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Image Search Results
Journal: bioRxiv
Article Title: Folate Receptor α Contributes to Radiation Resistance in Neuroendocrine Prostate Cancer by Regulating Redox Homeostasis
doi: 10.64898/2026.03.26.714502
Figure Lengend Snippet: A. Total spectrum counts of differentially expressed surface proteins between control and radioresistant LNCaP cells is shown. B. FOLR1 expression counts (Log(Fragments per Kilobase million) were plotted using RNA-seq data from prostate tumors available at cBioportal. C . FOLR1 mRNA levels were quantified in LNCaP and LNCaP-RR cells using qPCR. D . FOLR1 mRNA levels were quantified in PC3 and PC3-RR cells using qPCR. E . Surface expression of FOLR1 was quantified in LNCaP, LNCaP-RR, PC3 and PC3-RR cells using flow cytometry.
Article Snippet: We used the following antibodies: Synaptophysin (Thermofisher, SP11, MA5-16402), GAPDH (Cell Signaling, 14C10, 2118S), HIF1alpha (Cell Signaling, 3716S), Vinculin (Abcam, Ab91459),
Techniques: Control, Expressing, RNA Sequencing, Flow Cytometry
Journal: bioRxiv
Article Title: Folate Receptor α Contributes to Radiation Resistance in Neuroendocrine Prostate Cancer by Regulating Redox Homeostasis
doi: 10.64898/2026.03.26.714502
Figure Lengend Snippet: A. HIF-1α protein was quantified in LNCaP and LNCaP-RR cells using immunoblotting. B . HIF-1α mRNA was quantified in LNCaP and LNCaP-RR cells using qPCR. C. HIF-1α protein was quantified in PC3 and PC3-RR cells using immunoblotting. D . HIF-1α mRNA was quantified in PC3 and PC3-RR cells by qPCR. E. Synaptophysin protein expression was quantified by immunoblotting in LNCaP-RR cells after shRNA mediated downregulation of HIF-1α. F. HIF-1α and FOLR1 mRNA expression was quantified by qPCR in LNCaP-RR cells after shRNA mediated downregulation of HIF-1α. G. FOLR1 surface expression was quantified by flow cytometry in LNCaP-RR cells after shRNA mediated downregulation of HIF-1α. H. HIF-1α and FOLR1 mRNA expression was quantified by qPCR in PC3-RR cells after shRNA mediated downregulation of HIF-1α. I. FOLR1 mRNA expression was quantified by qPCR in LNCaP and PC3 cells after culturing cells in CoCl 2 for 2, 4 and 6 days. J. Synaptophysin protein expression was quantified by immunoblotting in LNCaP-RR cells after culturing cells in 1 uM methotrexate for 24h. K. Synaptophysin mRNA expression was quantified by qPCR in LNCaP-RR cells after shRNA mediated downregulation of FOLR1. L. Synaptophysin protein expression was quantified by immunoblotting in PC3 cells after culturing cells in CoCl2 and methotrexate for 24 hours.
Article Snippet: We used the following antibodies: Synaptophysin (Thermofisher, SP11, MA5-16402), GAPDH (Cell Signaling, 14C10, 2118S), HIF1alpha (Cell Signaling, 3716S), Vinculin (Abcam, Ab91459),
Techniques: Western Blot, Expressing, shRNA, Flow Cytometry
Journal: bioRxiv
Article Title: Folate Receptor α Contributes to Radiation Resistance in Neuroendocrine Prostate Cancer by Regulating Redox Homeostasis
doi: 10.64898/2026.03.26.714502
Figure Lengend Snippet: A. FOLR1 surface expression was quantified by flow cytometry in LNCaP-RR cells after shRNA mediated downregulation of HIF1A (shRNA-2). B. HIF1A mRNA expression was quantified by qPCR in LNCaP-RR cells after shRNA (shRNA-2) mediated downregulation of FOLR1. C. Synaptophysin protein expression was quantified by immunoblotting in PC3-RR cells after shRNA mediated downregulation of HIF-1α. D. Syp mRNA expression was quantified by qPCR in LNCaP-RR cells after culturing them in CoCl 2 for 24 hours. E. HIF-1α protein levels were quantified by immunoblotting in PC3 cells after culturing cells in CoCl 2 for 2, 4 and 6 days. F. SLC7A11 and GPX4 mRNA expression was quantified by qPCR in LNCaP-RR cells after shRNA mediated downregulation of FOLR1.
