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Procell Inc a2780 ovc cell line cl-0013
Effect of Bifidobacterium longum ‐EVs on the proliferation, apoptosis, migration, and invasion of <t>A2780</t> cells. A2780 cells were incubated with 1, 5, and 10 μg/mL of B. longum ‐EVs (defined as B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups, respectively). (A) Cell viability was measured by the Cell Counting Kit‐8 (CCK‐8) after treatment for 24, 48, and 72 h. After a 24 h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. ** P < 0.01 and *** P < 0.001, versus the control group.
A2780 Ovc Cell Line Cl 0013, 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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1) Product Images from "Extracellular vesicles of Bifidobacterium longum reverse the acquired carboplatin resistance in ovarian cancer cells via p53 phosphorylation on Ser15"

Article Title: Extracellular vesicles of Bifidobacterium longum reverse the acquired carboplatin resistance in ovarian cancer cells via p53 phosphorylation on Ser15

Journal: The Kaohsiung Journal of Medical Sciences

doi: 10.1002/kjm2.12837

Effect of Bifidobacterium longum ‐EVs on the proliferation, apoptosis, migration, and invasion of A2780 cells. A2780 cells were incubated with 1, 5, and 10 μg/mL of B. longum ‐EVs (defined as B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups, respectively). (A) Cell viability was measured by the Cell Counting Kit‐8 (CCK‐8) after treatment for 24, 48, and 72 h. After a 24 h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. ** P < 0.01 and *** P < 0.001, versus the control group.
Figure Legend Snippet: Effect of Bifidobacterium longum ‐EVs on the proliferation, apoptosis, migration, and invasion of A2780 cells. A2780 cells were incubated with 1, 5, and 10 μg/mL of B. longum ‐EVs (defined as B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups, respectively). (A) Cell viability was measured by the Cell Counting Kit‐8 (CCK‐8) after treatment for 24, 48, and 72 h. After a 24 h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. ** P < 0.01 and *** P < 0.001, versus the control group.

Techniques Used: Migration, Incubation, Cell Counting, CCK-8 Assay, Staining, Double Staining, Control

Bifidobacterium longum ‐EVs enhances the sensitivity of A2780‐CBP/R cells to carboplatin (CBP). A2780‐CBP/R cells from different groups were treated with 10 μM of CBP, 1 μg/mL of B. longum ‐EVs, or the combination, whereas cells treated with PBS were considered the control. (A) The cell viability was detected by CCK‐8 assay after treatment for 24, 48, and 72 h. After a 24‐h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. * P < 0.05, ** P < 0.01, and *** P < 0.001, versus the control group; # # P < 0.01, and ### P < 0.001, versus the CBP group.
Figure Legend Snippet: Bifidobacterium longum ‐EVs enhances the sensitivity of A2780‐CBP/R cells to carboplatin (CBP). A2780‐CBP/R cells from different groups were treated with 10 μM of CBP, 1 μg/mL of B. longum ‐EVs, or the combination, whereas cells treated with PBS were considered the control. (A) The cell viability was detected by CCK‐8 assay after treatment for 24, 48, and 72 h. After a 24‐h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. * P < 0.05, ** P < 0.01, and *** P < 0.001, versus the control group; # # P < 0.01, and ### P < 0.001, versus the CBP group.

Techniques Used: Control, CCK-8 Assay, Migration, Staining, Double Staining

Bifidobacterium longum ‐EVs promote p53 Ser15 phosphorylation to increase p53 accumulation in A2780‐CBP/R cells. (A) A2780‐CBP/R cells from different groups were treated with 10 μM carboplatin (CBP), 1 μg/mL of B. longum ‐EVs, or the combination, whereas the cells treated with PBS were considered the control. After treatment for 24 h, cells from each group were harvested to analyze the expression levels of MRP1, ATP7A, ATP7B, and p53. (B) Extracts from A2780‐CBP/R cells from the B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups were immunoprecipitated with either control IgG or p53 antibodies, and the presence of p53 Ser15, Ser20, and Ser46 phosphorylation was determined by western blot analysis. (C) A2780‐CBP/R cells were transfected with p53S15D or p53wt or the combination with or without B. longum ‐EVs. The cells were then treated with MG132 for an additional 6 h before collecting cell lysates for the ubiquitination assay. *** P < 0.001, versus the control group; # # P < 0.01, and ### P < 0.001, versus the CBP group.
Figure Legend Snippet: Bifidobacterium longum ‐EVs promote p53 Ser15 phosphorylation to increase p53 accumulation in A2780‐CBP/R cells. (A) A2780‐CBP/R cells from different groups were treated with 10 μM carboplatin (CBP), 1 μg/mL of B. longum ‐EVs, or the combination, whereas the cells treated with PBS were considered the control. After treatment for 24 h, cells from each group were harvested to analyze the expression levels of MRP1, ATP7A, ATP7B, and p53. (B) Extracts from A2780‐CBP/R cells from the B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups were immunoprecipitated with either control IgG or p53 antibodies, and the presence of p53 Ser15, Ser20, and Ser46 phosphorylation was determined by western blot analysis. (C) A2780‐CBP/R cells were transfected with p53S15D or p53wt or the combination with or without B. longum ‐EVs. The cells were then treated with MG132 for an additional 6 h before collecting cell lysates for the ubiquitination assay. *** P < 0.001, versus the control group; # # P < 0.01, and ### P < 0.001, versus the CBP group.

