Article Snippet: Human osteosarcoma cell lines (HOS, 143B), human bone marrow stromal cells (HS-5), human proximal renal tubular epithelial cells (HK-2), and human normal liver cells (LO2) were all purchased from the American Type Culture Collection (ATCC).

    Techniques: CCK-8 Assay, Migration, Transwell Assay, Flow Cytometry, Standard Deviation

    YHD can induce mitochondrial dysfunction in osteosarcoma (OS) cells. (A) Real-time quantitative PCR was used to measure mitochondrial DNA (mtDNA) levels. (B, C) Western blot analysis detected the effect of YHD on the expression levels of proteins related to mitochondrial biogenesis in OS cells. (D, E) JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. (F, G) MitoSOX staining detected the effect of YHD on mitochondrial ROS levels in OS cells. (H) Seahorse XFe24 analyzer measured the effect of YHD on the oxygen consumption rate (OCR) in OS cells. (I) The effect of YHD on ATP content in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Journal: Genes & Diseases

    Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

    doi: 10.1016/j.gendis.2025.101862

    Figure Lengend Snippet: YHD can induce mitochondrial dysfunction in osteosarcoma (OS) cells. (A) Real-time quantitative PCR was used to measure mitochondrial DNA (mtDNA) levels. (B, C) Western blot analysis detected the effect of YHD on the expression levels of proteins related to mitochondrial biogenesis in OS cells. (D, E) JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. (F, G) MitoSOX staining detected the effect of YHD on mitochondrial ROS levels in OS cells. (H) Seahorse XFe24 analyzer measured the effect of YHD on the oxygen consumption rate (OCR) in OS cells. (I) The effect of YHD on ATP content in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Article Snippet: Human osteosarcoma cell lines (HOS, 143B), human bone marrow stromal cells (HS-5), human proximal renal tubular epithelial cells (HK-2), and human normal liver cells (LO2) were all purchased from the American Type Culture Collection (ATCC).

    Techniques: Real-time Polymerase Chain Reaction, Western Blot, Expressing, Staining, Membrane, Standard Deviation

    YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and p38 signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Journal: Genes & Diseases

    Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

    doi: 10.1016/j.gendis.2025.101862

    Figure Lengend Snippet: YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and p38 signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Article Snippet: Human osteosarcoma cell lines (HOS, 143B), human bone marrow stromal cells (HS-5), human proximal renal tubular epithelial cells (HK-2), and human normal liver cells (LO2) were all purchased from the American Type Culture Collection (ATCC).

    Techniques: Protein-Protein interactions, Gene Expression, Control, Western Blot, Migration, Staining, Membrane, Standard Deviation