Article Snippet: We used the following antibodies: Synaptophysin (Thermofisher, SP11, MA5-16402), GAPDH (Cell Signaling, 14C10, 2118S), HIF1alpha (Cell Signaling, 3716S), Vinculin (Abcam, Ab91459),
Techniques: Expressing, Flow Cytometry, shRNA, Western Blot
Journal: bioRxiv
Article Title: Folate Receptor α Contributes to Radiation Resistance in Neuroendocrine Prostate Cancer by Regulating Redox Homeostasis
doi: 10.64898/2026.03.26.714502
Figure Lengend Snippet: A. FOLR1 mRNA expression was quantified by qPCR in LNCaP-RR cells after shRNA mediated downregulation of FOLR1. B. Clonogenic assay of LNCaP-RR control and shFOLR1 cells after irradiation (0-8 Gy) is shown. C. Clonogenic assay of LNCaP-RR cells treated with 1uM methotrexate after irradiation (0-8 Gy) is shown. D . Overexpression of FOLR1 in PC3 cells was confirmed by flow cytometry. E. Clonogenic assay of PC3 cells (control or overexpressing FOLR1) after irradiation (0-10 Gy) is shown. F. Clonogenic assay of LNCaP-RR cells performed under control or folate-reduced conditions after irradiation (0-8 Gy) is shown. G. Clonogenic assay of PC3-RR cells performed under control or folate-reduced conditions after irradiation (0-10 Gy) is shown.
Article Snippet: We used the following antibodies: Synaptophysin (Thermofisher, SP11, MA5-16402), GAPDH (Cell Signaling, 14C10, 2118S), HIF1alpha (Cell Signaling, 3716S), Vinculin (Abcam, Ab91459),
Techniques: Expressing, shRNA, Clonogenic Assay, Control, Irradiation, Over Expression, Flow Cytometry
Journal: bioRxiv
Article Title: Folate Receptor α Contributes to Radiation Resistance in Neuroendocrine Prostate Cancer by Regulating Redox Homeostasis
doi: 10.64898/2026.03.26.714502
Figure Lengend Snippet: A. The levels of GSH were quantified in LNCaP and LNCaP-RR cells. B. The relative levels of GSH were quantified in LNCaP-RR cells after shRNA mediated downregulation of FOLR1. C. Relative levels of total ROS measured by DCF fluorescence is compared between LNCaP, LNCaP-RR and LNCaP-shFOLR1 at 24 hrs post radiation (4 Gy). D. Relative levels of total ROS measured by DCF fluorescence in LNCaP-RR cells cultured with or without Methotrexate (1uM) is shown 24 hrs after radiation (4 Gy). E. Bar graph plotted using mean fluorescence intensty to show retention of cell tracer violet dye in control, RR and RR with FOLR1 shRNAs populations of LNCaP cells. F . Level of Ki-67 mRNA levels was quantified by qPCR in control and PC3-RR cells. G . Effect of FOLR1 overexpression in PC3 cells on mRNA levels of Myc, Ki-67 and CDC25 was quantified by qPCR. H. Level of Ki-67 mRNA levels was quantified by qPCR in control, LNCaP-RR and LNCaP-RR-FOLR1shRNAs cells
Article Snippet: We used the following antibodies: Synaptophysin (Thermofisher, SP11, MA5-16402), GAPDH (Cell Signaling, 14C10, 2118S), HIF1alpha (Cell Signaling, 3716S), Vinculin (Abcam, Ab91459),
Techniques: shRNA, Fluorescence, Cell Culture, Control, Over Expression
Journal: Advanced Science
Article Title: TRIM47 Regulates Energy Metabolism via Glycolytic Reprogramming to Drive Hepatocellular Carcinoma Progression and Represents an Efficient Therapeutic Target
doi: 10.1002/advs.202416996
Figure Lengend Snippet: Mechanism of TRIM47 in HCC progression, and therapeutic potential of siTRIM47 nanoparticles (NPs). (A) TRIM47 is significantly upregulated in HCC tissues compared to normal tissues ( n = 72, *** p < 0.001. Data are expressed in mean ± SD), correlating with poorer patient survival (High = 36, Low = 36). (B) Schematic representation of TRIM47's role in HCC progression. TRIM47 promotes ubiquitin‐mediated degradation of FBP1, enhancing glycolysis, increasing lactic acid, adenosine triphosphate (ATP), and reactive oxygen species (ROS) production, which supports cancer cell proliferation and metastasis. Bortezomib inhibits TRIM47‐mediated FBP1 degradation, thereby reducing glycolytic activity. siTRIM47@PD NPs, consisting of PLA and DC‐Chol, target TRIM47, resulting in significant inhibition of tumor growth and metastasis, as demonstrated in an orthotopic HCC model.
Article Snippet: The appropriate primary antibodies, Flag and
Techniques: Ubiquitin Proteomics, Activity Assay, Inhibition
Journal: Advanced Science
Article Title: TRIM47 Regulates Energy Metabolism via Glycolytic Reprogramming to Drive Hepatocellular Carcinoma Progression and Represents an Efficient Therapeutic Target
doi: 10.1002/advs.202416996
Figure Lengend Snippet: TRIM47 Interacts with FBP1 and Regulates its Protein Expression. (A) CoIP results of TRIM47 with key enzymes of the gluconeogenesis pathway in HepG2 and HCCLM3 cells. (B) Subcellular localisation of TRIM47 and FBP1 in HepG2 and HCCLM3 cells visualized by IF imaging. (C) CoIP results of ectopically expressed Flag‐TRIM47 and Myc‐FBP1 in HEK293T cells. (D, E) Impact of TRIM47 expression on the protein and mRNA levels of FBP1 ( n = 3, Data are expressed in mean ± SD). (F,G) Changes in FBP1 protein levels in HepG2 and HCCLM3 cells upon MG132 treatment. (H) MG132 treatment abolished the effect of TRIM47 overexpression on FBP1 protein levels. (I,J) Under MG132 treatment, the impact of TRIM47 overexpression or knockdown on FBP1 ubiquitination levels was analyzed. (K) CHX chase assay demonstrated that TRIM47 knockdown affects the stability of FBP1 protein ( n = 3, *** p < 0.001. Data are expressed in mean ± SD). (L) Immunoprecipitation analysis of the types of polyubiquitination of FBP1 in HCC cells (with or without Flag‐TRIM47 lentiviral transfection) co‐transfected with Myc‐FBP1 and HA‐Ub‐K48 (K48‐linked ubiquitin only) or HA‐Ub‐K63 (K63‐linked ubiquitin only). (M) Immunoprecipitation analysis of FBP1 polyubiquitination in HCC cells (control and TRIM47 knockdown conditions) co‐transfected with Myc‐FBP1 and HA‐Ub‐K48. (N) CoIP between co‐transfected HA‐Ub and Myc‐FBP1 WT or lysine mutants to verify potential ubiquitination sites. (O) WB analysis of FBP1 protein levels in HCC cells (with or without Flag‐TRIM47 lentiviral transfection) transfected with WT or K51R Myc‐FBP1 plasmids.
Article Snippet: The appropriate primary antibodies, Flag and
Techniques: Expressing, Imaging, Over Expression, Knockdown, Ubiquitin Proteomics, Immunoprecipitation, Transfection, Control
Journal: Advanced Science
Article Title: TRIM47 Regulates Energy Metabolism via Glycolytic Reprogramming to Drive Hepatocellular Carcinoma Progression and Represents an Efficient Therapeutic Target
doi: 10.1002/advs.202416996
Figure Lengend Snippet: FBP1 Mediates the Oncogenic Role of TRIM47 in HCC. (A, B) Changes in the mRNA and protein levels of FBP1 after transfection with siTRIM47 and siFBP1 ( n = 3, *** p < 0.001. Data are expressed in mean ± SD). (C–F) Knockdown of FBP1 can rescue the reduction in key glycolysis‐related gene expression, lactate production, ATP generation, and glucose uptake caused by siTRIM47 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001. Data are expressed in mean ± SD). (G–J) Cell function rescue experiments demonstrate that knocking down FBP1 can restore the decreased proliferation, migration, and invasion abilities of HCC cells induced by siTRIM47 ( n = 3, *** p < 0.001. Data are expressed in mean ± SD). (K, L) Changes in the mRNA and protein levels of FBP1 after transfection with siTRIM47 and bortezomib treatment. (M–P) Bortezomib treatment can inhibit the increase in key glycolysis‐related gene expression, lactate production, ATP generation, and glucose uptake induced by TRIM47 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001. Data are expressed in mean ± SD). (Q–T) Bortezomib treatment can suppress the enhanced proliferation, migration, and invasion abilities of HCC cells induced by TRIM47 ( n = 3, *** p < 0.001. Data are expressed in mean ± SD).