Techniques Used: Phospho-proteomics, Control, Expressing, Immunoprecipitation, Western Blot, Transfection, Ubiquitin Proteomics

Bifidobacterium longum ‐EVs reverse carboplatin (CBP) resistance by promoting p53 Ser15 phosphorylation in A2780‐CBP/R cells. The p53S15D mutant was generated in A2780‐CBP/R cells. A2780‐CBP/R cells with the p53S15A mutant were treated with CBP alone or combined with B. longum‐ EVs, whereas the cells treated with PBS served as the control group. (A) Cell viability was measured by the CCK‐8 assay after treatment for 24, 48, and 72 h. After a 24‐h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. * P < 0.05, ** P < 0.01, and *** P < 0.001.
Figure Legend Snippet: Bifidobacterium longum ‐EVs reverse carboplatin (CBP) resistance by promoting p53 Ser15 phosphorylation in A2780‐CBP/R cells. The p53S15D mutant was generated in A2780‐CBP/R cells. A2780‐CBP/R cells with the p53S15A mutant were treated with CBP alone or combined with B. longum‐ EVs, whereas the cells treated with PBS served as the control group. (A) Cell viability was measured by the CCK‐8 assay after treatment for 24, 48, and 72 h. After a 24‐h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Techniques Used: Phospho-proteomics, Mutagenesis, Generated, Control, CCK-8 Assay, Migration, Staining, Double Staining



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Procell Inc a2780 ovc cell line cl-0013
Effect of Bifidobacterium longum ‐EVs on the proliferation, apoptosis, migration, and invasion of <t>A2780</t> cells. A2780 cells were incubated with 1, 5, and 10 μg/mL of B. longum ‐EVs (defined as B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups, respectively). (A) Cell viability was measured by the Cell Counting Kit‐8 (CCK‐8) after treatment for 24, 48, and 72 h. After a 24 h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. ** P < 0.01 and *** P < 0.001, versus the control group.
A2780 Ovc Cell Line Cl 0013, 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/a2780 ovc cell line cl-0013/product/Procell Inc
Average 90 stars, based on 1 article reviews
a2780 ovc cell line cl-0013 - by Bioz Stars, 2026-03
90/100 stars
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Effect of Bifidobacterium longum ‐EVs on the proliferation, apoptosis, migration, and invasion of A2780 cells. A2780 cells were incubated with 1, 5, and 10 μg/mL of B. longum ‐EVs (defined as B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups, respectively). (A) Cell viability was measured by the Cell Counting Kit‐8 (CCK‐8) after treatment for 24, 48, and 72 h. After a 24 h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. ** P < 0.01 and *** P < 0.001, versus the control group.

Journal: The Kaohsiung Journal of Medical Sciences

Article Title: Extracellular vesicles of Bifidobacterium longum reverse the acquired carboplatin resistance in ovarian cancer cells via p53 phosphorylation on Ser15

doi: 10.1002/kjm2.12837

Figure Lengend Snippet: Effect of Bifidobacterium longum ‐EVs on the proliferation, apoptosis, migration, and invasion of A2780 cells. A2780 cells were incubated with 1, 5, and 10 μg/mL of B. longum ‐EVs (defined as B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups, respectively). (A) Cell viability was measured by the Cell Counting Kit‐8 (CCK‐8) after treatment for 24, 48, and 72 h. After a 24 h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. ** P < 0.01 and *** P < 0.001, versus the control group.

Article Snippet: The A2780 OVC cell line (Procell no. CL‐0013) was grown in DMEM media with 10% FBS at 37°C.

Techniques: Migration, Incubation, Cell Counting, CCK-8 Assay, Staining, Double Staining, Control

Bifidobacterium longum ‐EVs enhances the sensitivity of A2780‐CBP/R cells to carboplatin (CBP). A2780‐CBP/R cells from different groups were treated with 10 μM of CBP, 1 μg/mL of B. longum ‐EVs, or the combination, whereas cells treated with PBS were considered the control. (A) The cell viability was detected by CCK‐8 assay after treatment for 24, 48, and 72 h. After a 24‐h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. * P < 0.05, ** P < 0.01, and *** P < 0.001, versus the control group; # # P < 0.01, and ### P < 0.001, versus the CBP group.

Journal: The Kaohsiung Journal of Medical Sciences

Article Title: Extracellular vesicles of Bifidobacterium longum reverse the acquired carboplatin resistance in ovarian cancer cells via p53 phosphorylation on Ser15

doi: 10.1002/kjm2.12837

Figure Lengend Snippet: Bifidobacterium longum ‐EVs enhances the sensitivity of A2780‐CBP/R cells to carboplatin (CBP). A2780‐CBP/R cells from different groups were treated with 10 μM of CBP, 1 μg/mL of B. longum ‐EVs, or the combination, whereas cells treated with PBS were considered the control. (A) The cell viability was detected by CCK‐8 assay after treatment for 24, 48, and 72 h. After a 24‐h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. * P < 0.05, ** P < 0.01, and *** P < 0.001, versus the control group; # # P < 0.01, and ### P < 0.001, versus the CBP group.

