prmt5 enzymatic activity  (MedChemExpress)

Journal: Frontiers in Neurology

Article Title: PRMT5 inhibition suppresses the PI3K/AKT pathway to attenuate vascular smooth muscle cell pathological phenotype in intracranial aneurysm

doi: 10.3389/fneur.2026.1771196

Figure Lengend Snippet: PRMT5 level was increased in IA models. In vivo analysis of PRMT5 level between the sham and model groups (A) . In vitro analysis of VSMC viability (B) and PRMT5 level (C) among the untreated, Ang II (0.1 μM), Ang II (0.5 μM), and Ang II (1 μM) groups. *: p < 0.05; **: p < 0.01; ***: p < 0.001; ns: not significant.

Article Snippet: EPZ015666 (MCE, China) is an orally bioavailable small-molecule inhibitor of PRMT5 enzymatic activity.

Techniques: In Vivo, In Vitro

Journal: Frontiers in Neurology

Article Title: PRMT5 inhibition suppresses the PI3K/AKT pathway to attenuate vascular smooth muscle cell pathological phenotype in intracranial aneurysm

doi: 10.3389/fneur.2026.1771196

Figure Lengend Snippet: EPZ015666 inhibited PRMT5 enzymatic activity, facilitated transition from synthetic phenotype to contractile phenotype, and suppressed PI3K/AKT pathway in Ang II-treated VSMCs. Comparison of PRMT5, H4R3me2s, α -SMA, OPN, and MMP9 levels among the Model, EPZ (1 μM), EPZ (5 μM), and EPZ (10 μM) groups (A) . Comparison of p-PI3K and p-AKT among the Model, EPZ (1 μM), EPZ (5 μM), and EPZ (10 μM) groups (B) . *: p < 0.05; **: p < 0.01; ***: p < 0.001; ns: not significant.

Article Snippet: EPZ015666 (MCE, China) is an orally bioavailable small-molecule inhibitor of PRMT5 enzymatic activity.

Techniques: Activity Assay, Comparison

Journal: bioRxiv

Article Title: PRMT5 as an Epigenetic Target for Group 3 (MYC-driven) Medulloblastoma

doi: 10.64898/2026.04.09.717536

Figure Lengend Snippet: (A) qPCR analysis for the expression of PRMT5/MYC mRNA in two MYC-amplified cell lines with transiently knocked-down of PRMT5 (using siRNAs) at 72 h. ****, p<0.0001 (student t test, SCR vs siPRMT5). (B) Effect of PRMT5 knockdown (siRNAs) on MYC-luciferase reporter gene (MYC-Luc) activity in HD-MB03 cells. *, p<0.05 (student t test) (C) ChIP analyses for the enrichment of PRMT5 and H4R3me2s on the proximal promoter region of the MYC gene in HD-MB03 cells. ****, p<0.0001 (student t test). ChIP analyses for the enrichment/binding of PRMT5 (D) and H4R3me2s (E) to the proximal promoter region of MYC gene, in PRMT5 knockdown (siRNAs) HD-MB03 cells. ( F ) Co-immunoprecipitation of BRD4 with PRMT5. ( G ) ChIP analyses for the enrichment/binding of PRMT5 and BRD4 to the proximal promoter region of MYC gene, in BRD4 knockdown (siRNAs) HD-MB03 cells. *, p<0.05; **, p<0.05 (student t test).

Article Snippet: Four PRMT5 inhibitors (EPZ015666, GSK332595, LLY-283, JNJ64619178) were purchased from MedChemExpress LLC or Selleckchem Company.

Techniques: Expressing, Amplification, Knockdown, Luciferase, Activity Assay, Binding Assay, Immunoprecipitation

Journal: bioRxiv

Article Title: PRMT5 as an Epigenetic Target for Group 3 (MYC-driven) Medulloblastoma

doi: 10.64898/2026.04.09.717536

Figure Lengend Snippet: RNA-sequencing was used to assess global gene expression changes in HD-MB03 cells 24 h after treatment with DMSO (vehicle) or JNJ64619178 (1 µM). (A) Volcano plot displaying genes significantly upregulated or downregulated in response to PRMT5 inhibition. (B) Gene Ontology Biological Process (GO-BP) functional analysis for top 10 pathways altered by JNJ. (C) Gene sets enrichment analysis (GSEA) (with p<0.01 and FDR<0.2) for top 10 pathways/gene sets (including MYC-associated target gene sets, RNA splicing, metabolism) altered by PRMT5 inhibition. (D) Number of the aberrant splicing events in protein coding genes disrupted by PRMT5 inhibition. (E) GO-BP functional analysis for the aberrant splicing events altered by PRMT5 inhibition. (F) Volcano plot represents all the significant (p<0.05) splicing events. Selected genes from the indicated GO-BP functional classification are highlighted. Metabolism associated genes GGT6, GPT2 and C1QBP1 are identified.

Article Snippet: Four PRMT5 inhibitors (EPZ015666, GSK332595, LLY-283, JNJ64619178) were purchased from MedChemExpress LLC or Selleckchem Company.

Techniques: RNA Sequencing, Gene Expression, Inhibition, Functional Assay

Journal: bioRxiv

Article Title: PRMT5 as an Epigenetic Target for Group 3 (MYC-driven) Medulloblastoma

doi: 10.64898/2026.04.09.717536

Figure Lengend Snippet: (A) MTT assay showing the effects of PRMT5 inhibitors (1-50 µM) on cell growth of MYC-amplified MB (HD-MB03, D341), non-MYC MB (ONS-76) and normal human astrocyte (NHA) cell lines. (B) IC 50 values of PRMT5 inhibitors in the indicated cell lines. (C) Annexin-V assay showing effects of PRMT5 inhibitors (JNJ, EPZ) on apoptosis in HD-MB03 cells. **, p<0.01, ***, p<0.001 (relative to ‘0’ (vehicle control)). (D) Cell cycle profile in HD-MB03 cells treated with PRMT5 inhibitors (EPZ, JNJ). (E) Western blot analysis for the expression of the indicated key proteins in JNJ-treated HD-MB03 cells. ( F) Quantification of spheres following treatment of JNJ and EPZ in two PDX-derived MB cell lines (MED-411FH, MED-114FH) at 72 h. Values, mean ± SEM. * p < 0.05; ** p < 0.01; *** p < 0.005; *** p < 0.001 (Student- t -test). (G) Representative sphere (MED-411FH) images showing disruption of spheres in each treatment. (H) Western blot results showing the expression of indicated proteins in MED-411 spheres treated with JNJ and EPZ.

Article Snippet: Four PRMT5 inhibitors (EPZ015666, GSK332595, LLY-283, JNJ64619178) were purchased from MedChemExpress LLC or Selleckchem Company.

Techniques: MTT Assay, Amplification, Annexin V Assay, Control, Western Blot, Expressing, Derivative Assay, Disruption

Journal: bioRxiv

Article Title: PRMT5 as an Epigenetic Target for Group 3 (MYC-driven) Medulloblastoma