Article Snippet: The appropriate primary antibodies, Flag and
Techniques: Transfection, Knockdown, Gene Expression, Cell Function Assay, Migration
Journal: Advanced Science
Article Title: TRIM47 Regulates Energy Metabolism via Glycolytic Reprogramming to Drive Hepatocellular Carcinoma Progression and Represents an Efficient Therapeutic Target
doi: 10.1002/advs.202416996
Figure Lengend Snippet: In Vivo Promoting Effect of TRIM47 on HCC Growth and Metastasis. (A) Representative images of xenograft tumors formed by HCCLM3 cells harbouring shNC or shTRIM47, along with comparisons of tumor growth rates and mass differences ( n = 6, *** p < 0.001. Data are expressed in mean ± SD). (B) Representative images of xenograft tumors formed by HepG2 cells harbouring vector or TRIM47, with or without bortezomib intervention, along with comparisons of tumor growth rates and mass differences ( n = 6, * p < 0.05, ** p < 0.01, *** p < 0.001. Data are expressed in mean ± SD). (C) Representative IHC images of TRIM47, FBP1, KI‐67, and PCNA in xenograft tumors from mice subjected to different treatments. (D) Hematoxylin‐eosin (HE) staining images and metastasis ratios of lung metastatic lesions formed by HCCLM3 cells harbouring shNC or shTRIM47 ( n = 8, * p < 0.05. Data are expressed in mean ± SD). (E) HE staining images and metastasis ratios of lung metastatic lesions formed by HepG2 cells harbouring vector or TRIM47 ( n = 8, * p < 0.05. Data are expressed in mean ± SD).
Article Snippet: The appropriate primary antibodies, Flag and
Techniques: In Vivo, Plasmid Preparation, Staining
Journal: Advanced Science
Article Title: TRIM47 Regulates Energy Metabolism via Glycolytic Reprogramming to Drive Hepatocellular Carcinoma Progression and Represents an Efficient Therapeutic Target
doi: 10.1002/advs.202416996
Figure Lengend Snippet: In Vivo Therapeutic Efficacy of siTRIM47@PD NPs in Orthotopic Liver Cancer Mice. (A) Schematic diagram of the NPs structure. (B) Transmission electron microscopy image of siTRIM47@PD NPs. (C) Particle size distribution of PD and siTRIM47@PD. (D) Zeta potential of PD and siTRIM47@PD. (E) Statistical analysis of PD DIO on siTRIM47@PD and the corresponding fluorescence signal of siTRIM47 Cy5 via the Pearson correlation test, with a correlation coefficient of 0.8651. (F) Bioluminescence and representative gross images of the liver in the saline, siNC@PD, and siTRIM47@PD groups. (G–I) Compared with those in the saline and siNC@PD groups, the fluorescence intensity in the siTRIM47@PD group was significantly lower. (J) Compared with those in the saline and siNC@PD groups, the liver tumor weight in the siTRIM47@PD group was significantly lower ( n = 5, *** p < 0.001. Data are expressed in mean ± SD). (K) Mouse weight change curve. (L,M) Lactate levels and ATP levels in liver tumor tissues of the saline group, siNC@PD group, and siTRIM47@PD group. (N) WB experiments explored the expression of TRIM47 and FBP1 proteins in liver tumor tissues of the saline group, siNC@PD group, and siTRIM47@PD group ( n = 5, *** p < 0.001. Data are expressed in mean ± SD).
Article Snippet: The appropriate primary antibodies, Flag and
Techniques: In Vivo, Drug discovery, Transmission Assay, Electron Microscopy, Zeta Potential Analyzer, Fluorescence, Saline, Expressing
Journal: BMC Oral Health
Article Title: Folate-receptor 1 level in periodontal disease: a pilot study
doi: 10.1186/s12903-019-0909-z
Figure Lengend Snippet: The Spearman’s rank correlation (r) among clinical parameters and FOLR1 levels
Article Snippet:
Techniques:
Journal: Cell systems
Article Title: Four key steps control glycolytic flux in mammalian cells
doi: 10.1016/j.cels.2018.06.003
Figure Lengend Snippet:
Article Snippet: FBP1: FBP1 ( {"type":"entrez-nucleotide","attrs":{"text":"NM_000507","term_id":"1677501380","term_text":"NM_000507"}} NM_000507 ) Human cDNA Clone ,
Techniques: Recombinant, Modification, Transfection, Clone Assay, Enzyme-linked Immunosorbent Assay, Colorimetric Assay, Lactate Dehydrogenase Assay, Bicinchoninic Acid Protein Assay, PK Assay, Plasmid Preparation, Sequencing, Expressing, Variant Assay, Cell Culture
Journal: International Journal of Molecular Sciences
Article Title: Accumulation of Cerebrospinal Fluid, Ventricular Enlargement, and Cerebral Folate Metabolic Errors Unify a Diverse Group of Neuropsychiatric Conditions Affecting Adult Neocortical Functions
doi: 10.3390/ijms251810205
Figure Lengend Snippet: Positive controls used.
Article Snippet: FOLR1 ,
Techniques: