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CLS Cell Lines Service GmbH
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Biopharm GmbH
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iCell Bioscience Inc
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Image Search Results
Journal: Stem Cell Research & Therapy
Article Title: Transplantation of gastric epithelial mitochondria into human gastric cancer cells inhibits tumor growth and enhances chemosensitivity by reducing cancer stemness and modulating gastric cancer metabolism
doi: 10.1186/s13287-025-04223-7
Figure Lengend Snippet: Transplanted GES-1 gastric epithelial mitochondria suppress gastric cancer cell stemness. ( A ) Protein expression of stemness markers (SOX2 and NANOG) after GES-1 mitochondrial transplantation for 24 h in MKN45 cells. ( B ) Quantification of SOX2 and NANOG expression. ( C ) GRP78 expression after GES-1 mitochondrial transplantation for 24 h. ( D ) Quantification of GRP78 expression. ( E ) CD44 positive cells on MKN45 or AGS cells after GES-1 mitochondrial transplantation for 24 h. ( F ) Quantification of CD44 positive cells. ( G ) ALDH1 activity after mitochondrial transplantation for 24 h in MKN45 cells. ( H ) Quantification of ALDH1 activity. ( I ) CD24 positive cells after GES-1 mitochondrial transplantation for 24 h in MKN45 cells. ( J ) Quantification of CD24 positive cells. ( K ) LGR5 positive cells after GES-1 mitochondrial transplantation for 24 h in MKN45 cells. ( L ) Quantification of LGR5 positive cells. ( M ) Expression of p-JNK and JNK after GES-1 mitochondrial transplantation for 24 h in MKN45 cells. ( N ) NOTCH1 expression after GES-1 mitochondrial transplantation for 24 h in MKN45 cells. The data are presented as the means ± SEMs; n ≥ 3 for independent experiments; two-tailed Student’s t test: * p < 0.05 and ** p < 0.01
Article Snippet: The normal
Techniques: Expressing, Transplantation Assay, Activity Assay, Two Tailed Test
Journal: Stem Cell Research & Therapy
Article Title: Transplantation of gastric epithelial mitochondria into human gastric cancer cells inhibits tumor growth and enhances chemosensitivity by reducing cancer stemness and modulating gastric cancer metabolism
doi: 10.1186/s13287-025-04223-7
Figure Lengend Snippet: Transplanted GES-1 gastric epithelial mitochondria into gastric cancer cells increased the level of intracellular ROS and modulated mitochondrial metabolism. ( A ) Superoxide generation in mitochondria was analyzed by performing mitoSOX Deep Red staining through flow cytometry after GES-1 mitochondrial transplantation for 24 h in MKN45 or AGS cells. ( B ) Quantification of mitochondrial superoxide generation. ( C ) Intracellular superoxide level was analyzed by performing DHE staining through flow cytometry after GES-1 mitochondrial transplantation for 24 h in MKN45 or AGS cells. ( D ) Quantification of intracellular superoxide level. ( E ) OXPHOS profiles, ( F ) spare respiratory capacity, ( G ) maximal respiration, and ( H ) basal respiration of MKN45 cells after GES-1 mitochondrial transplantation for 24 h were evaluated via a Seahorse bioanalyzer. ( I ) ATP concentration was analyzed via an ATPlite kit. Data are presented as the means ± SEMs; n ≥ 3 for independent experiments; two-tailed Student’s t test: * p < 0.05 and ** p < 0.01
Article Snippet: The normal
Techniques: Staining, Flow Cytometry, Transplantation Assay, Concentration Assay, Two Tailed Test
Journal: Stem Cell Research & Therapy
Article Title: Transplantation of gastric epithelial mitochondria into human gastric cancer cells inhibits tumor growth and enhances chemosensitivity by reducing cancer stemness and modulating gastric cancer metabolism
doi: 10.1186/s13287-025-04223-7
