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fdft1 inhibitor ym  (MedChemExpress)
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Identification of the antitumor targets of ATA. ( A ) Overlap of the predicted targets of ATA (blue) and disease targets from the transcriptomic data (pink). ( B ) Function analysis of fifteen common targets via GeneMANIA. (C) Binding pattern diagram of ATA and the target proteins <t>FDFT1,</t> PPARA, and PPARG. The yellow dashed line represents the hydrogen bond interaction. ( D – F ) After pre-incubation with or without YM-53601 (2.5 μM and 5 µM, ( D )), GW6471 (2.5 μM and 5 µM, ( E )), or GW9662 (5 μM and 10 µM, ( F )) for 30 min, HCT116 cells were treated with ATA (0 μM, 10 μM, and 15 µM) for 48 h. The cell viabilities were detected via the MTT assay. The data are expressed as means ± SD ( n = 3). ** p < 0.01 and *** p < 0.001 vs. control (Ctrl). ( G ) Venn diagram of predicted targets for ATA, OA, and UA. Five genes in red were identified as ATA-specific targets. ( H ) The cell viabilities of HCT116 cells treated with ATA, UA, and OA for 48 h were detected via the MTT assay and the IC 50 values were calculated using Graphpad Prism 9.0 software.
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Identification of the antitumor targets of ATA. ( A ) Overlap of the predicted targets of ATA (blue) and disease targets from the transcriptomic data (pink). ( B ) Function analysis of fifteen common targets via GeneMANIA. (C) Binding pattern diagram of ATA and the target proteins FDFT1, PPARA, and PPARG. The yellow dashed line represents the hydrogen bond interaction. ( D – F ) After pre-incubation with or without YM-53601 (2.5 μM and 5 µM, ( D )), GW6471 (2.5 μM and 5 µM, ( E )), or GW9662 (5 μM and 10 µM, ( F )) for 30 min, HCT116 cells were treated with ATA (0 μM, 10 μM, and 15 µM) for 48 h. The cell viabilities were detected via the MTT assay. The data are expressed as means ± SD ( n = 3). ** p < 0.01 and *** p < 0.001 vs. control (Ctrl). ( G ) Venn diagram of predicted targets for ATA, OA, and UA. Five genes in red were identified as ATA-specific targets. ( H ) The cell viabilities of HCT116 cells treated with ATA, UA, and OA for 48 h were detected via the MTT assay and the IC 50 values were calculated using Graphpad Prism 9.0 software.

Journal: International Journal of Molecular Sciences

Article Title: 3 β -Hydroxy-12-oleanen-27-oic Acid Exerts an Antiproliferative Effect on Human Colon Carcinoma HCT116 Cells via Targeting FDFT1

doi: 10.3390/ijms241915020

Figure Lengend Snippet: Identification of the antitumor targets of ATA. ( A ) Overlap of the predicted targets of ATA (blue) and disease targets from the transcriptomic data (pink). ( B ) Function analysis of fifteen common targets via GeneMANIA. (C) Binding pattern diagram of ATA and the target proteins FDFT1, PPARA, and PPARG. The yellow dashed line represents the hydrogen bond interaction. ( D – F ) After pre-incubation with or without YM-53601 (2.5 μM and 5 µM, ( D )), GW6471 (2.5 μM and 5 µM, ( E )), or GW9662 (5 μM and 10 µM, ( F )) for 30 min, HCT116 cells were treated with ATA (0 μM, 10 μM, and 15 µM) for 48 h. The cell viabilities were detected via the MTT assay. The data are expressed as means ± SD ( n = 3). ** p < 0.01 and *** p < 0.001 vs. control (Ctrl). ( G ) Venn diagram of predicted targets for ATA, OA, and UA. Five genes in red were identified as ATA-specific targets. ( H ) The cell viabilities of HCT116 cells treated with ATA, UA, and OA for 48 h were detected via the MTT assay and the IC 50 values were calculated using Graphpad Prism 9.0 software.

Article Snippet: Ursolic acid (UA, ≥ 98%), oleanolic acid (OA, ≥ 98%), and 23-hydroxybetulinic acid (23-HA, ≥ 98%) were purchased from Chengdu Lemeitian Pharmaceutical Technology Co., Ltd., Sichuan, China; β -elemene (≥ 98%) was obtained from Shanghai Yuanye Bio-Technology Co., Ltd., Shanghai, China; cisplatin, oxaliplatin, PPARγ inhibitor GW9662, and PPARα inhibitor GW6471 were purchased from Selleck Chemicals, Houston, TX, USA; the FDFT1 inhibitor YM-53601 was obtained from MedChemExpress Technology, Monmouth Junction, NJ, USA.

