Journal: The Journal of Clinical Investigation

Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models

doi: 10.1172/JCI199056

Figure Lengend Snippet: ( A ) Strategy for identification of 4 key genes encoding secreted proteins that are downregulated (fold change > 2) by CLOCK depletion in GSC272 with inducible CLOCK shRNA (ish CLOCK ) versus inducible shRNA control (ishC), and by BMAL1 depletion in T387 and T3565 with BMAL1 shRNA (sh BMAL1 ) versus shRNA control (shC). ( B ) Heat map shows the expression of TFPI2 , COL8A1 , LRRC17, and PLA2R1 in GSC272, T387, and T3565 harboring ishC versus ish CLOCK and shC versus sh BMAL1 . Red and blue indicate higher and lower expression, respectively. ( C and D ) ChIP-seq data analysis shows the heatmap ( C ) and quantification ( D ) of BMAL1-enriched profiles at TFPI2 , COL8A1 , LRRC17, and PLA2R1 promotors in GSCs (T387 and T3565) and NSCs (ENSA and hNP1). n = 4. ( E ) ChIP-seq data analysis shows BMAL1-enriched profiles at the TFPI2 promotor in NSC #1 and #2 (ENSA and hNP1) and GSC #1 and #2 (T387 and T3565). ( F and G ) RT-qPCR for CLOCK and TFPI2 in control, CLOCK-depleted ( F , n = 4), and BMAL1-depleted ( G , n = 3) GSC272. ( H ) RT-qPCR for TFPI2 in GSC20 and GSC272 treated with or without SR9009 (5 μmol/L). n = 3 independent samples. ( I and J ) RT-qPCR for CLOCK and TFPI2 in GSC17 ( I ) or GSC23 ( J ) harboring CLOCK overexpression (OE). n = 3. ( K and L ) Immunoblots for CLOCK, BMAL1, and TFPI2 in GSC272 harboring shC and sh CLOCK ( K ), or shC and sh BMAL1 ( L ). ( M ) Immunoblots for CLOCK and TFPI2 in GSC20 and GSC272 treated with or without SR9009 (1 and 5 μmol/L). ( N and O ) Immunoblots for CLOCK, BMAL1, and TFPI2 in GSC17 ( N ) or GSC23 ( O ) harboring CLOCK OE. Data from multiple replicates are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, Student’s t test ( D and F – J ).

Article Snippet: Plasmids of human Tagged ORF Clone of CLOCK (Origene, # RC221408), and TFPI2 (Origene, #RC202760) and mouse Tagged ORF Clone of Clock (Origene, #MR226315), and Tfpi2 (Origene, #MR202782) were used.

Techniques: shRNA, Control, Expressing, ChIP-sequencing, Quantitative RT-PCR, Over Expression, Western Blot

Journal: The Journal of Clinical Investigation

Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models

doi: 10.1172/JCI199056

Figure Lengend Snippet: ( A – D ) Immunoblots ( A and B ) and RT-qPCR ( C and D , n = 3) for CD133 ( PROM1 ) and SOX2 in GSC272 harboring shRNA control (shC), CLOCK shRNA (sh CLOCK , A ), or sh BMAL1 ( B ) in the presence or absence of TFPI2 overexpression (OE). n = 3. ( E and F ) In vitro limiting dilution assays in GSC272 harboring shC, sh CLOCK ( E ), or sh BMAL1 ( F ) in the presence or absence of TFPI2 OE. ( G – I ) Representative images ( G ) and quantification of relative tumorsphere number ( H ) and size ( I ) of GSC272 expressing shC, sh CLOCK, or sh BMAL1 in the presence or absence of TFPI2 OE. Scale bar: 200 μm. n = 8. ( J – M ) Representative images and quantification of proliferation in GSC272 harboring shC, sh CLOCK ( J and K ), and sh BMAL1 ( L and M ) with or without TFPI2 OE. n = 3. ( N – Q ) Immunoblots ( N and O ) and RT-qPCR ( P and Q , n = 3) for CD133 ( PROM1 ) and SOX2 in GSC17 and GSC23 harboring Control or CLOCK OE with or without sh TFPI2 . ( R and S ) In vitro limiting dilution assays in GSC17 ( R ) and GSC23 ( S ) expressing Control or CLOCK OE with or without sh TFPI2 . ( T and U ) Representative images ( T ) and quantification of relative tumorsphere number ( U ) of GSC17 or GSC23 harboring CLOCK OE in the presence or absence of sh TFPI2 . Scale bar: 200 μm. n = 8. ( V – Y ) Representative images and quantification of proliferation in GSC17 ( V and W ) and GSC23 ( X and Y ) harboring CLOCK OE in the presence or absence of sh TFPI2 . n = 3. Data from multiple replicates are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, 1-way ANOVA test ( C , D , H , I , K , M , P , Q , U , W , and Y ), 2-way ANOVA test ( E , F , R , and S ).

Article Snippet: Plasmids of human Tagged ORF Clone of CLOCK (Origene, # RC221408), and TFPI2 (Origene, #RC202760) and mouse Tagged ORF Clone of Clock (Origene, #MR226315), and Tfpi2 (Origene, #MR202782) were used.

Techniques: Western Blot, Quantitative RT-PCR, shRNA, Control, Over Expression, In Vitro, Expressing

Journal: The Journal of Clinical Investigation

Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models

doi: 10.1172/JCI199056

Figure Lengend Snippet: ( A ) Amplification pattern TFPI2 and CLOCK in TCGA GBM patient tumors from indicated datasets. ( B ) High-resolution uniform manifold approximation and projection (UMAP) showing expression of CLOCK and TFPI2 in GSCs (the population of cells are highlighted in circle) of GBM patient tumors based on scRNA-Seq data ( GSE182109 ). ( C ) Relationship between CLOCK and TFPI2 expression in GSCs from GBM patient tumors based on scRNA-Seq data ( GSE182109 ). R and P values are shown. Pearson’s correlation test. ( D ) In vitro limiting dilution assays in GSC272 harboring shRNA control (shC) and TFPI2 shRNA (sh TFPI2 ) treated with or without SR9009 (5 μM). ( E – G ) Representative images ( E ) and quantification of relative tumorsphere number ( F ) and size ( G ) of GSC272 harboring shC and sh TFPI2 and treated with or without SR9009 (5 μM). Scale bar: 200 μm. n = 8. ( H ) Survival curves of nude mice implanted with 2 × 10 5 shC and sh TFPI2 GSC272. Mice were treated with SR9009 (100 mg/kg, i.p., daily) for 10 days beginning at day 7 after orthotopic injection ( n = 8 mice per group). ( I – L ) Representative images and quantification of IHC staining for SOX2 ( I and J ) and CD133 ( K and L ) in shC and sh TFPI2 GSC272 tumors from mice treated with or without SR9009. Scale bar: 100 μm. n = 7. Data from multiple replicates are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, 1-way ANOVA test ( F , G , J , and L ), 2-way ANOVA test ( D ), log-rank test ( H ).

Article Snippet: Plasmids of human Tagged ORF Clone of CLOCK (Origene, # RC221408), and TFPI2 (Origene, #RC202760) and mouse Tagged ORF Clone of Clock (Origene, #MR226315), and Tfpi2 (Origene, #MR202782) were used.

Techniques: Amplification, Expressing, In Vitro, shRNA, Control, Injection, Immunohistochemistry

Journal: The Journal of Clinical Investigation

Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models

doi: 10.1172/JCI199056

Figure Lengend Snippet: ( A – D ) RT-qPCR ( A and B , n = 3) and immunoblots ( C and D ) for TFPI2, CLOCK, and BMAL1 in GSC17 and GSC23 harboring control or TFPI2 overexpression (OE). ( E ) RT-qPCR ( E , n = 3) and immunoblots ( F ) for TFPI2, CLOCK, and BMAL1 in GSC272 harboring shRNA control (shC) or TFPI2 shRNA (sh TFPI2 ). ( G and H ) Immunoblots for CD133 and SOX2 in GSC17 ( G ) and GSC23 ( H ) harboring control or TFPI2 OE and treated with or without SR9009 (5 μM). ( I ) In vitro limiting dilution assays in GSC17 harboring control or TFPI2 OE and treated with or without SR9009 (5 μM). ( J – L ) Representative images ( J ) and quantification of relative tumorsphere number ( K ) and size ( L ) of GSC17 harboring control or TFPI2 OE treated with or without SR9009 (5 μM). Scale bar: 200 μm. n = 8. ( M ) In vitro limiting dilution assays in GSC23 harboring control or TFPI2 OE and treated with or without SR9009 (5 μM). ( N – P ) Representative images ( N ) and quantification of relative tumorsphere number ( O ) and size ( P ) of GSC23 harboring control or TFPI2 OE treated with or without SR9009 (5 μM). Scale bar: 200 μm. n = 8. ( Q ) Survival curves of nude mice implanted with 2 × 10 5 Control and TFPI2 OE GSC23 and treated with SR9009 (100 mg/kg, i.p., daily) for 10 days beginning at day 7 (n = 8 mice per group). ( R – U ) Representative images and quantification of IHC staining for SOX2 ( R and S ) and CD133 ( T and U ) in Control and TFPI2 OE GSC23 tumors from mice treated with or without SR9009. Scale bar: 100 μm. n = 7. Data from multiple replicates are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, 1-way ANOVA test ( A , B , E , K , L , O , P , S , and U ), 2-way ANOVA test ( I and M ), log-rank test ( Q ).

Article Snippet: Plasmids of human Tagged ORF Clone of CLOCK (Origene, # RC221408), and TFPI2 (Origene, #RC202760) and mouse Tagged ORF Clone of Clock (Origene, #MR226315), and Tfpi2 (Origene, #MR202782) were used.

Techniques: Quantitative RT-PCR, Western Blot, Control, Over Expression, shRNA, In Vitro, Immunohistochemistry

Journal: The Journal of Clinical Investigation

Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models

doi: 10.1172/JCI199056

Figure Lengend Snippet: ( A ) GSEA analysis shows the top 10 enriched hallmark pathways in shRNA control (shC) GSC272 compared with TFPI2 shRNA (sh TFPI2 ) GSC272. Blue bars indicate the top 2 enriched signatures ( FDR < 0.25). ( B and C ) Immunoblots for HIF-1α, P-P65, and P65 in cell lysates of GSC17 ( B ) and GSC23 ( C ) harboring control and TFPI2 overexpression (OE). ( D ) Immunoblots for HIF-1α, P-P6,5 and P65 in cell lysates of shC and sh TFPI2 GSC272. ( E and F ) Immunoblots for HIF-1α, P-P65, and P65 in cell lysates of GSC17 ( E ) and GSC23 ( F ) harboring control and TFPI2 OE treated with or without HIF-1α inhibitor ACF (2 μM). ( G and H ) Quantification of p65 ChIP-PCR in the CLOCK promoter ( G ) and BMAL1 promoter ( H ) of GSC272. IgG was used as Control. n = 3. ( I and J ) RT-qPCR for CLOCK and BMAL1 in GSC17 ( I ) and GSC23 ( J ) harboring TFPI2 OE treated with or without ACF. n = 3. ( K and L ) RT-qPCR for CLOCK and BMAL1 in GSC17 ( K ) and GSC23 ( L ) harboring control or TFPI2 OE treated with or without P65 inhibitor SC75741. n = 3. ( M and N ) Immunoblots for CLOCK and BMAL1 in cell lysates of control and TFPI2 OE GSC17 ( M ) or GSC23 ( N ) treated with or without ACF. ( O and P ) Immunoblots for CLOCK and BMAL1 in cell lysates of control and TFPI2 OE GSC17 ( O ) or GSC23 ( P ) treated with or without SC75741. Data from multiple replicates are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, Student’s t test ( G and H ), 1-way ANOVA test ( I – L ).

Article Snippet: Plasmids of human Tagged ORF Clone of CLOCK (Origene, # RC221408), and TFPI2 (Origene, #RC202760) and mouse Tagged ORF Clone of Clock (Origene, #MR226315), and Tfpi2 (Origene, #MR202782) were used.

Techniques: shRNA, Control, Western Blot, Over Expression, Quantitative RT-PCR

Journal: The Journal of Clinical Investigation

Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models

doi: 10.1172/JCI199056

Figure Lengend Snippet: ( A and B ) Immunoblots for CD133 and SOX2 in cell lysates of GSC17 ( A ) and GSC23 ( B ) harboring control or TFPI2 overexpression (OE) and treated with or without HIF-1α inhibitor ACF (2 μM). ( C and D ) Immunoblots for CD133 and SOX2 in cell lysates of control and TFPI2 -OE GSC17 ( C ) and GSC23 ( D ) treated with or without P65 inhibitor SC75741 (5 μM). ( E ) In vitro limiting dilution assays in control and TFPI2 -OE GSC17 treated with or without ACF (2 μM) or SC75741 (5 μM). ( F – H ) Representative images ( F ) and quantification of relative tumorsphere number ( G ) and size ( H ) of control and TFPI2 -OE GSC17 treated with or without ACF or SC75741. Scale bar: 200 μm. n = 8. ( I ) In vitro limiting dilution assays in control and TFPI2 -OE GSC23 treated with or without ACF (2 μM) or SC75741 (5 μM). ( J – L ) Representative images ( J ) and quantification of relative tumorsphere number ( K ) and size ( L ) of control and TFPI2 -OE GSC23 treated with or without ACF or SC75741. Scale bar: 200 μm. n = 8. ( M – P ) Representative and quantification of proliferation in GSC17 ( M and N ) and GSC23 ( O and P ) harboring control or TFPI2 OE treated with or without ACF (2 μM) or SC75741 (5 μM). n = 3. Data from multiple replicates are presented as mean ± SD. ** P < 0.01, *** P < 0.001, 1-way ANOVA test ( G , H , K , L , N , and P ), 2-way ANOVA test ( E and I ).

Article Snippet: Plasmids of human Tagged ORF Clone of CLOCK (Origene, # RC221408), and TFPI2 (Origene, #RC202760) and mouse Tagged ORF Clone of Clock (Origene, #MR226315), and Tfpi2 (Origene, #MR202782) were used.

Techniques: Western Blot, Control, Over Expression, In Vitro

Journal: The Journal of Clinical Investigation

Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models

doi: 10.1172/JCI199056

Figure Lengend Snippet: ( A ) Schematic diagram depicting the positive feedback loop between TFPI2 and the CLOCK-BMAL1 complex in GSCs and the strategy of dual targeting their downstream signaling pathways to block GSC self renewal. ( B ) Survival curves of nude mice implanted with 2 × 10 5 GSC272 and treated with LDHA inhibitor Stiripentol (150 mg/kg, i.p., every other day), JNK inhibitor JNK-IN-8 (30 mg/kg, i.p., daily), STAT3 inhibitor WP1066 (30 mg/kg, i.p., daily), or Stiripentol in combination with JNK-IN-8 or WP1066 for 2 weeks beginning at day 7. n = 8 mice per group. ( C – F ) Representative images and quantification of IHC staining for SOX2 ( C and D ) and CD133 ( E and F ) in GSC272 tumors from mice with indicated treatments. Scale bar: 100 μm. n = 4. ( G and H ) Representative images ( G ) and quantification ( H ) of flow cytometry for the percentage of CD45 low CD11b + TMEM119 + CD206 + microglia (out of CD45 low CD11b + TMEM119 + microglia) in tumors from 005 GSC-bearing mice with indicated treatments. n = 3. ( I and J ) Representative images ( I ) and quantification ( J ) of flow cytometry for the percentage of CD45 + CD3 + CD8 + IFNγ + T cells (out of CD45 + CD3 + CD8 + T cells) in tumors from 005 GSC-bearing mice with indicated treatments. n = 3. ( K ) Survival curves of C57BL/6J mice implanted with 2 × 10 5 005 GSCs and treated with Stiripentol, JNK-IN-8, or WP1066, and Stiripentol in combination with JNK-IN-8 or WP1066 for 2 weeks beginning at day 7, and with anti-PD1 (10 mg/kg, i.p.) treatment on days 11, 14, and 17. n = 8 mice per group. Data from multiple replicates are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, 1-way ANOVA test ( D , F , H , and J ), log-rank test ( B and K ).

Article Snippet: Plasmids of human Tagged ORF Clone of CLOCK (Origene, # RC221408), and TFPI2 (Origene, #RC202760) and mouse Tagged ORF Clone of Clock (Origene, #MR226315), and Tfpi2 (Origene, #MR202782) were used.

Techniques: Protein-Protein interactions, Blocking Assay, Immunohistochemistry, Flow Cytometry

Journal: bioRxiv

Article Title: TL1A-activated T cells remodel the rectal mucosa in Crohn’s disease patients with perianal fistulizing disease

doi: 10.1101/2025.06.26.657455

Figure Lengend Snippet: A: Violin plot for LTB expression in the T-cell compartment. The adjusted p-values obtained by DEG analysis are indicated for each comparison. B: ELISA for TFPI2 in the supernatants of primary intestinal fibroblasts stimulated with LTα 1 β 2 (100ng/ml) for 24 hours compared to the unstimulated condition. Paired T test, nonparametric, n=10, ** = p < 0.01. C: Violin plot for LTB and TNFRSF25 expression in the CD4+ T cell compartment, comparing CDun and CDinf patients. The adjusted p-values generated by DEG analysis are indicated. D: Violin plot for LTB and TNFRSF25 expression in the CD4+ T cell compartment, comparing CDinf and CD+PFDinf patients. The adjusted p-values generated by DEG analysis are indicated. E: On the left, Uniform Manifold Approximation and Projection (UMAP) plots of the whole object showing the expression of TNFSF15 . On the right, violin plots indicating the expression of TNFSF15 . F: Graphical representation of the flow cytometry approach to detect LTα 1 β 2 + T cells.

Article Snippet: Supernatants of stimulated fibroblasts and tissue explants were used for cytokine detection using the DuoSet ELISA Kits from R&D for human MMP1 (DY901B) and IL-22 (DY782), and the human TFPI2 ELISA Kit from MyBioSource (MBS2507217) according to the manufacturer’s instructions.

Techniques: Expressing, Comparison, Enzyme-linked Immunosorbent Assay, Generated, Flow Cytometry

Journal: Cancers

Article Title: Reassessing the Role of Tissue Factor Pathway Inhibitor 2 in Neoplastic and Non-Neoplastic Lesions

doi: 10.3390/cancers17091447

Figure Lengend Snippet: Relationship between the regulation of TFPI2 expression in cancer cells and host cells. The signaling pathway constituents numbered 1 to 21 in the figure are described in sections of the text labeled as (1,2), and so forth. Arrows denote activation, while T-shaped symbols represent inhibition. ACTN4, actinin 4; AP-1, activator protein 1; AP-2α, activator protein 2 alpha; CLIP1, CAP-Gly domain-containing linker protein 1 (CLIP1); COX-2, cyclooxygenase-2; DNMT1, DNA methyltransferase 1; EGF, epidermal growth factor; ERK, extracellular signal-regulated kinase; HGF, hepatocyte growth factor; IL-10, interleukin-10; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; MBD3, methyl-CpG-binding domain protein 3; MMP, matrix metalloproteinase; MYH9, myosin 9; MITF, melanocyte-induced transcription factor; NF-κB, nuclear factor kappa B; PPARγ, peroxisome proliferator-activated receptor gamma; PSAP, prosaposin; SLUG, snail family transcriptional repressor 2; TAM, tumor-associated macrophages; TFPI2, tissue factor pathway inhibitor 2; TGF-β, transforming growth factor beta; TGFBI, transforming growth factor beta-induced; TIRAP, TIR domain containing adaptor protein; TMPRSS4, transmembrane protease serine 4; uPA, urokinase-type plasminogen activator; VEC, vascular endothelial cells; VEGF, vascular endothelial growth factor; VSMC, vascular smooth muscle cells.

Article Snippet: Tosoh Corporation has developed an automated immunoassay for quantifying TFPI2 concentrations in blood, using a one-step immunofluorescence technique with two anti-TFPI2 monoclonal antibodies [ ].

Techniques: Expressing, Labeling, Activation Assay, Inhibition, Binding Assay

Journal: Cancers

Article Title: Reassessing the Role of Tissue Factor Pathway Inhibitor 2 in Neoplastic and Non-Neoplastic Lesions

doi: 10.3390/cancers17091447

Figure Lengend Snippet: Molecules and signaling pathways regulated by TFPI2. The left pie chart illustrates molecules and signaling pathways modulated by TFPI2 that are implicated in the regulation of glucose and lipid metabolism, macrophage polarization, inflammatory responses, immune modulation, and cellular proliferation and survival. In contrast, the right pie chart depicts molecules and signaling cascades associated with extracellular matrix remodeling, cytoskeletal integrity, and cellular motility.

Article Snippet: Tosoh Corporation has developed an automated immunoassay for quantifying TFPI2 concentrations in blood, using a one-step immunofluorescence technique with two anti-TFPI2 monoclonal antibodies [ ].

Techniques: Protein-Protein interactions

Journal: Cancers

Article Title: Reassessing the Role of Tissue Factor Pathway Inhibitor 2 in Neoplastic and Non-Neoplastic Lesions

doi: 10.3390/cancers17091447

Figure Lengend Snippet: Molecular and signaling pathways governing the regulation of TFPI2 expression. The left pie chart depicts factors that promote the upregulation of TFPI2, while the right pie chart illustrates those that facilitate its downregulation. These genes contribute to cancer invasion and metastasis by modulating inflammatory responses, promoting angiogenesis, regulating immune functions, and influencing tumor cell proliferation, survival, and apoptotic pathways.

Article Snippet: Tosoh Corporation has developed an automated immunoassay for quantifying TFPI2 concentrations in blood, using a one-step immunofluorescence technique with two anti-TFPI2 monoclonal antibodies [ ].

Techniques: Protein-Protein interactions, Expressing

Journal: Cancers

Article Title: Reassessing the Role of Tissue Factor Pathway Inhibitor 2 in Neoplastic and Non-Neoplastic Lesions

doi: 10.3390/cancers17091447

Figure Lengend Snippet: The role of TFPI2 in pregnancy-induced hypertension, diabetes, and atherosclerosis. TFPI2 orchestrates extracellular matrix (ECM) remodeling, tissue regeneration, angiogenesis, and immune modulation. The preservation or disturbance of cellular homeostasis through inflammatory processes may result in TFPI2 dysregulation, thereby contributing to the onset and progression of diabetes, atherosclerosis, and pregnancy-induced hypertension. Superscript arrows represent the upregulation of each factor or the activation of pathological or functional processes, whereas subscript arrows denote downregulation or functional inhibition. DNMT1, DNA methyltransferase 1; ERK, extracellular signal-regulated kinase; EZH1, enhancer of zeste 1 polycomb repressive complex 2 subunit; H3K27me3, tri-methylation at lysine 27 of histone H3; IL-1, interleukin-1; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; MΦ, macrophage; PI3K, phosphatidylinositol-3-kinase; PPARγ, peroxisome proliferator-activated receptor gamma; TFPI2, tissue factor pathway inhibitor 2; TGF-β, transforming growth factor-beta; TNF-α, tumor necrosis factor-alfa; VEC, vascular endothelial cells; VEGFR, vascular endothelial growth factor receptor; VSMC, vascular smooth muscle cells.

Article Snippet: Tosoh Corporation has developed an automated immunoassay for quantifying TFPI2 concentrations in blood, using a one-step immunofluorescence technique with two anti-TFPI2 monoclonal antibodies [ ].

Techniques: Preserving, Activation Assay, Functional Assay, Inhibition, Methylation

Journal: Cancers

Article Title: Reassessing the Role of Tissue Factor Pathway Inhibitor 2 in Neoplastic and Non-Neoplastic Lesions

doi: 10.3390/cancers17091447

Figure Lengend Snippet: Role of TFPI2 in cancer invasion and metastasis. As illustrated in the upper left panel, TFPI2 overexpression suppresses ECM remodeling and inhibits tumor invasion in vitro. Conversely, the upper right panel shows that TFPI2 downregulation facilitates invasion through MMP-mediated ECM degradation. In vivo, TFPI2 influences not only cancer cells but also diverse components of the TME, including inflammatory and immune cells, endothelial cells, cytokines, ECM constituents, and angiogenic factors, thereby playing a pivotal role in modulating tumor malignancy and metastatic dissemination. Superscript arrows represent the upregulation of each factor or the activation of pathological or functional processes, whereas subscript arrows denote downregulation or functional inhibition.

Article Snippet: Tosoh Corporation has developed an automated immunoassay for quantifying TFPI2 concentrations in blood, using a one-step immunofluorescence technique with two anti-TFPI2 monoclonal antibodies [ ].

Techniques: Over Expression, In Vitro, In Vivo, Activation Assay, Functional Assay, Inhibition