Figure Lengend Snippet: Glycolytic and mitochondrial biogenesis proteins were downregulated after epithelial mitochondrial transplantation. ( A ) Protein expression of PKM2, MCT1, and MCT4 after GES-1 mitochondrial transplantation for 24 h in MKN45 cells. ( B ) Quantification of PKM2, MCT1, and MCT4 expression after GES-1 mitochondrial transplantation for 24 h. ( C ) Lactate metabolism were analyzed using a Lactate-Glo Assay Kit after GES-1 mitochondrial transplantation for 24 h in MKN45 cells. ( D ) Lactate secretion by MKN45 and GES-1 cells was analyzed using a Lactate-Glo Assay Kit. ( E ) Protein expression of PGC-1α after GES-1 mitochondrial transplantation for 24 h in MKN45 cells. ( F ) Quantification of PGC-1α. The data are presented as the means ± SEMs; n ≥ 3 for independent experiments; two-tailed Student’s t test: * p < 0.05 and *** p < 0.005
Article Snippet: The normal
Techniques: Transplantation Assay, Expressing, Glo Assay, Two Tailed Test
Journal: Stem Cell Research & Therapy
Article Title: Transplantation of gastric epithelial mitochondria into human gastric cancer cells inhibits tumor growth and enhances chemosensitivity by reducing cancer stemness and modulating gastric cancer metabolism
doi: 10.1186/s13287-025-04223-7
Figure Lengend Snippet: Pretreatment of epithelial mitochondria into gastric cancer cells suppressed tumor growth in a mouse tumor xenograft model. ( A ) Experimental design and flowchart of the mouse xenograft model and mitochondrial treatment. AGS cells were pretreated with GES-1 mitochondria for 24 h before injection. ( B ) Schematic of the gastric cancer xenografts in each group. ( C ) Body weights of mice in each group. ( D ) Tumor growth curves of each group. ( E ) Gastric tumors harvested from each group. ( F ) Representative images of hematoxylin and eosin and IHC staining of Ki-67 and GRP78 in each group. ( G ). Representative IHC analysis of ki-67 staining in each group. ( H ) Representative IHC analysis of GRP78 in each group. The data are presented as the means ± SEMs; n ≥ 3 for independent experiments; two-tailed Student’s t test: ** p < 0.01 and *** p < 0.005
Article Snippet: The normal
Techniques: Injection, Immunohistochemistry, Staining, Two Tailed Test
Journal: Stem Cell Research & Therapy
Article Title: Transplantation of gastric epithelial mitochondria into human gastric cancer cells inhibits tumor growth and enhances chemosensitivity by reducing cancer stemness and modulating gastric cancer metabolism
doi: 10.1186/s13287-025-04223-7
Figure Lengend Snippet: Transplantation of gastric epithelial mitochondria promoted gastric cancer cell apoptosis under hypoxic conditions and enhanced chemosensitivity. ( A ) MKN45 or ( B ) AGS cells ( C ) were treated with CoCl 2 and GES-1 mitochondria for 48 h. Cell viability was analyzed via an SRB assay. Protein expression and quantification of HIF-1α in ( C ) MKN45 or ( D ) AGS cells were measured after GES-1 mitochondrial transplantation under hypoxic conditions for 24 h. ( E ) Protein expression and quantification of Drp1 in ( C ) MKN45 or ( D ) AGS cells were analyzed after GES-1 mitochondrial transplantation under hypoxic conditions. ( G ) Apoptotic protein expression was quantified on the basis of the c-csapase3/caspase3 ratio via Western blotting. ( H , I ) Caspase activity in AGS cells was analyzed through flow cytometry. ( J , K ) Caspase activity in MKN45 cells was analyzed through flow cytometry. The data are presented as the means ± SEMs; n ≥ 3 for independent experiments; two-tailed Student’s t test: * p < 0.05, ** p < 0.01 and *** p < 0.001; # p < 0.05, ## p < 0.01 and ### p < 0.005
Article Snippet: The normal
Techniques: Transplantation Assay, Sulforhodamine B Assay, Expressing, Western Blot, Activity Assay, Flow Cytometry, Two Tailed Test
Journal: Stem Cell Research & Therapy
Article Title: Transplantation of gastric epithelial mitochondria into human gastric cancer cells inhibits tumor growth and enhances chemosensitivity by reducing cancer stemness and modulating gastric cancer metabolism
doi: 10.1186/s13287-025-04223-7
