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ATCC a549 stat1

OptiLAIV is attenuated and safe in <t>Stat1</t> −/− mice. (A) Scheme of mouse immunization. (B) 8-week-old Stat1 −/− mice were vaccinated intranasally under anesthesia with 10 4 PFU LAIV or optiLAIV in 25 μL and body weight (left panel) and survival (right panel) were monitored for 14 days postvaccination ( n = 4 mock-vaccinated group; n = 8 per vaccinated group). (C) 8-week-old Stat1 −/− mice were vaccinated intranasally under anesthesia with 10 5 PFU LAIV or optiLAIV in 25 μL PBS. At 2, 4 and 6 days postvaccination snouts (left panel) and lungs (right panel) were collected and viral titers were determined by plaque assay ( n = 5 per group). The statistical significances between LAIV group and optiLAIV group were determined using two-way ANOVA with the Geisser-Greenhouse correction and post hoc Dunn’s multiple-comparison test in panel B and Mantel-Cox test for survival curve; multiple Mann-Whitney tests in panel C;. P-values are indicated in the figure. *, comparison between LAIV and optiLAIV. L.o.D. = limit of detection (5 PFU/mL). Graphs are representative of 2 independent experiments and indicate mean ± SEM for panel B and geometric mean for panel C. Symbols represent data from individual mice for panel B. In C, black dotted line represents 15% body weight loss cutoff.

A549 Stat1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 31811 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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a549 stat1 - by Bioz Stars, 2026-08

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1) Product Images from "Optimizing the Live Attenuated Influenza A Vaccine Backbone for High-Risk Patient Groups"

Article Title: Optimizing the Live Attenuated Influenza A Vaccine Backbone for High-Risk Patient Groups

Journal: Journal of Virology

doi: 10.1128/jvi.00871-22

OptiLAIV is attenuated and safe in Stat1 −/− mice. (A) Scheme of mouse immunization. (B) 8-week-old Stat1 −/− mice were vaccinated intranasally under anesthesia with 10 4 PFU LAIV or optiLAIV in 25 μL and body weight (left panel) and survival (right panel) were monitored for 14 days postvaccination ( n = 4 mock-vaccinated group; n = 8 per vaccinated group). (C) 8-week-old Stat1 −/− mice were vaccinated intranasally under anesthesia with 10 5 PFU LAIV or optiLAIV in 25 μL PBS. At 2, 4 and 6 days postvaccination snouts (left panel) and lungs (right panel) were collected and viral titers were determined by plaque assay ( n = 5 per group). The statistical significances between LAIV group and optiLAIV group were determined using two-way ANOVA with the Geisser-Greenhouse correction and post hoc Dunn’s multiple-comparison test in panel B and Mantel-Cox test for survival curve; multiple Mann-Whitney tests in panel C;. P-values are indicated in the figure. *, comparison between LAIV and optiLAIV. L.o.D. = limit of detection (5 PFU/mL). Graphs are representative of 2 independent experiments and indicate mean ± SEM for panel B and geometric mean for panel C. Symbols represent data from individual mice for panel B. In C, black dotted line represents 15% body weight loss cutoff.

Figure Legend Snippet: OptiLAIV is attenuated and safe in Stat1 −/− mice. (A) Scheme of mouse immunization. (B) 8-week-old Stat1 −/− mice were vaccinated intranasally under anesthesia with 10 4 PFU LAIV or optiLAIV in 25 μL and body weight (left panel) and survival (right panel) were monitored for 14 days postvaccination ( n = 4 mock-vaccinated group; n = 8 per vaccinated group). (C) 8-week-old Stat1 −/− mice were vaccinated intranasally under anesthesia with 10 5 PFU LAIV or optiLAIV in 25 μL PBS. At 2, 4 and 6 days postvaccination snouts (left panel) and lungs (right panel) were collected and viral titers were determined by plaque assay ( n = 5 per group). The statistical significances between LAIV group and optiLAIV group were determined using two-way ANOVA with the Geisser-Greenhouse correction and post hoc Dunn’s multiple-comparison test in panel B and Mantel-Cox test for survival curve; multiple Mann-Whitney tests in panel C;. P-values are indicated in the figure. *, comparison between LAIV and optiLAIV. L.o.D. = limit of detection (5 PFU/mL). Graphs are representative of 2 independent experiments and indicate mean ± SEM for panel B and geometric mean for panel C. Symbols represent data from individual mice for panel B. In C, black dotted line represents 15% body weight loss cutoff.

Techniques Used: Plaque Assay, Comparison, MANN-WHITNEY

OptiLAIV NS1 allows unfolded protein response activation in human cell models. (A–B) A549 cells were infected at an MOI of 5 with LAIV or optiLAIV or treated with tunicamycin at 5 μg/mL. At 16 h and 24 h postinfection RT-PCR was performed from isolated RNA for the spliced form of XBP1 mRNA (A). In parallel at 8 h, 16 h and 24 h postinfection, lysates were analyzed by Western blot for expression of sXBP1, actin, NP and NS1 proteins (B). (C) A549 wt cells (upper panel) or A549 Stat1 −/− cells (lower panel) were infected at an MOI of 5 with LAIV or optiLAIV and RT-qPCR for UPR-induced genes DNAJB9 and DDIT3 was performed in RNA lysates at 16 h and 24 h postinfection. (D) A549 wt cells (upper panel) or A549 Stat1 −/− cells (lower panel) were infected at an MOI of 0.01 with either LAIV or optiLAIV. Supernatants were collected at indicated time postinfection and viral titers determined by plaque assay. (E) Primary human nasal epithelial cells (Mucilair) were infected at an MOI of 5 with LAIV or optiLAIV. Cells were lysed at 24 h postinfection and RT-qPCR for each respective gene was performed. The statistical significances between LAIV group and optiLAIV group were determined using one-way ANOVA with post hoc Tukey’s multiple-comparison test for panels A, C and E; two-way ANOVA with the Geisser-Greenhouse correction and post hoc Dunn’s multiple-comparison test for panel D. *, comparison between LAIV and optiLAIV; # : comparison between mock and optiLAIV; ns = nonsignificant. Graphs are representative of 3 independent experiments and indicate mean ± SD.

Figure Legend Snippet: OptiLAIV NS1 allows unfolded protein response activation in human cell models. (A–B) A549 cells were infected at an MOI of 5 with LAIV or optiLAIV or treated with tunicamycin at 5 μg/mL. At 16 h and 24 h postinfection RT-PCR was performed from isolated RNA for the spliced form of XBP1 mRNA (A). In parallel at 8 h, 16 h and 24 h postinfection, lysates were analyzed by Western blot for expression of sXBP1, actin, NP and NS1 proteins (B). (C) A549 wt cells (upper panel) or A549 Stat1 −/− cells (lower panel) were infected at an MOI of 5 with LAIV or optiLAIV and RT-qPCR for UPR-induced genes DNAJB9 and DDIT3 was performed in RNA lysates at 16 h and 24 h postinfection. (D) A549 wt cells (upper panel) or A549 Stat1 −/− cells (lower panel) were infected at an MOI of 0.01 with either LAIV or optiLAIV. Supernatants were collected at indicated time postinfection and viral titers determined by plaque assay. (E) Primary human nasal epithelial cells (Mucilair) were infected at an MOI of 5 with LAIV or optiLAIV. Cells were lysed at 24 h postinfection and RT-qPCR for each respective gene was performed. The statistical significances between LAIV group and optiLAIV group were determined using one-way ANOVA with post hoc Tukey’s multiple-comparison test for panels A, C and E; two-way ANOVA with the Geisser-Greenhouse correction and post hoc Dunn’s multiple-comparison test for panel D. *, comparison between LAIV and optiLAIV; # : comparison between mock and optiLAIV; ns = nonsignificant. Graphs are representative of 3 independent experiments and indicate mean ± SD.