Article Snippet: The A2780 OVC cell line (Procell no. CL‐0013) was grown in DMEM media with 10% FBS at 37°C.

Techniques: Control, CCK-8 Assay, Migration, Staining, Double Staining

Bifidobacterium longum ‐EVs promote p53 Ser15 phosphorylation to increase p53 accumulation in A2780‐CBP/R cells. (A) A2780‐CBP/R cells from different groups were treated with 10 μM carboplatin (CBP), 1 μg/mL of B. longum ‐EVs, or the combination, whereas the cells treated with PBS were considered the control. After treatment for 24 h, cells from each group were harvested to analyze the expression levels of MRP1, ATP7A, ATP7B, and p53. (B) Extracts from A2780‐CBP/R cells from the B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups were immunoprecipitated with either control IgG or p53 antibodies, and the presence of p53 Ser15, Ser20, and Ser46 phosphorylation was determined by western blot analysis. (C) A2780‐CBP/R cells were transfected with p53S15D or p53wt or the combination with or without B. longum ‐EVs. The cells were then treated with MG132 for an additional 6 h before collecting cell lysates for the ubiquitination assay. *** P < 0.001, versus the control group; # # P < 0.01, and ### P < 0.001, versus the CBP group.

Journal: The Kaohsiung Journal of Medical Sciences

Article Title: Extracellular vesicles of Bifidobacterium longum reverse the acquired carboplatin resistance in ovarian cancer cells via p53 phosphorylation on Ser15

doi: 10.1002/kjm2.12837

Figure Lengend Snippet: Bifidobacterium longum ‐EVs promote p53 Ser15 phosphorylation to increase p53 accumulation in A2780‐CBP/R cells. (A) A2780‐CBP/R cells from different groups were treated with 10 μM carboplatin (CBP), 1 μg/mL of B. longum ‐EVs, or the combination, whereas the cells treated with PBS were considered the control. After treatment for 24 h, cells from each group were harvested to analyze the expression levels of MRP1, ATP7A, ATP7B, and p53. (B) Extracts from A2780‐CBP/R cells from the B. longum ‐EVs‐L, B. longum ‐EVs‐M, and B. longum ‐EVs‐H groups were immunoprecipitated with either control IgG or p53 antibodies, and the presence of p53 Ser15, Ser20, and Ser46 phosphorylation was determined by western blot analysis. (C) A2780‐CBP/R cells were transfected with p53S15D or p53wt or the combination with or without B. longum ‐EVs. The cells were then treated with MG132 for an additional 6 h before collecting cell lysates for the ubiquitination assay. *** P < 0.001, versus the control group; # # P < 0.01, and ### P < 0.001, versus the CBP group.

Article Snippet: The A2780 OVC cell line (Procell no. CL‐0013) was grown in DMEM media with 10% FBS at 37°C.

Techniques: Phospho-proteomics, Control, Expressing, Immunoprecipitation, Western Blot, Transfection, Ubiquitin Proteomics

Bifidobacterium longum ‐EVs reverse carboplatin (CBP) resistance by promoting p53 Ser15 phosphorylation in A2780‐CBP/R cells. The p53S15D mutant was generated in A2780‐CBP/R cells. A2780‐CBP/R cells with the p53S15A mutant were treated with CBP alone or combined with B. longum‐ EVs, whereas the cells treated with PBS served as the control group. (A) Cell viability was measured by the CCK‐8 assay after treatment for 24, 48, and 72 h. After a 24‐h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Journal: The Kaohsiung Journal of Medical Sciences

Article Title: Extracellular vesicles of Bifidobacterium longum reverse the acquired carboplatin resistance in ovarian cancer cells via p53 phosphorylation on Ser15

doi: 10.1002/kjm2.12837

Figure Lengend Snippet: Bifidobacterium longum ‐EVs reverse carboplatin (CBP) resistance by promoting p53 Ser15 phosphorylation in A2780‐CBP/R cells. The p53S15D mutant was generated in A2780‐CBP/R cells. A2780‐CBP/R cells with the p53S15A mutant were treated with CBP alone or combined with B. longum‐ EVs, whereas the cells treated with PBS served as the control group. (A) Cell viability was measured by the CCK‐8 assay after treatment for 24, 48, and 72 h. After a 24‐h treatment, (B) cell proliferation, (C) apoptosis, (D) migration, and (E) invasion were detected by Edu staining, Annexin V‐FITC/PI double staining, wound healing, and Transwell assays, respectively. * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: The A2780 OVC cell line (Procell no. CL‐0013) was grown in DMEM media with 10% FBS at 37°C.

Techniques: Phospho-proteomics, Mutagenesis, Generated, Control, CCK-8 Assay, Migration, Staining, Double Staining