Figure Lengend Snippet: Human gastric epithelial mitochondria reduce gastric cancer cell chemoresistance by promoting apoptosis. ( A , B ) MKN45 or AGS cells were treated with 5-FU or GES-1 mitochondria or both in combination for 24 h. Cell viability was analyzed via SRB Assay. ( C , D ) Protein expression and quantification of BAX in MKN45 or AGS cells were analyzed after treatment for 72 h. ( E – H ) Caspase activity in MKN45 or AGS cells was analyzed through flow cytometry. ( J ) Quantification of protein expression (p-AKT/AKT ratio) in MKN45 cells after GES-1 mitochondrial transplantation. The data are presented as the means ± SEMs; n ≥ 3 for independent experiments; two-tailed Student’s t test: ** p < 0.01 and *** p < 0.001; # p < 0.05, ## p < 0.01 and ### p < 0.005
Article Snippet: The normal
Techniques: Sulforhodamine B Assay, Expressing, Activity Assay, Flow Cytometry, Transplantation Assay, Two Tailed Test
Journal: Experimental and Therapeutic Medicine
Article Title: KLF5‑mediated expression of CARD11 promotes the progression of gastric cancer
doi: 10.3892/etm.2023.12121
Figure Lengend Snippet: CARD11 is highly expressed in gastric cancer and is associated with poor prognosis. (A) The ENCORI database predicted the expression of CARD11 in tissues of patients with gastric cancer. *** P<0.001 vs. the cancer group. (B) The ENCORI database predicted the association of CARD11 overexpression with overall survival. Cutoff-High, median 50% and Cutoff-Low, median 50%. The expression levels of CARD11 in normal gastric epithelial cells and in gastric cancer cells were detected by (C) reverse transcription-quantitative PCR and (D) western blotting. ** P<0.01 and *** P<0.001 vs. the GES-1 group. CARD, caspase recruitment domain-containing protein; ENCORI, the encyclopedia of RNA interactomes.
Article Snippet:
Techniques: Expressing, Over Expression, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot
Journal: Experimental and Therapeutic Medicine
Article Title: KLF5‑mediated expression of CARD11 promotes the progression of gastric cancer
doi: 10.3892/etm.2023.12121
Figure Lengend Snippet: Interference of CARD11 expression inhibits gastric cancer cell metastasis. The (A) migratory and (B) invasive abilities of gastric cancer cells transfected with si-CARD11 were detected by wound healing and Transwell assays. (C) The expression levels of EMT-related proteins in gastric cancer cells transfected with si-CARD11 were detected by western blot analysis. *** P<0.001 vs. the control group. ### P<0.001 vs. the si-NC group. CARD, caspase recruitment domain-containing protein; si, small interfering; EMT, epithelial-to-mesenchymal transition.
Article Snippet:
Techniques: Expressing, Transfection, Western Blot, Control
Journal: Experimental and Therapeutic Medicine
Article Title: KLF5‑mediated expression of CARD11 promotes the progression of gastric cancer
doi: 10.3892/etm.2023.12121
Figure Lengend Snippet: KLF5 regulates CARD11 to promote malignant progression of gastric cancer might by activating mTOR pathway. The viability, proliferation and cell cycle of gastric cancer cells transfected with si-CARD11 and oe-KLF5 was analyzed by (A) CCK-8, (B and C) EdU staining and (D) flow cytometry analysis. The (E) migration and (F) invasion of gastric cancer cells transfected with si-CARD11 and oe-KLF5 was detected by wound healing and Transwell assays. (G) The expression of EMT-related proteins in gastric cancer cells transfected with si-CARD11 and oe-KLF5 was detected by western blotting. (H) The expression of mTOR pathway related proteins n gastric cancer cells transfected with si-CARD11 and oe-KLF5 was detected by western blotting. *** P<0.001 vs. Control group. # P<0.05, ## P<0.01 and ### P<0.001 vs. si-CARD11 group. KLF5, Krüppel-like factor 5; CARD, caspase recruitment domain-containing protein; si, small interfering; oe, overexpression; EMT, epithelial-to-mesenchymal transition; p-. phosphorylated.
Article Snippet:
Techniques: Transfection, CCK-8 Assay, Staining, Flow Cytometry, Migration, Expressing, Western Blot, Control, Over Expression