doi: 10.64898/2026.04.09.717536

Figure Lengend Snippet: (A ) JNJ brain concentration in BALB/c mice (N=3) following oral administration of 10 mg/kg JNJ at different timepoints. **p<0.01 (Student’s t-test). (B) NSG mice (N=5) with subcutaneously xenografted HD-MB03 cells were treated orally with vehicle or JNJ (10 mg/kg) five times a week for three weeks. Tumor volume measurement of xenografted mice following treatments. The differences noted between treatment groups show comparison by Student ‘s t-test of the tumor volumes on 21 days post treatment (p<0.005). (C) Representative IHC images (40 × magnification with 60 µm scale bar) of PRMT5, MYC, Ki-67, and CC3 expression in xenografts 21 days post-treatment, as indicated. Bar graphs below show the percentages of PRMT5, MYC, Ki-67 and CC3 positive cells derived from immunohistology scores, which were semi-quantitated in the tumors of three xenografted mice. **p<0.01; ***p<0.005 (Student’s t-test). (D) NSG mice (N=6) with orthotopically xenografted HD-MB03 cells were treated daily with vehicle or JNJ (10 mg/kg) or JNJ (F) (10 mg/kg) for two weeks. Survival analysis of xenografted mice using Kaplan-Meier (long-rank test). *p<0.05, **p<0.01, ***p<0.001. (E) Representative IHC images (4x magnification with 600 µm scale bar) and respective quantification showing MYC-positive tumors in the mouse cerebellum. The percentage of MYC, derived from immunohistology scores, was semi-quantitated in the tumors of three xenografted mice 21 days post-treatment. *p< **p<0.01 (Student’s t-test).

Article Snippet: Four PRMT5 inhibitors (EPZ015666, GSK332595, LLY-283, JNJ64619178) were purchased from MedChemExpress LLC or Selleckchem Company.

Techniques: Concentration Assay, Comparison, Expressing, Derivative Assay

Journal: Cell Death & Disease

Article Title: Targeting ENO1 reprograms macrophage polarization to trigger antitumor immunity and improves the therapeutic effect of radiotherapy

doi: 10.1038/s41419-026-08416-7

Figure Lengend Snippet: A The expression of total and surface ENO1 in human CRC cell lines was evaluated by immunoblotting and flow cytometry. B The expression of total and surface ENO1 in human BRCA cell lines was evaluated by immunoblotting and flow cytometry. C HT29 and LoVo cells were treated with different doses of recombinant human TGFβ1 protein (rhTGFβ1) for 24 hr, after which surface ENO1 expression was analyzed via flow cytometry. D HS578T and MDA-MB-468 cells were treated with different doses of the rhTGFβ1 protein for 24 hr, after which the surface ENO1 level was analyzed via flow cytometry. E LoVo cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) in combination with a PRMT5 inhibitor (AMG-193, 1 μM) or a PRMT6 inhibitor (EPZ020411 hydrochloride, 1 μM) for 24 hr. The surface ENO1 level was analyzed via flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). F HT29 cells were treated with rhTGFβ1 protein in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The surface ENO1 expression was analyzed via flow cytometry. ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). G LoVo shNC and LoVo shPRMT5 cells were treated with LPS (1 μg/mL), rhTGFβ1 protein (10 ng/mL) or H 2 O 2 (50 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). H HT29 and LoVo cells were treated with LPS (1 μg/mL) and RT (5 Gy) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3). I HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. *** p < 0.001. One-Way ANOVA test ( n = 3). J HT29 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05. One-Way ANOVA test ( n = 3). K MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The surface level of ENO1 was examined by flow cytometry. * p < 0.05, ** p < 0.01 and *** p < 0.001. One-Way ANOVA test ( n = 3). L MDA-MB-468 cells were treated with RT (5 Gy) in combination with a TGFβR1 inhibitor (1 μM), a Smad3 inhibitor (1 μM), or a PRMT5 inhibitor (1 μM) for 24 hr. The level of plasmin activity was examined via an ELISA kit. * p < 0.05, and ** p < 0.01. One-Way ANOVA test ( n = 3). M HT29 cells were treated with RT (5 Gy) in combination with a PRMT5 inhibitor (1 μM) for 24 hr. The level of surface-methylated ENO1 was evaluated by immunoprecipitation and immunoblotting.

Article Snippet: The TGFβR1 inhibitor galunisertib (HY-13226, MCE, USA) [ ], Smad3 inhibitor SIS3 (HY-13013, MCE, USA) and PRMT5 inhibitor EPZ015666 (HY-12727, MCE, USA) were dissolved in DMSO to a concentration of 10 mM.

Techniques: Expressing, Western Blot, Flow Cytometry, Recombinant, Activity Assay, Enzyme-linked Immunosorbent Assay, Methylation, Immunoprecipitation

Journal: Cell Death & Disease

Article Title: Targeting ENO1 reprograms macrophage polarization to trigger antitumor immunity and improves the therapeutic effect of radiotherapy

doi: 10.1038/s41419-026-08416-7

Figure Lengend Snippet: A A total of 5 × 10 5 CT26 cells were subcutaneously injected into the left legs of BALB/c mice for 5 days and then intraperitoneally administered with anti-ENO1 antibodies (HuL001, 40 mg/kg) or clodronate liposomes (50 μL/mouse) on the indicated days ( n = 5). Local radiotherapy was given on Day 10. The tumor volume was recorded every three days. * p < 0.05. Two-Way ANOVA test ( n = 4). B The densities of M1 (CD80 + ) and M2 (CD206 + ) macrophages in resected tumors were analyzed by immunofluorescence staining. The quantification of M1 (CD80 + ) and M2 (CD206 + ) macrophages in resected tumors. * p < 0.05 and *** p < 0.001. One-Way ANOVA test ( n = 3). C 4T1 cells (5 ×10 4 ) were subcutaneously injected into the left legs of BALB/c mice for 4 days and then intraperitoneally administered anti-ENO1 antibodies (HuL001, 20 mg/kg) six times on the indicated days ( n = 5). Local radiotherapy was given on Days 10 and 12. The tumor volume was recorded every three days. * p < 0.05 and *** p < 0.001. Two-Way ANOVA test ( n = 4). D The resected tumors were weighed on Day 40. * p < 0.05. One-Way ANOVA test ( n = 4). E The densities of M1 (CD80 + ) and M2 (CD206 + ) macrophages in resected tumors were analyzed by immunofluorescence staining. F The quantification of M1 (CD80 + ) and M2 (CD206 + ) macrophages in resected tumors. * p < 0.05. One-Way ANOVA test ( n = 3). G The frequencies of M1 (CD11c + CD11b + F4/80 + CD45 + 7AAD - CD3 - CD19 - ) and M2 (CD1206 + CD11b + F4/80 + CD45 + 7AAD - CD3 - CD19 - ) tumor-infiltrating macrophages were analyzed by flow cytometry. * p < 0.05. One-Way ANOVA test ( n = 3-4). H The quantification of the M1/M2 ratio is shown. * p < 0.05. One-Way ANOVA test ( n = 3). I A representative image of flow cytometric analysis of GzmB + (GzmB hi CD8 + CD3 + CD45 + 7AAD - ) T cells. J The frequency of GzmB + (GzmB hi CD8 + CD3 + CD45 + 7AAD - ) T cells was analyzed by flow cytometry. * p < 0.05. One-Way ANOVA test ( n = 3-4). K The density of GzmB + (GzmB hi CD8 + CD3 + CD45 + 7AAD - ) T cells is shown. * p < 0.05. One-Way ANOVA test ( n = 3-4). L The density of IFNγ + (IFNγ hi CD8 + CD3 + CD45 + 7AAD - ) T cells is shown ( n = 3-4). * p < 0.05 and ** p < 0.01. One-Way ANOVA test ( n = 3-4). M The proposed mechanism of TGFβ1/TGFβR/Smad3/PRMT5-mediated ENO1 translocation for lactate release via MCT4.

Article Snippet: The TGFβR1 inhibitor galunisertib (HY-13226, MCE, USA) [ ], Smad3 inhibitor SIS3 (HY-13013, MCE, USA) and PRMT5 inhibitor EPZ015666 (HY-12727, MCE, USA) were dissolved in DMSO to a concentration of 10 mM.

Techniques: Injection, Liposomes, Immunofluorescence, Staining, Flow Cytometry, Translocation Assay

Journal: bioRxiv

Article Title: PRMT5 inhibitors actively promote metastatic progression of lung adenocarcinoma

doi: 10.64898/2026.01.30.702866

Figure Lengend Snippet: a. Schematic of LUAD dedifferentiation spectrum, including the relative states of KP Early and KP Late . Each bar represents the general expression pattern of the given dedifferentiation state marker. b. Schematic of generation of PRMT5i-resistant variants of KP Late (KP1 36 ) and KP Early (KP2 36 ) cell lines. c. Dose response curves for KP Late (blue) and a representative KP Late -R line, KP Late -R1 (red) treated with JNJ-64619178 (PRMT5i) for 5 days. Data are mean ± SD of 3 technical replicates/line. p=0.0012, Welch’s t-test. d. GSEA results for gene sets listed in Supplementary Fig. 1c comparing KP Early and KP Late to their resistant lines. Color represents normalized enrichment score, while size inversely correlates with significance. e. Western blot of core LUAD dedifferentiation markers (Nkx2.1, Hnf4a, Hmga2) and Hsp90 loading control in KP Early and KP Late , as well as one control (DMSO selection) and three PRMT5i-resistant populations. f. UMAP of scRNA-seq dataset from an autochthonous KP model of LUAD with ( Left panel ) all clusters marked, ( Center panel ) Stmn2 expression, or ( Right panel ) Sox11 expression within the individual clusters. Cluster 12 (circled) was previously described to contain late-stage, pro-metastatic cells 44 .

Article Snippet: The PRMT5 inhibitor JNJ-64619178 was used for all PRMT5i treatment experiments and obtained from MedChemExpress (HY-101564).

Techniques: Expressing, Marker, Western Blot, Control, Selection

Journal: bioRxiv

Article Title: PRMT5 inhibitors actively promote metastatic progression of lung adenocarcinoma

doi: 10.64898/2026.01.30.702866

Figure Lengend Snippet: a. Differentially accessible loci in KP Early after 5-day vehicle or 100nM PRMT5i treatment. Points represent individual loci that are more accessible (pink, p adj <0.01, log 2 FC>1), less accessible (blue, p adj <0.01, log 2 FC<-1), or not differentially accessible (gray). b. Cumulative fraction of the coefficient of variation for significant loci of KP Early after 5-day vehicle or PRMT5i treatment, indicating vehicle-derepressed (blue) and PRMT5i-derepressed (red) loci. p<10 -44 , F test. c. ChromVAR deviation score differences between vehicle- and PRMT5i-treated parental cells (x-axis) and resistant and parental cells (y-axis) for KP Early and KP Late . Points indicate differentially accessible (dark gray or colored, p adj <0.01) and not significant (light gray) motifs. Colored points represent motifs within the same TF family. d. Accessibility of indicated TF family motifs across: ( Top panel ) UMAP projections of a scATAC-seq dataset from an autochthonous model of LUAD, and ( Bottom panel ) chromVAR deviation scores for each biological replicate (n=3) of parental (blue), PRMT5i-treated parental (pink), and resistant (red) lines. e. Four categories of genome-wide representation of loci indicating derepression or repression of peak accessibility in response to a 5-day PRMT5i treatment of KP Early and whether this is established or not, in the stably-resistant KP Early -R1. ( Left panel ) Representative accessibility track, ( Center panel ) genome-wide accessibility heatmap, and ( Right panel ) all enriched TF motifs (p<10 -50 ) are shown. Colors denote: parental (blue), PRMT5i-treated parental (pink), and stable resistant (red) lines. f. Comparison of loci that show differentially accessible in response to a 5-day PRMT5i treatment of KP Early (drug-responsive) versus ones established in stably-resistant cells for ( Top panel ) KP Early and ( Bottom panel ) KP Late . Proportion of drug-responsive peaks that are also resistance state peaks is shown as a percentage. g. CTCF chromVAR deviation score in KP Early and KP Late treated with vehicle (blue) or PRMT5i for 5 days (pink). h. Genomic annotation of PRMT5-derepressed loci in KP Early and KP Late .

Article Snippet: The PRMT5 inhibitor JNJ-64619178 was used for all PRMT5i treatment experiments and obtained from MedChemExpress (HY-101564).

Techniques: Genome Wide, Stable Transfection, Comparison

Journal: bioRxiv

Article Title: PRMT5 inhibitors actively promote metastatic progression of lung adenocarcinoma

doi: 10.64898/2026.01.30.702866

Figure Lengend Snippet: a. Schematic of the CDKN2A and adjacent MTAP loci indicating gene products and functions. b. Frequents of CDKN2A copy number losses in various tumor types, with SKCM (skin cutaneous melanoma) and LUAD highlighted. c. Schematic of effects of CDKN2A- deficiency on MTAP and PRMT5 biology. d. Normalized RNA expression counts for HMGA2 and RUNX2 in CDKN2A / MTAP -deficient LU99 cells treated with vehicle (blue) or MRTX1719 (red), an MTA-cooperative PRMT5i, for 3 or 5 days. Data are mean ± SD of 2 biological replicates/line. *p<0.05, **p<0.01, ***p<0.001, Student’s t-test. e-f. Differentially expressed genes comparing CDKN2A DKO to the rest of the tumors (+) in the TCGA LUAD ( e ) Firehose Legacy or ( f ) PanCancer cohorts. ( Left panel ) Points represent individual genes that have increased expression (red, p<0.05, log 2 FC>0.5) or decreased expression (blue, p<0.05, log 2 FC<-0.5). ( Right panel ) Expression of HMGA2 in indicated groups. Points represent individual patients with the total number of patients per group listed below the axis. p=0.00068 Legacy cohort and p=0.00003 PanCancer cohort, Student’s t-test.

Article Snippet: The PRMT5 inhibitor JNJ-64619178 was used for all PRMT5i treatment experiments and obtained from MedChemExpress (HY-101564).

Techniques: RNA Expression, Expressing

Journal: Biomolecules

Article Title: Enhancing CD8 + T Cells Infiltration Through the Protein Arginine Methyltransferase 5 (PRMT5)/CXCL10 Axis Restricts Cervical Cancer Progression

doi: 10.3390/biom15121717

Figure Lengend Snippet: Increases in PRMT5 expression were found to be linked to adverse prognosis in cervical cancer. ( A ) PRMT5 expression was conducted in both healthy cervical tissues and tumor tissues obtained from the TCGA database (num (T) = 306; num (N) = 13). ( B ) Correlation between PRMT5 expression and immune cells from TCGA database (ssgsea test). ( C ) The analyses were performed to investigate the association among high/low PRMT5 expression levels and T cells/CD8 + T cells/Macrophages/NK/DC in cervical cancer patients derived from TCGA database. ( D ) The relationship between PRMT5 expression and T cells, CD8 + T cells, Macrophages, NK, DC using the TCGA database (ssgsea test). OS ( E ), DSS ( F ) and PFI ( G ) analyses were conducted on cervical cancer patients with high/low levels of PRMT5 using data from the TCGA database. The data represent the mean ± SEM. Blue represents low PRMT5 expression, red represents high PRMT5 expression. ns = no significance, * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: PRMT5 inhibitor EPZ015666 (also known as GSK3235025; Selleckchem, Houston, TX, USA) was utilized in the experiments.

Techniques: Expressing, Derivative Assay

Journal: Biomolecules

Article Title: Enhancing CD8 + T Cells Infiltration Through the Protein Arginine Methyltransferase 5 (PRMT5)/CXCL10 Axis Restricts Cervical Cancer Progression

doi: 10.3390/biom15121717

Figure Lengend Snippet: Downregulation of PRMT5 resulted in the inhibition of tumor cell migration, invasion and apoptosis. ( A ) Plasmid vector containing Control shRNA and shRNA targeting PRMT5. ( B ) Comparison of PRMT5 expression between control cells and U14 cells with PRMT5 knockdown. ( C ) Assessment of cell proliferation in U14 cells following PRMT5 knockdown. ( D ) Evaluation of cell migration in U14 cells following PRMT5 knockdown through the Scratch assay. ( E ) Analysis of cell migration and invasion in U14 cells following PRMT5 knockdown through the transwell assay. ( F ) Examination of apoptosis in U14 cells following PRMT5 knockdown. The data represent the mean ± SEM. * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: PRMT5 inhibitor EPZ015666 (also known as GSK3235025; Selleckchem, Houston, TX, USA) was utilized in the experiments.

Techniques: Inhibition, Migration, Plasmid Preparation, Control, shRNA, Comparison, Expressing, Knockdown, Wound Healing Assay, Transwell Assay

Journal: Biomolecules

Article Title: Enhancing CD8 + T Cells Infiltration Through the Protein Arginine Methyltransferase 5 (PRMT5)/CXCL10 Axis Restricts Cervical Cancer Progression

doi: 10.3390/biom15121717

Figure Lengend Snippet: Disruption of PRMT5 suppressed less tumor growth in CD8 KO mice. 6-week-old female C57BL/6 mice and CD8 KO mice received subcutaneous injections of either control cells or U14 cells with PRMT5 knockdown ( n = 5 per group). ( A – C ) The mice were euthanized, and the tumors that were resected were subsequently analyzed on day 16 after inoculation. ( A ) The tumor growth curve observed on the mice is depicted in a line graph. On day 16, images ( B ) and weight measurements ( C ) of the excised tumor were recorded. ( D ) A survival curve was generated for tumor-bearing mice that received subcutaneous injections of control and U14 cells with PRMT5 knockdown. The data represent the mean ± SEM. * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: PRMT5 inhibitor EPZ015666 (also known as GSK3235025; Selleckchem, Houston, TX, USA) was utilized in the experiments.

Techniques: Disruption, Control, Knockdown, Generated

Journal: Biomolecules

Article Title: Enhancing CD8 + T Cells Infiltration Through the Protein Arginine Methyltransferase 5 (PRMT5)/CXCL10 Axis Restricts Cervical Cancer Progression

doi: 10.3390/biom15121717

Figure Lengend Snippet: Disruption of PRMT5 enhanced CXCL10 secretion by tumor cells. ( A ) Venn analysis comparing control cells and U14 cells with PRMT5 knockdown using RNA-seq. ( B ) Comparison of chemokine expression profiles between control cells and U14 cells with PRMT5 knockdown analyzed through RNA-seq. ( C ) Real-time PCR experiments were conducted to examine CCL5, CCL11, CCL4, CXCL9, and CXCL10 expression in control cells and U14 cells with PRMT5 knockdown. ( D ) CXCL10 level was measured by ELISA. ( E ) Correlation between CXCL10 expression and immune cell populations was assessed using the Kruskal–Wallis test from TCGA database. ( F ) Analysis of high PRMT5 expression enrichment compared to low PRMT5 expression in T cells and CD8 + T cells of cervical cancer patients from TCGA database. Blue represents low CXCL10 expression, red represents high CXCL10 expression. Correlation between CXCL10 expression and T cells ( G )/CD8 + T cells ( H ) was evaluated using the Kruskal–Wallis test from TCGA database. The data represent the mean ± SEM. ns = no significance, * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: PRMT5 inhibitor EPZ015666 (also known as GSK3235025; Selleckchem, Houston, TX, USA) was utilized in the experiments.

Techniques: Disruption, Control, Knockdown, RNA Sequencing, Comparison, Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

Journal: Biomolecules

Article Title: Enhancing CD8 + T Cells Infiltration Through the Protein Arginine Methyltransferase 5 (PRMT5)/CXCL10 Axis Restricts Cervical Cancer Progression

doi: 10.3390/biom15121717

Figure Lengend Snippet: PRMT5 regulated CD8 + T cells recruitment through CXCL10/CXCR3 axis. Control cells and PRMT5 knockdown U14 cells were subcutaneously injected into 6-week-old female C57BL/6 mice and CXCR3 KO mice. Mice were euthanized at day 18 after inoculation ( n = 4 per group). The tumor single cell suspension was prepared and analyzed by flow cytometry. ( A ) A line graph shows the tumor growth curve of mice. Images ( B ) and weight ( C ) of the resected tumor at day 18 after inoculation. ( D ) The percentage of CD4 + and CD8 + T cells in CD45 + cells. The data represent the mean ± SEM. * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: PRMT5 inhibitor EPZ015666 (also known as GSK3235025; Selleckchem, Houston, TX, USA) was utilized in the experiments.

Techniques: Control, Knockdown, Injection, Suspension, Flow Cytometry

Journal: Biomolecules

Article Title: Enhancing CD8 + T Cells Infiltration Through the Protein Arginine Methyltransferase 5 (PRMT5)/CXCL10 Axis Restricts Cervical Cancer Progression

doi: 10.3390/biom15121717

Figure Lengend Snippet: EPZ015666 inhibited dimethylation levels at H3R2, H3R8, and H4R3 sites. ( A ) Analyis of PRMT5 expression in the cytoplasm and nucleus was assessed via Western blot. ( B ) Effect of EPZ015666 on PRMT5 expression in cytoplasm and nucleus by Western blot. ( C ) Impact of EPZ015666 on the expression of PRMT5, H3R2me2s, H3R8me2s, and H4R3me2s in cervical cancer cells was assessed using Western blot. H3 or H4 served as a loading control. Original western blots can be found at .

Article Snippet: PRMT5 inhibitor EPZ015666 (also known as GSK3235025; Selleckchem, Houston, TX, USA) was utilized in the experiments.

Techniques: Expressing, Western Blot, Control

Journal: Biomolecules

Article Title: Enhancing CD8 + T Cells Infiltration Through the Protein Arginine Methyltransferase 5 (PRMT5)/CXCL10 Axis Restricts Cervical Cancer Progression

doi: 10.3390/biom15121717

Figure Lengend Snippet: EPZ015666 effectively suppressed cervical cancer growth by enhancing intracellular cytokine expression in T cells. ( A – I ) 6-week-old female C57BL/6 mice received daily intraperitoneal injections of EPZ015666 (150 mg kg −1 ) 3 days after inoculation of U14 cells ( n = 5 per group). ( A ) The growth curve of tumors in the mice is illustrated by a line graph. On day 12 post-inoculation, images ( B ) and weight measurements ( C ) of the excised tumors were collected. ( D ) Analysis was conducted to determine PRMT5 expression and SDMA levels within the tumor. ( E ) The proportion of CD4 + and CD8 + T cells among CD45 + cells was determined. ( F ) IFN-γ, TNF-α and granzyme B expression levels were assessed in CD8 + T cells. ( G ) PD-1, TIM-3 and LAG-3 expression levels were revealed through surface examination on CD8 + T cells. ( H ) IFN-γ, TNF-α and Foxp3 expression levels were examined in CD4 + T cells. ( I ) PD-1, TIM-3 and LAG-3 expression levels was assessed on CD4 + T cells. The data represent the mean ± SEM. * p < 0.05 and *** p < 0.001.

Article Snippet: PRMT5 inhibitor EPZ015666 (also known as GSK3235025; Selleckchem, Houston, TX, USA) was utilized in the experiments.

Techniques: Expressing

Journal: Biomolecules

Article Title: Enhancing CD8 + T Cells Infiltration Through the Protein Arginine Methyltransferase 5 (PRMT5)/CXCL10 Axis Restricts Cervical Cancer Progression

doi: 10.3390/biom15121717

Figure Lengend Snippet: Schematic illustration elucidating the mechanistic function of PRMT5 in facilitating the progression of cervical carcinoma. →: activation effect; ┤: inhibitory effect.

Article Snippet: PRMT5 inhibitor EPZ015666 (also known as GSK3235025; Selleckchem, Houston, TX, USA) was utilized in the experiments.

Techniques: Activation Assay