mv3 (braf wild-type) cells Search Results


mv3 braf wild type melanoma cells  (Cyagen Biosciences)
90
Cyagen Biosciences mv3 braf wild type melanoma cells
Figure 2. Transcriptomic analysis on public datasets highlighted the role of HMOX-1 in aggressiveness and <t>BRAF</t> inhibitor resistance in melanoma. (A,B) Kaplan–Meier curves representing the disease- free survival (DFS) of patients with a high expression of HMOX-1 compared to samples with low expression of HMOX-1 in a TCGA melanoma cohort (406 samples with survival information) (A) and in BRAF mutant samples (165 samples) (B) HMOX-1 expression was stratified as “high” and “low” with an optimized cut-off. (C) Boxplot representing the distribution of HMOX-1 expression in sensitive and resistant mice after A375 cell inoculation and BRAF inhibitor treatment (GSE74729, 4 sensitive and 5 resistant samples). (D) Boxplot representing the distribution of HMOX-1 expression in sensitive and resistant patients in a merge of 3 melanoma patient datasets (43 BRAF inhibitor sensitive (before treatment) and 48 resistant and relapse of disease (after treatment)). FC, fold change; DFS, disease-free survival.
Mv3 Braf Wild Type Melanoma Cells, supplied by Cyagen Biosciences, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mv3+(braf+wild-type)+cells/Braf/pm35053476-107-4-49
Average 90 stars, based on 1 article reviews
mv3 braf wild type melanoma cells - by Bioz Stars, 2026-09
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glass-bottom coverslip dishes p35g-1.5-14-c  (MatTek)
90
MatTek glass-bottom coverslip dishes p35g-1.5-14-c
Figure 2. Transcriptomic analysis on public datasets highlighted the role of HMOX-1 in aggressiveness and <t>BRAF</t> inhibitor resistance in melanoma. (A,B) Kaplan–Meier curves representing the disease- free survival (DFS) of patients with a high expression of HMOX-1 compared to samples with low expression of HMOX-1 in a TCGA melanoma cohort (406 samples with survival information) (A) and in BRAF mutant samples (165 samples) (B) HMOX-1 expression was stratified as “high” and “low” with an optimized cut-off. (C) Boxplot representing the distribution of HMOX-1 expression in sensitive and resistant mice after A375 cell inoculation and BRAF inhibitor treatment (GSE74729, 4 sensitive and 5 resistant samples). (D) Boxplot representing the distribution of HMOX-1 expression in sensitive and resistant patients in a merge of 3 melanoma patient datasets (43 BRAF inhibitor sensitive (before treatment) and 48 resistant and relapse of disease (after treatment)). FC, fold change; DFS, disease-free survival.
Glass Bottom Coverslip Dishes P35g 1.5 14 C, supplied by MatTek, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mv3+(braf+wild-type)+cells/glass+bottom+culture+dishes/pm36859545-573-11-10
Average 90 stars, based on 1 article reviews
glass-bottom coverslip dishes p35g-1.5-14-c - by Bioz Stars, 2026-09
90/100 stars
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Image Search Results


Figure 2. Transcriptomic analysis on public datasets highlighted the role of HMOX-1 in aggressiveness and BRAF inhibitor resistance in melanoma. (A,B) Kaplan–Meier curves representing the disease- free survival (DFS) of patients with a high expression of HMOX-1 compared to samples with low expression of HMOX-1 in a TCGA melanoma cohort (406 samples with survival information) (A) and in BRAF mutant samples (165 samples) (B) HMOX-1 expression was stratified as “high” and “low” with an optimized cut-off. (C) Boxplot representing the distribution of HMOX-1 expression in sensitive and resistant mice after A375 cell inoculation and BRAF inhibitor treatment (GSE74729, 4 sensitive and 5 resistant samples). (D) Boxplot representing the distribution of HMOX-1 expression in sensitive and resistant patients in a merge of 3 melanoma patient datasets (43 BRAF inhibitor sensitive (before treatment) and 48 resistant and relapse of disease (after treatment)). FC, fold change; DFS, disease-free survival.

Journal: Cancers

Article Title: Nuclear Localization of BRAF V600E Is Associated with HMOX-1 Upregulation and Aggressive Behavior of Melanoma Cells.

doi: 10.3390/cancers14020311

Figure Lengend Snippet: Figure 2. Transcriptomic analysis on public datasets highlighted the role of HMOX-1 in aggressiveness and BRAF inhibitor resistance in melanoma. (A,B) Kaplan–Meier curves representing the disease- free survival (DFS) of patients with a high expression of HMOX-1 compared to samples with low expression of HMOX-1 in a TCGA melanoma cohort (406 samples with survival information) (A) and in BRAF mutant samples (165 samples) (B) HMOX-1 expression was stratified as “high” and “low” with an optimized cut-off. (C) Boxplot representing the distribution of HMOX-1 expression in sensitive and resistant mice after A375 cell inoculation and BRAF inhibitor treatment (GSE74729, 4 sensitive and 5 resistant samples). (D) Boxplot representing the distribution of HMOX-1 expression in sensitive and resistant patients in a merge of 3 melanoma patient datasets (43 BRAF inhibitor sensitive (before treatment) and 48 resistant and relapse of disease (after treatment)). FC, fold change; DFS, disease-free survival.

Article Snippet: MEF (BRAF KO) and MV3 (BRAF wild-type) melanoma cells expressing nuclear localization signal (NLS)-BRAFV600E and BRAFV600E were established by infecting the cells with lentiviral particles expressing human BRAFV600E with NLS sequence pLV[Exp]Neo-CMV>DsRed_Express2: ORF_2373bp/ Myc(hBRAFV600E/3xNLS) or without NLS pLV[Exp]-NeoCMV>DsRed_ Express2:ORF_2301bp/Myc(hBRAFV600E) tagged with DsRed fluorescent protein according to the standard protocols (Cyagen, Santa Clara, CA, USA).

Techniques: Expressing, Mutagenesis

Figure 3. Nuclear BRAFV600E and HMOX-1 expression in xenograft mouse and human melanoma tissue cores. (A) The plasmid (BRAFV600E) or (3XNLS-BRAFV600E), containing BRAFV600E with nu- clear localization sequences (NLS), was transfected into the melanoma cell line MV3 (BRAFwt/wt) and selected with antibiotic G418. (B) MV3 cells transduced with BRAFV600E, NLS-BRAFV600E, and control cells were injected in mice (n = 5 for each group), and representative tumor images were taken. Xenograft mouse tissues were stained with an anti-HOMX1 antibody. Mag. 400×. Scale bars = 50 µm (C) Human malignant melanoma tissue array: immunoreactivity to BRAFV600E and HMOX1 in the human melanoma cores was detected and counterstained for the nuclear and cy- toplasm location. Mag. 400×. Scale bars = 50 µm. (Figure S3) provides the whole IHC analysis. (D) phosphoERK and phosphoAKT were assessed in MEF stably transfected with BRAFV600E or NLS-BRAFV600E after treatment with 5 µM PLX-4032 at different time points. A representative gel is shown. Two additional independent experiments provided similar results.

Journal: Cancers

Article Title: Nuclear Localization of BRAF V600E Is Associated with HMOX-1 Upregulation and Aggressive Behavior of Melanoma Cells.

doi: 10.3390/cancers14020311

Figure Lengend Snippet: Figure 3. Nuclear BRAFV600E and HMOX-1 expression in xenograft mouse and human melanoma tissue cores. (A) The plasmid (BRAFV600E) or (3XNLS-BRAFV600E), containing BRAFV600E with nu- clear localization sequences (NLS), was transfected into the melanoma cell line MV3 (BRAFwt/wt) and selected with antibiotic G418. (B) MV3 cells transduced with BRAFV600E, NLS-BRAFV600E, and control cells were injected in mice (n = 5 for each group), and representative tumor images were taken. Xenograft mouse tissues were stained with an anti-HOMX1 antibody. Mag. 400×. Scale bars = 50 µm (C) Human malignant melanoma tissue array: immunoreactivity to BRAFV600E and HMOX1 in the human melanoma cores was detected and counterstained for the nuclear and cy- toplasm location. Mag. 400×. Scale bars = 50 µm. (Figure S3) provides the whole IHC analysis. (D) phosphoERK and phosphoAKT were assessed in MEF stably transfected with BRAFV600E or NLS-BRAFV600E after treatment with 5 µM PLX-4032 at different time points. A representative gel is shown. Two additional independent experiments provided similar results.