Techniques: Binding Assay, Incubation, MTT Assay, Control, Software

FDFT1 mediated the cytotoxicity of ATA towards HCT116 cells. ( A ) The gene expression levels of FDFT1 in the HCT116 cells treated with ATA for different times via the RT-qPCR assay. ( B , C ) The protein expression levels of FDFT1 in the HCT116 cells treated with ATA (7.5, 15 and 30 μM) for 24 h via Western blotting. The figure ( B ) shown is representative of three independent experiments. The data ( C ) are expressed as means ± SD ( n = 3). * p < 0.05 and ** p < 0.01 vs. Ctrl (0 μM). ( D – F ) After pre-incubation with or without the FDFT1 inhibitor YM-53601 (2 and 4 µM) for 30 min, HCT116 cells were treated with ATA (0 µM, 5 µM, and 7.5 µM, D), OA (100 μM, E), or UA (40 μM, F) for 24 h. The cell viabilities were detected via the MTT assay. The data are expressed as means ± SD ( n = 3). * p < 0.05 vs. the control (Ctrl). ( G – H ) After pre-incubation with or without YM-53601 (4 µM, 30 min), the HCT116 cells were treated with ATA (20 μM) for 24 h. The autophagic flux was observed through the mRFP-GFP-LC3 assay. The figure ( G ) shown is representative of three independent experiments. The cell apoptosis was determined using FCM. The figure ( H ) is representative of three independent experiments. The apoptotic percentages ( I ) are expressed as means ± SD ( n = 3). *** p < 0.001 vs. Ctrl. ( J – L ) The mRNA ( J ) and protein ( K , L ) expression levels of FDFT1 in HCT116 cells were detected using RT-qPCR and Western blotting after transfection with FDFT1 siRNA for 24 h and 48 h, respectively. siNC—negative control siRNA. The figure ( K ) shown is representative of three independent experiments. The data ( J , L ) are expressed as means ± SD ( n = 3). * p < 0.05 and *** p < 0.001 vs. siNC. ( M ) The HCT116 cells were transfected with FDFT1 siRNAs for 48 h, followed by exposure to ATA at indicated concentrations for another 48 h. The cell viabilities were detected through the MTT assay. The data are expressed as means ± SD ( n = 3). * p < 0.05 and *** p < 0.001 vs. siNC.

Journal: International Journal of Molecular Sciences

Article Title: 3 β -Hydroxy-12-oleanen-27-oic Acid Exerts an Antiproliferative Effect on Human Colon Carcinoma HCT116 Cells via Targeting FDFT1

doi: 10.3390/ijms241915020

Figure Lengend Snippet: FDFT1 mediated the cytotoxicity of ATA towards HCT116 cells. ( A ) The gene expression levels of FDFT1 in the HCT116 cells treated with ATA for different times via the RT-qPCR assay. ( B , C ) The protein expression levels of FDFT1 in the HCT116 cells treated with ATA (7.5, 15 and 30 μM) for 24 h via Western blotting. The figure ( B ) shown is representative of three independent experiments. The data ( C ) are expressed as means ± SD ( n = 3). * p < 0.05 and ** p < 0.01 vs. Ctrl (0 μM). ( D – F ) After pre-incubation with or without the FDFT1 inhibitor YM-53601 (2 and 4 µM) for 30 min, HCT116 cells were treated with ATA (0 µM, 5 µM, and 7.5 µM, D), OA (100 μM, E), or UA (40 μM, F) for 24 h. The cell viabilities were detected via the MTT assay. The data are expressed as means ± SD ( n = 3). * p < 0.05 vs. the control (Ctrl). ( G – H ) After pre-incubation with or without YM-53601 (4 µM, 30 min), the HCT116 cells were treated with ATA (20 μM) for 24 h. The autophagic flux was observed through the mRFP-GFP-LC3 assay. The figure ( G ) shown is representative of three independent experiments. The cell apoptosis was determined using FCM. The figure ( H ) is representative of three independent experiments. The apoptotic percentages ( I ) are expressed as means ± SD ( n = 3). *** p < 0.001 vs. Ctrl. ( J – L ) The mRNA ( J ) and protein ( K , L ) expression levels of FDFT1 in HCT116 cells were detected using RT-qPCR and Western blotting after transfection with FDFT1 siRNA for 24 h and 48 h, respectively. siNC—negative control siRNA. The figure ( K ) shown is representative of three independent experiments. The data ( J , L ) are expressed as means ± SD ( n = 3). * p < 0.05 and *** p < 0.001 vs. siNC. ( M ) The HCT116 cells were transfected with FDFT1 siRNAs for 48 h, followed by exposure to ATA at indicated concentrations for another 48 h. The cell viabilities were detected through the MTT assay. The data are expressed as means ± SD ( n = 3). * p < 0.05 and *** p < 0.001 vs. siNC.