Techniques Used: Activation Assay, Infection, Reverse Transcription Polymerase Chain Reaction, Isolation, Western Blot, Expressing, Quantitative RT-PCR, Plaque Assay, Comparison

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a Evaluation of colony formation efficacy of HCT116 and HK2-8 cells after treatments with either scramble siRNAs or STAT1 siRNAs. The graphs represent data obtained from 3 biological replicates, each of which included 3 technical replicates, and represent ±SEM ( * ) P < 0.05 ( ** ) P < 0.01; ( t -test), NS, non-significant. b Immunoblotting of indicated protein from extracts of siRNA-treated cells. Quantifications show the relative intensity of STAT1 normalized to ACTIN from 3 biological replicates and represent ±SEM * P < 0.05 ( t -test). c Volcano Diagram illustrates the number of genes differentially expressed in STAT1-replete (WT; control) compared to STAT1 -/- HCT116 cells. Essential genes of sterol and lipid biosynthetic pathways are indicated. Dashed horizontal and vertical lines indicate significance thresholds (|FC | > 0.5, P < 0.05). Genes are colored in gray (non-significant), blue ( P -value significant), and red (both P -values and fold change are significant). A positive fold change means that the gene is upregulated by STAT1. All labeled genes exhibit statistically significant upregulation (logFC > 0.5, P < 0.0005), consistent with their role in cholesterol biosynthesis and lipid metabolism. d Bar plot of biological processes (BP) from gene ontology (ON) significantly enriched in STAT1-dependent genes in HCT116 cells. e KEGG pathways under the control of STAT1 in HCT116 cells.

Journal: Communications Biology

Article Title: A feedforward loop between STAT1 and YAP1 stimulates lipid biosynthesis, accelerates tumor growth, and promotes chemotherapy resistance in mutant KRAS colorectal cancer

doi: 10.1038/s42003-025-08740-2

Figure Lengend Snippet: a Evaluation of colony formation efficacy of HCT116 and HK2-8 cells after treatments with either scramble siRNAs or STAT1 siRNAs. The graphs represent data obtained from 3 biological replicates, each of which included 3 technical replicates, and represent ±SEM ( * ) P < 0.05 ( ** ) P < 0.01; ( t -test), NS, non-significant. b Immunoblotting of indicated protein from extracts of siRNA-treated cells. Quantifications show the relative intensity of STAT1 normalized to ACTIN from 3 biological replicates and represent ±SEM * P < 0.05 ( t -test). c Volcano Diagram illustrates the number of genes differentially expressed in STAT1-replete (WT; control) compared to STAT1 -/- HCT116 cells. Essential genes of sterol and lipid biosynthetic pathways are indicated. Dashed horizontal and vertical lines indicate significance thresholds (|FC | > 0.5, P < 0.05). Genes are colored in gray (non-significant), blue ( P -value significant), and red (both P -values and fold change are significant). A positive fold change means that the gene is upregulated by STAT1. All labeled genes exhibit statistically significant upregulation (logFC > 0.5, P < 0.0005), consistent with their role in cholesterol biosynthesis and lipid metabolism. d Bar plot of biological processes (BP) from gene ontology (ON) significantly enriched in STAT1-dependent genes in HCT116 cells. e KEGG pathways under the control of STAT1 in HCT116 cells.

Article Snippet: Plasmids containing the green fluorescence protein (GFP)-tagged forms of wild type STAT1, STAT1 Y701F or STAT1 S727A cDNA were obtained from Addgene (plasmid #12301,12302 and 12304) .

Techniques: Western Blot, Control, Labeling

a Detection of SREBF mRNAs in colon cancer cells with intact or impaired STAT1. SREBF 1 and 2 mRNA levels were normalized to ACTIN and TUBULIN mRNAs used as internal controls. Data obtained from 3 biological replicates each of which contained 3 technical replicates and represent ±SEM ** P < 0.01: *** P < 0.001 ( t -test), NS, non-significant. b Immunoblotting for SREBP1 and 2 in colon cancer cells with intact or downregulated STAT1. Quantifications show the relative intensity of proteins normalized to TUBULIN. FL, full length; M, mature form. c Schematic representation of the mevalonate pathway. Genes in red are SREBP-dependent genes. d ChIP-seq data from ENCODE (UCSC data base) indicating the binding of SREBP1 and 2 to transcriptional regulatory regions of mevalonate pathway genes. Graphs show the expression of ACAT1 , HMGCR and IDI1 mRNAs by qPCR in cells treated with scrambled or STAT1 siRNAs. Gene expressions were normalized to ACTIN and TUBULIN mRNAs used as internal controls. Data were obtained from 3 independent experiments performed in triplicates and represent ±SEM *P < 0.05, **P < 0.01, *** P < 0.001 ( t -test). e Immunoblotting of HCT116 protein extracts replete (control) or deplete ( −/− ) for STAT1 by CRISPR (cell line #1 and #2). Detection of STAT1 and rate-limiting enzymes of sterol and lipid biosynthetic pathway HMGCR and FAS, respectively.

Journal: Communications Biology

Article Title: A feedforward loop between STAT1 and YAP1 stimulates lipid biosynthesis, accelerates tumor growth, and promotes chemotherapy resistance in mutant KRAS colorectal cancer

doi: 10.1038/s42003-025-08740-2

Figure Lengend Snippet: a Detection of SREBF mRNAs in colon cancer cells with intact or impaired STAT1. SREBF 1 and 2 mRNA levels were normalized to ACTIN and TUBULIN mRNAs used as internal controls. Data obtained from 3 biological replicates each of which contained 3 technical replicates and represent ±SEM ** P < 0.01: *** P < 0.001 ( t -test), NS, non-significant. b Immunoblotting for SREBP1 and 2 in colon cancer cells with intact or downregulated STAT1. Quantifications show the relative intensity of proteins normalized to TUBULIN. FL, full length; M, mature form. c Schematic representation of the mevalonate pathway. Genes in red are SREBP-dependent genes. d ChIP-seq data from ENCODE (UCSC data base) indicating the binding of SREBP1 and 2 to transcriptional regulatory regions of mevalonate pathway genes. Graphs show the expression of ACAT1 , HMGCR and IDI1 mRNAs by qPCR in cells treated with scrambled or STAT1 siRNAs. Gene expressions were normalized to ACTIN and TUBULIN mRNAs used as internal controls. Data were obtained from 3 independent experiments performed in triplicates and represent ±SEM *P < 0.05, **P < 0.01, *** P < 0.001 ( t -test). e Immunoblotting of HCT116 protein extracts replete (control) or deplete ( −/− ) for STAT1 by CRISPR (cell line #1 and #2). Detection of STAT1 and rate-limiting enzymes of sterol and lipid biosynthetic pathway HMGCR and FAS, respectively.

Techniques: Western Blot, ChIP-sequencing, Binding Assay, Expressing, Control, CRISPR

a ChIP-seq data from ENCODE (UCSC database) indicating STAT1 binding to the regulatory regions of SREBF1 and 2 genes. b ChIP assays of endogenous STAT1 bound to SREBF gene segments containing STAT1 binding sites in HCT116 and HK2-8 cells. IgG, non-specific control antibody. c Expression of GFP (control) and GFP-tagged STAT1 proteins that are either intact (wild type, WT), impaired for phosphorylation (Y701F or S727A) or S727 phosphomimetic (S727E) in HCT116 STAT1 −/− cells. GFP+ cells were sorted by flow cytometry, and extracts were immunoblotted for GFP or ACTIN. d Detection of SREBF-1 and 2 mRNAs by qPCR in HCT116 STAT1 −/− cells expressing either GFP or GFP-STAT1 forms. e ChIP assays of GFP-STAT1 for binding to STAT1 sites of SREBF genes in reconstituted HCT116 STAT1 −/− cells using GFP antibody. b–e Data obtained from 3 biological replicates and represent ±SEM *P < 0.05, **P < 0.01, *** P < 0.001 ( t -test).

Journal: Communications Biology

Article Title: A feedforward loop between STAT1 and YAP1 stimulates lipid biosynthesis, accelerates tumor growth, and promotes chemotherapy resistance in mutant KRAS colorectal cancer

doi: 10.1038/s42003-025-08740-2

Figure Lengend Snippet: a ChIP-seq data from ENCODE (UCSC database) indicating STAT1 binding to the regulatory regions of SREBF1 and 2 genes. b ChIP assays of endogenous STAT1 bound to SREBF gene segments containing STAT1 binding sites in HCT116 and HK2-8 cells. IgG, non-specific control antibody. c Expression of GFP (control) and GFP-tagged STAT1 proteins that are either intact (wild type, WT), impaired for phosphorylation (Y701F or S727A) or S727 phosphomimetic (S727E) in HCT116 STAT1 −/− cells. GFP+ cells were sorted by flow cytometry, and extracts were immunoblotted for GFP or ACTIN. d Detection of SREBF-1 and 2 mRNAs by qPCR in HCT116 STAT1 −/− cells expressing either GFP or GFP-STAT1 forms. e ChIP assays of GFP-STAT1 for binding to STAT1 sites of SREBF genes in reconstituted HCT116 STAT1 −/− cells using GFP antibody. b–e Data obtained from 3 biological replicates and represent ±SEM *P < 0.05, **P < 0.01, *** P < 0.001 ( t -test).

Techniques: ChIP-sequencing, Binding Assay, Control, Expressing, Phospho-proteomics, Flow Cytometry

$a HCT116 and HK2-8 cells replete or deplete of STAT1 were serum-starved for 18 h (untreated; UT) and stimulated with either 10% fetal bovine serum or 25 μM LPA for 1 h. Cells were subjected to IF analyses of YAP1 (red) along with DAPI staining of DNA (blue). Graphs show the quantification of YAP1 nuclear localization in 300 cells. Scale bar: 25 μm. b , c Cells were subjected to cytoplasmic (C), and nuclear (N) fractionation followed by immunoblotting for the indicated proteins. TUBULIN or THO complex 1 (THOC1) was used as cytoplasmic or nuclear marker, respectively. Quantification in panel b is based on three biological replicates, while panel c is based on two biological replicates. d , e HCT116 STAT1 +/+ and STAT1 −/− cells were transfected with either pGL3-luciferase reporter plasmid (control) or 8xGTIIC plasmid containing the firefly luciferase reporter gene under the control of 8x TEAD binding sites in CTGF minimal promoter. Transfected cells were serum-starved for 18 h followed by stimulation with either 10% fetal bovine serum or 25 μM LPA for 6 h. A plasmid expressing the renilla luciferase gene was used as internal control. f , g HCT116 cells were serum starved for 18 h followed by stimulation of 10% fetal bovine serum in the absence or presence of 2.5 mM cerivastatin (panel f, g) or 10 μM ROCK kinase inhibitor Y-27632 (panel f) for 18 h. Protein extracts were subjected to immunoblotting for the indicated proteins. a , b , d , e Graphs show the quantifications from 3 biological replicates and represent ±SEM *P < 0.05, **P < 0.01, *** P < 0.001 ( t -test), NS, non-significant. In c , data represent the quantification of 2 biological replicates.$

Journal: Communications Biology

Article Title: A feedforward loop between STAT1 and YAP1 stimulates lipid biosynthesis, accelerates tumor growth, and promotes chemotherapy resistance in mutant KRAS colorectal cancer

doi: 10.1038/s42003-025-08740-2

Figure Lengend Snippet: a HCT116 and HK2-8 cells replete or deplete of STAT1 were serum-starved for 18 h (untreated; UT) and stimulated with either 10% fetal bovine serum or 25 μM LPA for 1 h. Cells were subjected to IF analyses of YAP1 (red) along with DAPI staining of DNA (blue). Graphs show the quantification of YAP1 nuclear localization in 300 cells. Scale bar: 25 μm. b , c Cells were subjected to cytoplasmic (C), and nuclear (N) fractionation followed by immunoblotting for the indicated proteins. TUBULIN or THO complex 1 (THOC1) was used as cytoplasmic or nuclear marker, respectively. Quantification in panel b is based on three biological replicates, while panel c is based on two biological replicates. d , e HCT116 STAT1 +/+ and STAT1 −/− cells were transfected with either pGL3-luciferase reporter plasmid (control) or 8xGTIIC plasmid containing the firefly luciferase reporter gene under the control of 8x TEAD binding sites in CTGF minimal promoter. Transfected cells were serum-starved for 18 h followed by stimulation with either 10% fetal bovine serum or 25 μM LPA for 6 h. A plasmid expressing the renilla luciferase gene was used as internal control. f , g HCT116 cells were serum starved for 18 h followed by stimulation of 10% fetal bovine serum in the absence or presence of 2.5 mM cerivastatin (panel f, g) or 10 μM ROCK kinase inhibitor Y-27632 (panel f) for 18 h. Protein extracts were subjected to immunoblotting for the indicated proteins. a , b , d , e Graphs show the quantifications from 3 biological replicates and represent ±SEM *P < 0.05, **P < 0.01, *** P < 0.001 ( t -test), NS, non-significant. In c , data represent the quantification of 2 biological replicates.

Techniques: Staining, Fractionation, Western Blot, Marker, Transfection, Luciferase, Plasmid Preparation, Control, Binding Assay, Expressing

a Volcano diagram showing the number of differentially expressed genes in YAP1-replete (WT; control) compared to YAP1 −/− HCT116 cells. Dashed horizontal and vertical lines indicate significance thresholds (|FC | > 0.5, P < 0.05). A positive fold change means that the gene is upregulated by YAP1. Genes are colored in gray (non-significant), blue ( P -value significant), and red (both P -values and fold change are significant). All labeled genes exhibit statistically significant upregulation (logFC > 0.5, P < 0.0005), consistent with their role in cholesterol biosynthesis and lipid metabolism. b Top KEGG pathways under the control of YAP1 in HCT116 cells. c Graphs assess the expression of SREBF1 and 2 mRNAs by qPCR in cells treated with scrambled or YAP1 siRNAs. Gene expressions were normalized to ACTIN and TUBULIN mRNAs used as internal controls. Data were obtained from 3 independent experiments performed in triplicates and represent ±SEM *P < 0.05, * *P < 0.01, *** P < 0.001 ( t -test). d ChIP-seq data from ENCODE indicating the binding of TEAD4 to transcriptional regulatory regions of SREBF genes. e ChIP assays of YAP1 for binding in complex with TEAD4 to SREBF genes in HCT116 cells, both in the presence and absence of STAT1 and/or YAP1. IgG, non-specific control antibody. f Immunoblotting of SREBP1 and 2 in isogenic pair colon cancer cells prior to and after YAP1 downregulation by siRNAs. FL, full length. g Immunoblotting of SREBP1, 2 and TEAD4 in isogenic pairs of colon cancer cells treated with scrambled or TEAD4 siRNAs. h Immunoblotting of SREBP1 and 2 proteins in HCT116 cells treated with TEAD inhibitor 15 μM VT104 for the indicated time points. f , g , h Quantification of proteins normalized to TUBULIN for each blot is indicated.

Journal: Communications Biology

Article Title: A feedforward loop between STAT1 and YAP1 stimulates lipid biosynthesis, accelerates tumor growth, and promotes chemotherapy resistance in mutant KRAS colorectal cancer

doi: 10.1038/s42003-025-08740-2

Figure Lengend Snippet: a Volcano diagram showing the number of differentially expressed genes in YAP1-replete (WT; control) compared to YAP1 −/− HCT116 cells. Dashed horizontal and vertical lines indicate significance thresholds (|FC | > 0.5, P < 0.05). A positive fold change means that the gene is upregulated by YAP1. Genes are colored in gray (non-significant), blue ( P -value significant), and red (both P -values and fold change are significant). All labeled genes exhibit statistically significant upregulation (logFC > 0.5, P < 0.0005), consistent with their role in cholesterol biosynthesis and lipid metabolism. b Top KEGG pathways under the control of YAP1 in HCT116 cells. c Graphs assess the expression of SREBF1 and 2 mRNAs by qPCR in cells treated with scrambled or YAP1 siRNAs. Gene expressions were normalized to ACTIN and TUBULIN mRNAs used as internal controls. Data were obtained from 3 independent experiments performed in triplicates and represent ±SEM *P < 0.05, * *P < 0.01, *** P < 0.001 ( t -test). d ChIP-seq data from ENCODE indicating the binding of TEAD4 to transcriptional regulatory regions of SREBF genes. e ChIP assays of YAP1 for binding in complex with TEAD4 to SREBF genes in HCT116 cells, both in the presence and absence of STAT1 and/or YAP1. IgG, non-specific control antibody. f Immunoblotting of SREBP1 and 2 in isogenic pair colon cancer cells prior to and after YAP1 downregulation by siRNAs. FL, full length. g Immunoblotting of SREBP1, 2 and TEAD4 in isogenic pairs of colon cancer cells treated with scrambled or TEAD4 siRNAs. h Immunoblotting of SREBP1 and 2 proteins in HCT116 cells treated with TEAD inhibitor 15 μM VT104 for the indicated time points. f , g , h Quantification of proteins normalized to TUBULIN for each blot is indicated.

Techniques: Control, Labeling, Expressing, ChIP-sequencing, Binding Assay, Western Blot

Journal: Communications Biology

Article Title: A feedforward loop between STAT1 and YAP1 stimulates lipid biosynthesis, accelerates tumor growth, and promotes chemotherapy resistance in mutant KRAS colorectal cancer

doi: 10.1038/s42003-025-08740-2

Figure Lengend Snippet: Venn diagram ( a ) and Volcano diagram ( b ) of genes that are commonly upregulated by STAT1 and YAP1 in HCT116 cells. Essential genes of sterol and lipid biosynthetic pathways are indicated in the Volcano diagram. b Dashed horizontal and vertical lines indicate significance thresholds (|FC | > 0.5, P < 0.05). A positive fold change means that the gene is upregulated by STAT1 and YAP1. Genes are colored in gray (non-significant), blue ( P -value significant), and Red (both P -values and fold change are significant). All labeled genes exhibit statistically significant upregulation (logFC > 0.5, P < 0.0005), consistent with their role in cholesterol biosynthesis and lipid metabolism. c Bar plot of biological processes (BP) from gene ontology (GO) significantly enriched in the common set of genes under the control of both YAP1 and STAT1 identified by gene expression profile analysis. d KEGG pathways under the control of STAT1 and YAP1 in HCT116 cells. e This schematic illustrates the cooperative role of STAT1 and YAP1 in promoting SREBP expression and activating the mevalonate pathway in mutant KRAS CRCs. The STAT1–YAP1 axis functions as a feedforward autoregulatory loop that sustains sterol biosynthesis. STAT1, phosphorylated at S727, directly induces the transcription of SREBF1 and SREBF2 genes. Elevated SREBP levels, in turn, enhance mevalonate pathway activity, leading to the prenylation, plasma membrane anchoring and activation of RHO GTPases. This activation promotes further phosphorylation of STAT1 at S727 and stimulates YAP1 nuclear localization and activation. Although YAP1 acts downstream of STAT1, it also reinforces the loop by cooperating with TEAD4 to transcriptionally upregulate SREBF genes. Created in BioRender. Koromilas, A. (2025) https://BioRender.com/nz5wlhr .

Techniques: Labeling, Control, Gene Expression, Expressing, Mutagenesis, Activity Assay, Clinical Proteomics, Membrane, Activation Assay, Phospho-proteomics

a , b HCT116 cells with intact or depleted STAT1 and/or YAP1 expression were subcutaneously transplanted into female nu/nu mice (n = 10 per group). Tumor volume (mm³) was measured over the indicated time course. At the end of the study, tumor tissues from 3 mice were analyzed by IHC to assess H&E staining and the subcellular localization of YAP1 ( b ). c , d Similarly, HCT116 cells with combined YAP1 and STAT1 deletion or expression were transplanted into nu/nu mice (n = 5 per group). When tumors reached ~200 mm 3 , mice were treated by oral gavage with either vehicle or cerivastatin (CERI). Tumor growth was monitored over time. Red and blue arrows indicate the start point of treatment of YAP1 +/+ STAT1 +/+ and YAP1 −/− STAT1 −/− tumors, respectively. At the endpoint, tumors from 3 mice were subjected to IHC for H&E and YAP1 detection ( d ). a–d Data represent mean ± SEM. Statistical significance was determined by t -test: * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bar in panels b and d: 50 μm and 25 μm (insert image). Quantification graphs panels b and d show Histo (H)-scores for nuclear and cytoplasmic YAP1 staining. e HCT116 xenografts were established in nu/nu mice (n = 5 per group). Upon tumor growth to ~200 mm 3 (red arrow), mice received either vehicle, cerivastatin (oral), afatinib (intraperitoneal), or the combination of both. Tumor volume was tracked for the indicated duration. Data represent mean ± SEM. *** P < 0.001 (t-test). f In a similar setup, mice bearing HCT116 xenografts (~200 mm 3 tumors) were treated with vehicle, cerivastatin (oral), VT104 (oral), or their combination. Tumor growth was monitored throughout the experiment. Data represent mean ± SEM. ** P < 0.01 (t-test). g This schematic model illustrates how the STAT1–YAP1 signaling axis enhances the mevalonate pathway, thereby supporting tumor growth and chemoresistance in mutant KRAS CRC. Inhibiting YAP1-TEAD4 activity (e.g., using VT104) disrupts the SREBP-driven feedback loop that sustains mevalonate pathway activation. Additionally, pharmacological blockade of the mevalonate pathway with statins increases tumor sensitivity to YAP1–TEAD4 inhibition in xenograft models of mutant KRAS CRC.

Journal: Communications Biology

Article Title: A feedforward loop between STAT1 and YAP1 stimulates lipid biosynthesis, accelerates tumor growth, and promotes chemotherapy resistance in mutant KRAS colorectal cancer

doi: 10.1038/s42003-025-08740-2

Figure Lengend Snippet: a , b HCT116 cells with intact or depleted STAT1 and/or YAP1 expression were subcutaneously transplanted into female nu/nu mice (n = 10 per group). Tumor volume (mm³) was measured over the indicated time course. At the end of the study, tumor tissues from 3 mice were analyzed by IHC to assess H&E staining and the subcellular localization of YAP1 ( b ). c , d Similarly, HCT116 cells with combined YAP1 and STAT1 deletion or expression were transplanted into nu/nu mice (n = 5 per group). When tumors reached ~200 mm 3 , mice were treated by oral gavage with either vehicle or cerivastatin (CERI). Tumor growth was monitored over time. Red and blue arrows indicate the start point of treatment of YAP1 +/+ STAT1 +/+ and YAP1 −/− STAT1 −/− tumors, respectively. At the endpoint, tumors from 3 mice were subjected to IHC for H&E and YAP1 detection ( d ). a–d Data represent mean ± SEM. Statistical significance was determined by t -test: * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bar in panels b and d: 50 μm and 25 μm (insert image). Quantification graphs panels b and d show Histo (H)-scores for nuclear and cytoplasmic YAP1 staining. e HCT116 xenografts were established in nu/nu mice (n = 5 per group). Upon tumor growth to ~200 mm 3 (red arrow), mice received either vehicle, cerivastatin (oral), afatinib (intraperitoneal), or the combination of both. Tumor volume was tracked for the indicated duration. Data represent mean ± SEM. *** P < 0.001 (t-test). f In a similar setup, mice bearing HCT116 xenografts (~200 mm 3 tumors) were treated with vehicle, cerivastatin (oral), VT104 (oral), or their combination. Tumor growth was monitored throughout the experiment. Data represent mean ± SEM. ** P < 0.01 (t-test). g This schematic model illustrates how the STAT1–YAP1 signaling axis enhances the mevalonate pathway, thereby supporting tumor growth and chemoresistance in mutant KRAS CRC. Inhibiting YAP1-TEAD4 activity (e.g., using VT104) disrupts the SREBP-driven feedback loop that sustains mevalonate pathway activation. Additionally, pharmacological blockade of the mevalonate pathway with statins increases tumor sensitivity to YAP1–TEAD4 inhibition in xenograft models of mutant KRAS CRC.

Techniques: Expressing, Staining, Mutagenesis, Activity Assay, Activation Assay, Inhibition

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