Article Snippet: MEF (BRAF KO) and MV3 (BRAF wild-type) melanoma cells expressing nuclear localization signal (NLS)-BRAFV600E and BRAFV600E were established by infecting the cells with lentiviral particles expressing human BRAFV600E with NLS sequence pLV[Exp]Neo-CMV>DsRed_Express2: ORF_2373bp/ Myc(hBRAFV600E/3xNLS) or without NLS pLV[Exp]-NeoCMV>DsRed_ Express2:ORF_2301bp/Myc(hBRAFV600E) tagged with DsRed fluorescent protein according to the standard protocols (Cyagen, Santa Clara, CA, USA).

Techniques: Expressing, Plasmid Preparation, Transfection, Transduction, Control, Injection, Staining, Stable Transfection

Figure 6. Pathway analysis revealed a key role of HMOX-1 in BRAF inhibitor therapy resistance in the xenograft model and in melanoma patients. (A) Dotplot representing the enrichment score obtained for the common pathways identified in the xenograft model and melanoma patients. (B) Heatmap representing the correlation matrix between the 36 genes involved in the 3 selected pathways (ferroptosis, fluid shear stress and atherosclerosis, and hepatocellular carcinoma) common in the xenograft model and melanoma patients. Values are from the patient dataset. (C) Network representation of the 36 genes (green nodes) involved in the 3 selected pathways (light yellow nodes), with their Spearman correlation as edges. Dark red ellipse, genes belonging to “fluid shear stress and atherosclerosis”; orange, genes belonging to “ferroptosis”; blue ellipse, genes belonging to “hepatocellular carcinoma”; thicker edges, correlation related to HMOX1; blue edges, negative correlation; red edges, positive correlation; edge transparency proportional to correlation value; blue node border, negative correlation with HMOX1; red node border, positive correlation with HMOX1. Correlation values are from the patient dataset.

Journal: Cancers

Article Title: Nuclear Localization of BRAF V600E Is Associated with HMOX-1 Upregulation and Aggressive Behavior of Melanoma Cells.

doi: 10.3390/cancers14020311

Figure Lengend Snippet: Figure 6. Pathway analysis revealed a key role of HMOX-1 in BRAF inhibitor therapy resistance in the xenograft model and in melanoma patients. (A) Dotplot representing the enrichment score obtained for the common pathways identified in the xenograft model and melanoma patients. (B) Heatmap representing the correlation matrix between the 36 genes involved in the 3 selected pathways (ferroptosis, fluid shear stress and atherosclerosis, and hepatocellular carcinoma) common in the xenograft model and melanoma patients. Values are from the patient dataset. (C) Network representation of the 36 genes (green nodes) involved in the 3 selected pathways (light yellow nodes), with their Spearman correlation as edges. Dark red ellipse, genes belonging to “fluid shear stress and atherosclerosis”; orange, genes belonging to “ferroptosis”; blue ellipse, genes belonging to “hepatocellular carcinoma”; thicker edges, correlation related to HMOX1; blue edges, negative correlation; red edges, positive correlation; edge transparency proportional to correlation value; blue node border, negative correlation with HMOX1; red node border, positive correlation with HMOX1. Correlation values are from the patient dataset.

Article Snippet: MEF (BRAF KO) and MV3 (BRAF wild-type) melanoma cells expressing nuclear localization signal (NLS)-BRAFV600E and BRAFV600E were established by infecting the cells with lentiviral particles expressing human BRAFV600E with NLS sequence pLV[Exp]Neo-CMV>DsRed_Express2: ORF_2373bp/ Myc(hBRAFV600E/3xNLS) or without NLS pLV[Exp]-NeoCMV>DsRed_ Express2:ORF_2301bp/Myc(hBRAFV600E) tagged with DsRed fluorescent protein according to the standard protocols (Cyagen, Santa Clara, CA, USA).

Techniques: Shear