Article Snippet: Ursolic acid (UA, ≥ 98%), oleanolic acid (OA, ≥ 98%), and 23-hydroxybetulinic acid (23-HA, ≥ 98%) were purchased from Chengdu Lemeitian Pharmaceutical Technology Co., Ltd., Sichuan, China; β -elemene (≥ 98%) was obtained from Shanghai Yuanye Bio-Technology Co., Ltd., Shanghai, China; cisplatin, oxaliplatin, PPARγ inhibitor GW9662, and PPARα inhibitor GW6471 were purchased from Selleck Chemicals, Houston, TX, USA; the FDFT1 inhibitor YM-53601 was obtained from MedChemExpress Technology, Monmouth Junction, NJ, USA.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Incubation, MTT Assay, Control, Transfection, Negative Control

ATA inhibited the tumor growth of HCT116 xenografts in nude mice. ( A ) Tumor anatomy of HCT116 subcutaneous tumor-bearing mice. Scale bar = 10 mm. ( B ) Growth curve of tumor volume. ( C ) Average final tumor weights of each group. ( D ) Body weights of tumor-bearing mice. ( E , F ) Expression levels of FDFT1, LC3, p62, cyclinD1, pro-caspase3, and GPX4 in tumor tissues from Ctrl and ATA (60 mg/kg) groups via Western blotting. The data were expressed as means ± SD ( n = 4). * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. Ctrl.

Journal: International Journal of Molecular Sciences

Article Title: 3 β -Hydroxy-12-oleanen-27-oic Acid Exerts an Antiproliferative Effect on Human Colon Carcinoma HCT116 Cells via Targeting FDFT1

doi: 10.3390/ijms241915020

Figure Lengend Snippet: ATA inhibited the tumor growth of HCT116 xenografts in nude mice. ( A ) Tumor anatomy of HCT116 subcutaneous tumor-bearing mice. Scale bar = 10 mm. ( B ) Growth curve of tumor volume. ( C ) Average final tumor weights of each group. ( D ) Body weights of tumor-bearing mice. ( E , F ) Expression levels of FDFT1, LC3, p62, cyclinD1, pro-caspase3, and GPX4 in tumor tissues from Ctrl and ATA (60 mg/kg) groups via Western blotting. The data were expressed as means ± SD ( n = 4). * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. Ctrl.

Article Snippet: Ursolic acid (UA, ≥ 98%), oleanolic acid (OA, ≥ 98%), and 23-hydroxybetulinic acid (23-HA, ≥ 98%) were purchased from Chengdu Lemeitian Pharmaceutical Technology Co., Ltd., Sichuan, China; β -elemene (≥ 98%) was obtained from Shanghai Yuanye Bio-Technology Co., Ltd., Shanghai, China; cisplatin, oxaliplatin, PPARγ inhibitor GW9662, and PPARα inhibitor GW6471 were purchased from Selleck Chemicals, Houston, TX, USA; the FDFT1 inhibitor YM-53601 was obtained from MedChemExpress Technology, Monmouth Junction, NJ, USA.

Techniques: Expressing, Western Blot

Hypothetical pathway of FDFT1 in mediating the cytotoxic effect of ATA against HCT116 cells.

Journal: International Journal of Molecular Sciences

Article Title: 3 β -Hydroxy-12-oleanen-27-oic Acid Exerts an Antiproliferative Effect on Human Colon Carcinoma HCT116 Cells via Targeting FDFT1

doi: 10.3390/ijms241915020

Figure Lengend Snippet: Hypothetical pathway of FDFT1 in mediating the cytotoxic effect of ATA against HCT116 cells.

Article Snippet: Ursolic acid (UA, ≥ 98%), oleanolic acid (OA, ≥ 98%), and 23-hydroxybetulinic acid (23-HA, ≥ 98%) were purchased from Chengdu Lemeitian Pharmaceutical Technology Co., Ltd., Sichuan, China; β -elemene (≥ 98%) was obtained from Shanghai Yuanye Bio-Technology Co., Ltd., Shanghai, China; cisplatin, oxaliplatin, PPARγ inhibitor GW9662, and PPARα inhibitor GW6471 were purchased from Selleck Chemicals, Houston, TX, USA; the FDFT1 inhibitor YM-53601 was obtained from MedChemExpress Technology, Monmouth Junction, NJ, USA.

Techniques: