human crc cell lines colo320dm  (ATCC)


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    Structured Review

    ATCC human crc cell lines colo320dm
    Downregulation of ERCC1 expression in KRAS-mutant <t>CRC</t> cells might be related to hypermethylation of ERCC1gene, which possibly induced by up-regulation of DNMT3B (DNA methyltransferase 3B). (A) Protein expression of ERCC1 in DLD-1(KRAS G13D mutation) cells is up-regulated after 5′-azacitidine (de-methylating agent) treatment for 96 hours, which implied that the downregulation of ERCC1 in KRAS-mutant CRC cells might be partly through ERCC1 hypermethylation. (B) Downregulation of ERCC1 in COLO320DM (KRAS wild-type) cells transfected by KRAS G13D -mutant-vector for 24 and 96 hours may not only be restored by 5′-azacitidine in 10 µM, but also caused up-regulation of DNMT3B.
    Human Crc Cell Lines Colo320dm, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human crc cell lines colo320dm/product/ATCC
    Average 94 stars, based on 1 article reviews
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    human crc cell lines colo320dm - by Bioz Stars, 2022-11
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    1) Product Images from "KRAS Mutation Is a Predictor of Oxaliplatin Sensitivity in Colon Cancer Cells"

    Article Title: KRAS Mutation Is a Predictor of Oxaliplatin Sensitivity in Colon Cancer Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0050701

    Downregulation of ERCC1 expression in KRAS-mutant CRC cells might be related to hypermethylation of ERCC1gene, which possibly induced by up-regulation of DNMT3B (DNA methyltransferase 3B). (A) Protein expression of ERCC1 in DLD-1(KRAS G13D mutation) cells is up-regulated after 5′-azacitidine (de-methylating agent) treatment for 96 hours, which implied that the downregulation of ERCC1 in KRAS-mutant CRC cells might be partly through ERCC1 hypermethylation. (B) Downregulation of ERCC1 in COLO320DM (KRAS wild-type) cells transfected by KRAS G13D -mutant-vector for 24 and 96 hours may not only be restored by 5′-azacitidine in 10 µM, but also caused up-regulation of DNMT3B.
    Figure Legend Snippet: Downregulation of ERCC1 expression in KRAS-mutant CRC cells might be related to hypermethylation of ERCC1gene, which possibly induced by up-regulation of DNMT3B (DNA methyltransferase 3B). (A) Protein expression of ERCC1 in DLD-1(KRAS G13D mutation) cells is up-regulated after 5′-azacitidine (de-methylating agent) treatment for 96 hours, which implied that the downregulation of ERCC1 in KRAS-mutant CRC cells might be partly through ERCC1 hypermethylation. (B) Downregulation of ERCC1 in COLO320DM (KRAS wild-type) cells transfected by KRAS G13D -mutant-vector for 24 and 96 hours may not only be restored by 5′-azacitidine in 10 µM, but also caused up-regulation of DNMT3B.

    Techniques Used: Expressing, Mutagenesis, Transfection, Plasmid Preparation

    Validating ERCC1 as the predictor of oxaliplatin sensitivity in CRC cells. (A) ERCC1-knocked-down COLO320DM cells were more sensitive to oxaliplatin than parental COLO320DM cells, as demonstrated by MTT assay. (B) Protein and mRNA levels of ERCC1 were downregulated when COLO320DM cells were knocked-down by ERCC1 siRNA. *: p
    Figure Legend Snippet: Validating ERCC1 as the predictor of oxaliplatin sensitivity in CRC cells. (A) ERCC1-knocked-down COLO320DM cells were more sensitive to oxaliplatin than parental COLO320DM cells, as demonstrated by MTT assay. (B) Protein and mRNA levels of ERCC1 were downregulated when COLO320DM cells were knocked-down by ERCC1 siRNA. *: p

    Techniques Used: MTT Assay

    Overexpressing KRAS by another KRAS overexpression vector (G12V) in KRAS wild-type CRC cells leads to oxaliplatin sensitivity and ERCC1 downregulation. (A) KRAS G12V -DDK-myc-COLO320DM cells were more sensitive to oxaliplatin, but have the same sensitivity to irinotecan, 5FU, and doxorubicin than parental COLO320DM cells, as demonstrated by MTT assay. (B) The protein level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G12V mutant vector. (C) The mRNA level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G12V mutant vector. **: p
    Figure Legend Snippet: Overexpressing KRAS by another KRAS overexpression vector (G12V) in KRAS wild-type CRC cells leads to oxaliplatin sensitivity and ERCC1 downregulation. (A) KRAS G12V -DDK-myc-COLO320DM cells were more sensitive to oxaliplatin, but have the same sensitivity to irinotecan, 5FU, and doxorubicin than parental COLO320DM cells, as demonstrated by MTT assay. (B) The protein level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G12V mutant vector. (C) The mRNA level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G12V mutant vector. **: p

    Techniques Used: Over Expression, Plasmid Preparation, MTT Assay, Transfection, Mutagenesis

    Overexpressing KRAS in KRAS wild-type CRC cells leads to oxaliplatin sensitivity and ERCC1 downregulation. (A) KRAS G13D -DDK-myc-COLO320DM cells were more sensitive to oxaliplatin, but have the same sensitivity to irinotecan, 5FU, and doxorubicin than parental COLO320DM cells, as demonstrated by MTT assay. (B) The protein level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G13D mutant vector. (C) The mRNA level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G13D mutant vector. **: p
    Figure Legend Snippet: Overexpressing KRAS in KRAS wild-type CRC cells leads to oxaliplatin sensitivity and ERCC1 downregulation. (A) KRAS G13D -DDK-myc-COLO320DM cells were more sensitive to oxaliplatin, but have the same sensitivity to irinotecan, 5FU, and doxorubicin than parental COLO320DM cells, as demonstrated by MTT assay. (B) The protein level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G13D mutant vector. (C) The mRNA level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G13D mutant vector. **: p

    Techniques Used: MTT Assay, Transfection, Mutagenesis, Plasmid Preparation

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    ATCC drugs human crc cell lines
    Methylation status of the miR-520c regulatory region and expression of miR-520c-3p and its target S100A4 in a cohort of <t>CRC</t> tumor specimens ( A ) Methylation specific PCR products of metachronous metastasis positive and metachronous negative CRC tumor specimens were analyzed using agarose gel electrophoresis. The miR-520c regulatory element was methylated in all specimens. The two cell lines <t>SW620</t> and Colo206f served as internal controls. ( B ) miR-520c-3p expression in metachronous metastasis positive ( n = 10) and negative ( n = 10) CRC tumor specimens in comparison to representative normal mucosa were quantified using qRT-PCR. ( C , D ) miR-520c-3p and S100A4 expression in CRC tumor specimens in comparison to representative normal mucosa were quantified using qRT-PCR. RPII and RNUB6 served as internal controls.
    Drugs Human Crc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC reagents human crc cell lines colo320dm
    Downregulation of ERCC1 expression in KRAS-mutant <t>CRC</t> cells might be related to hypermethylation of ERCC1gene, which possibly induced by up-regulation of DNMT3B (DNA methyltransferase 3B). (A) Protein expression of ERCC1 in DLD-1(KRAS G13D mutation) cells is up-regulated after 5′-azacitidine (de-methylating agent) treatment for 96 hours, which implied that the downregulation of ERCC1 in KRAS-mutant CRC cells might be partly through ERCC1 hypermethylation. (B) Downregulation of ERCC1 in <t>COLO320DM</t> (KRAS wild-type) cells transfected by KRAS G13D -mutant-vector for 24 and 96 hours may not only be restored by 5′-azacitidine in 10 µM, but also caused up-regulation of DNMT3B.
    Reagents Human Crc Cell Lines Colo320dm, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Methylation status of the miR-520c regulatory region and expression of miR-520c-3p and its target S100A4 in a cohort of CRC tumor specimens ( A ) Methylation specific PCR products of metachronous metastasis positive and metachronous negative CRC tumor specimens were analyzed using agarose gel electrophoresis. The miR-520c regulatory element was methylated in all specimens. The two cell lines SW620 and Colo206f served as internal controls. ( B ) miR-520c-3p expression in metachronous metastasis positive ( n = 10) and negative ( n = 10) CRC tumor specimens in comparison to representative normal mucosa were quantified using qRT-PCR. ( C , D ) miR-520c-3p and S100A4 expression in CRC tumor specimens in comparison to representative normal mucosa were quantified using qRT-PCR. RPII and RNUB6 served as internal controls.

    Journal: Oncotarget

    Article Title: Epigenetic silencing of miR-520c leads to induced S100A4 expression and its mediated colorectal cancer progression

    doi: 10.18632/oncotarget.15499

    Figure Lengend Snippet: Methylation status of the miR-520c regulatory region and expression of miR-520c-3p and its target S100A4 in a cohort of CRC tumor specimens ( A ) Methylation specific PCR products of metachronous metastasis positive and metachronous negative CRC tumor specimens were analyzed using agarose gel electrophoresis. The miR-520c regulatory element was methylated in all specimens. The two cell lines SW620 and Colo206f served as internal controls. ( B ) miR-520c-3p expression in metachronous metastasis positive ( n = 10) and negative ( n = 10) CRC tumor specimens in comparison to representative normal mucosa were quantified using qRT-PCR. ( C , D ) miR-520c-3p and S100A4 expression in CRC tumor specimens in comparison to representative normal mucosa were quantified using qRT-PCR. RPII and RNUB6 served as internal controls.

    Article Snippet: Cell lines, cultures and drugs Human CRC cell lines (SW480, Rko, DLD-1, HCT116, SW620, HT-29, Colo320DM, WiDr, Caco-2 and HCT-15) were purchased from American Type Culture Collection (ATCC; Manassas, VA), and Colo206f from German Collection of Microorganisms and Cell culture (DSMZ Leibniz Institute; Braunschweig, Germany).

    Techniques: Methylation, Expressing, Polymerase Chain Reaction, Agarose Gel Electrophoresis, Quantitative RT-PCR

    miR-520c regulatory region is hypermethylated in CRC cell lines and treatment with 5-Aza induces the expression of miR-520c-3p and downregulates S100A4 expression ( A , B ) SW480, SW620 and HCT116 cells were treated with 5-Aza (2 mM) for 3 days. qRT-PCR and Western blots were performed to analyze the impact of 5-Aza treatment on miR-520c-3p and S100A4 expression. RNUB6, RPII and β-actin served as internal controls. ( C ) HCT116 and SW620 cells transfected with the wild type S100A4-3′-UTR were treated with 5-Aza (2 μM) for 24 h and the luciferase activity was measured. Renilla luciferase activity was used for normalization. Percentage luciferase activity was significantly reduced after 5-Aza. ( *p

    Journal: Oncotarget

    Article Title: Epigenetic silencing of miR-520c leads to induced S100A4 expression and its mediated colorectal cancer progression

    doi: 10.18632/oncotarget.15499

    Figure Lengend Snippet: miR-520c regulatory region is hypermethylated in CRC cell lines and treatment with 5-Aza induces the expression of miR-520c-3p and downregulates S100A4 expression ( A , B ) SW480, SW620 and HCT116 cells were treated with 5-Aza (2 mM) for 3 days. qRT-PCR and Western blots were performed to analyze the impact of 5-Aza treatment on miR-520c-3p and S100A4 expression. RNUB6, RPII and β-actin served as internal controls. ( C ) HCT116 and SW620 cells transfected with the wild type S100A4-3′-UTR were treated with 5-Aza (2 μM) for 24 h and the luciferase activity was measured. Renilla luciferase activity was used for normalization. Percentage luciferase activity was significantly reduced after 5-Aza. ( *p

    Article Snippet: Cell lines, cultures and drugs Human CRC cell lines (SW480, Rko, DLD-1, HCT116, SW620, HT-29, Colo320DM, WiDr, Caco-2 and HCT-15) were purchased from American Type Culture Collection (ATCC; Manassas, VA), and Colo206f from German Collection of Microorganisms and Cell culture (DSMZ Leibniz Institute; Braunschweig, Germany).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Transfection, Luciferase, Activity Assay

    COBRA and bisulfite sequencing analysis of miR-520c regulatory region ( A , B ) COBRA analysis using the restriction enzyme BstUI was performed to estimate the methylation status of miR-520c-3p in CRC cell lines. Colo206f, Colo320DM and WiDr were also analyzed after 5-Aza (2 μm) treatment for 3 days. ( C ) Colo320DM cells were treated with 2 μM 5-Aza for 3 days and the methylation of miR-520c-3p was analyzed by bisulfite sequencing. From each group 10 representative clones were sequenced. Each circle represents CpG islands in the sequenced region, and the black circle represents the methylated and the empty white circle represents unmethylated CpG island. ( D , E ) qRT-PCR of miR-520c-3p, S100A4 and Western blot analysis of S100A4 were performed after 5-Aza treatment of Colo206f, Colo320DM for 3 days (20 μg of total protein used for Western blot) and WiDr (5 μg of total protein used for Western blot) cell lines (from low to moderate S100A4 expressing cells). RNUB6, RPII and β-actin served as internal controls. ( *p

    Journal: Oncotarget

    Article Title: Epigenetic silencing of miR-520c leads to induced S100A4 expression and its mediated colorectal cancer progression

    doi: 10.18632/oncotarget.15499

    Figure Lengend Snippet: COBRA and bisulfite sequencing analysis of miR-520c regulatory region ( A , B ) COBRA analysis using the restriction enzyme BstUI was performed to estimate the methylation status of miR-520c-3p in CRC cell lines. Colo206f, Colo320DM and WiDr were also analyzed after 5-Aza (2 μm) treatment for 3 days. ( C ) Colo320DM cells were treated with 2 μM 5-Aza for 3 days and the methylation of miR-520c-3p was analyzed by bisulfite sequencing. From each group 10 representative clones were sequenced. Each circle represents CpG islands in the sequenced region, and the black circle represents the methylated and the empty white circle represents unmethylated CpG island. ( D , E ) qRT-PCR of miR-520c-3p, S100A4 and Western blot analysis of S100A4 were performed after 5-Aza treatment of Colo206f, Colo320DM for 3 days (20 μg of total protein used for Western blot) and WiDr (5 μg of total protein used for Western blot) cell lines (from low to moderate S100A4 expressing cells). RNUB6, RPII and β-actin served as internal controls. ( *p

    Article Snippet: Cell lines, cultures and drugs Human CRC cell lines (SW480, Rko, DLD-1, HCT116, SW620, HT-29, Colo320DM, WiDr, Caco-2 and HCT-15) were purchased from American Type Culture Collection (ATCC; Manassas, VA), and Colo206f from German Collection of Microorganisms and Cell culture (DSMZ Leibniz Institute; Braunschweig, Germany).

    Techniques: Combined Bisulfite Restriction Analysis Assay, Methylation Sequencing, Methylation, Clone Assay, Quantitative RT-PCR, Western Blot, Expressing

    miR-218 inhibits the MACC1 mediated tumor metastasis events of CRC ( A , B ) SW480 cells were transfected with miR-218 or anti-miR-218. After 48 h cells were plated on top of the Boyden chambers for migration and matrigel-coated Boyden chambers for invasion. After 15 h the migrated or invaded cells were measured as described in the materials and methods. ( C ) After 48 h of respective control-miR (ctrl), miR-218 and anti-miR-218 (anti-218) transfection, cells were seeded in agar plates and counted as described in material and methods. Numbers of colonies are represented in relation with the control condition as percentage. ( D ) Relative expression of miR-218 after transfection in SW480-empty vector (e.v.) control cells and SW480-MACC1 stably expressing cells. ( E , F ) MACC1 mRNA and protein expression after miR-218 transfection were quantified using qRT-PCR and Western blotting. ( G – I ) Migration, invasion and colony formation assays of SW480-e.v and SW480-MACC1 either with control-miR or miR-218. Data are represented as the percentage of migrating or invading cells and colonies as mean ± SEM of their biological replicates, each experiment performed in three technical replicates. Densitometric analysis of MACC1 protein bands normalized to β-actin represented as a mean value of triplicates, in comparison to the respective control. (* P

    Journal: Oncotarget

    Article Title: MACC1 is post-transcriptionally regulated by miR-218 in colorectal cancer

    doi: 10.18632/oncotarget.10803

    Figure Lengend Snippet: miR-218 inhibits the MACC1 mediated tumor metastasis events of CRC ( A , B ) SW480 cells were transfected with miR-218 or anti-miR-218. After 48 h cells were plated on top of the Boyden chambers for migration and matrigel-coated Boyden chambers for invasion. After 15 h the migrated or invaded cells were measured as described in the materials and methods. ( C ) After 48 h of respective control-miR (ctrl), miR-218 and anti-miR-218 (anti-218) transfection, cells were seeded in agar plates and counted as described in material and methods. Numbers of colonies are represented in relation with the control condition as percentage. ( D ) Relative expression of miR-218 after transfection in SW480-empty vector (e.v.) control cells and SW480-MACC1 stably expressing cells. ( E , F ) MACC1 mRNA and protein expression after miR-218 transfection were quantified using qRT-PCR and Western blotting. ( G – I ) Migration, invasion and colony formation assays of SW480-e.v and SW480-MACC1 either with control-miR or miR-218. Data are represented as the percentage of migrating or invading cells and colonies as mean ± SEM of their biological replicates, each experiment performed in three technical replicates. Densitometric analysis of MACC1 protein bands normalized to β-actin represented as a mean value of triplicates, in comparison to the respective control. (* P

    Article Snippet: Cell lines, cultures and drugs Human CRC cell lines (RKO, HCT15, Colo320DM, HCT116, SW480, SW620, HT-29, Caco-2, WiDr and DLD-1) were purchased from American Type Culture Collection (ATCC; Manassas, VA) and Colo206f from German Collection of Microorganisms and Cell culture (DSMZ Leibniz Institute; Braunschweig, Germany).

    Techniques: Transfection, Migration, Expressing, Plasmid Preparation, Stable Transfection, Quantitative RT-PCR, Western Blot

    Downregulation of ERCC1 expression in KRAS-mutant CRC cells might be related to hypermethylation of ERCC1gene, which possibly induced by up-regulation of DNMT3B (DNA methyltransferase 3B). (A) Protein expression of ERCC1 in DLD-1(KRAS G13D mutation) cells is up-regulated after 5′-azacitidine (de-methylating agent) treatment for 96 hours, which implied that the downregulation of ERCC1 in KRAS-mutant CRC cells might be partly through ERCC1 hypermethylation. (B) Downregulation of ERCC1 in COLO320DM (KRAS wild-type) cells transfected by KRAS G13D -mutant-vector for 24 and 96 hours may not only be restored by 5′-azacitidine in 10 µM, but also caused up-regulation of DNMT3B.

    Journal: PLoS ONE

    Article Title: KRAS Mutation Is a Predictor of Oxaliplatin Sensitivity in Colon Cancer Cells

    doi: 10.1371/journal.pone.0050701

    Figure Lengend Snippet: Downregulation of ERCC1 expression in KRAS-mutant CRC cells might be related to hypermethylation of ERCC1gene, which possibly induced by up-regulation of DNMT3B (DNA methyltransferase 3B). (A) Protein expression of ERCC1 in DLD-1(KRAS G13D mutation) cells is up-regulated after 5′-azacitidine (de-methylating agent) treatment for 96 hours, which implied that the downregulation of ERCC1 in KRAS-mutant CRC cells might be partly through ERCC1 hypermethylation. (B) Downregulation of ERCC1 in COLO320DM (KRAS wild-type) cells transfected by KRAS G13D -mutant-vector for 24 and 96 hours may not only be restored by 5′-azacitidine in 10 µM, but also caused up-regulation of DNMT3B.

    Article Snippet: Cell Culture and Reagents Human CRC cell lines COLO320DM (KRAS-wild-type), DLD-1G13D (KRAS G13D mutation), and SW480G12V (KRAS G12V mutation) were all obtained from American Type Culture Collection.

    Techniques: Expressing, Mutagenesis, Transfection, Plasmid Preparation

    Validating ERCC1 as the predictor of oxaliplatin sensitivity in CRC cells. (A) ERCC1-knocked-down COLO320DM cells were more sensitive to oxaliplatin than parental COLO320DM cells, as demonstrated by MTT assay. (B) Protein and mRNA levels of ERCC1 were downregulated when COLO320DM cells were knocked-down by ERCC1 siRNA. *: p

    Journal: PLoS ONE

    Article Title: KRAS Mutation Is a Predictor of Oxaliplatin Sensitivity in Colon Cancer Cells

    doi: 10.1371/journal.pone.0050701

    Figure Lengend Snippet: Validating ERCC1 as the predictor of oxaliplatin sensitivity in CRC cells. (A) ERCC1-knocked-down COLO320DM cells were more sensitive to oxaliplatin than parental COLO320DM cells, as demonstrated by MTT assay. (B) Protein and mRNA levels of ERCC1 were downregulated when COLO320DM cells were knocked-down by ERCC1 siRNA. *: p

    Article Snippet: Cell Culture and Reagents Human CRC cell lines COLO320DM (KRAS-wild-type), DLD-1G13D (KRAS G13D mutation), and SW480G12V (KRAS G12V mutation) were all obtained from American Type Culture Collection.

    Techniques: MTT Assay

    Overexpressing KRAS by another KRAS overexpression vector (G12V) in KRAS wild-type CRC cells leads to oxaliplatin sensitivity and ERCC1 downregulation. (A) KRAS G12V -DDK-myc-COLO320DM cells were more sensitive to oxaliplatin, but have the same sensitivity to irinotecan, 5FU, and doxorubicin than parental COLO320DM cells, as demonstrated by MTT assay. (B) The protein level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G12V mutant vector. (C) The mRNA level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G12V mutant vector. **: p

    Journal: PLoS ONE

    Article Title: KRAS Mutation Is a Predictor of Oxaliplatin Sensitivity in Colon Cancer Cells

    doi: 10.1371/journal.pone.0050701

    Figure Lengend Snippet: Overexpressing KRAS by another KRAS overexpression vector (G12V) in KRAS wild-type CRC cells leads to oxaliplatin sensitivity and ERCC1 downregulation. (A) KRAS G12V -DDK-myc-COLO320DM cells were more sensitive to oxaliplatin, but have the same sensitivity to irinotecan, 5FU, and doxorubicin than parental COLO320DM cells, as demonstrated by MTT assay. (B) The protein level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G12V mutant vector. (C) The mRNA level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G12V mutant vector. **: p

    Article Snippet: Cell Culture and Reagents Human CRC cell lines COLO320DM (KRAS-wild-type), DLD-1G13D (KRAS G13D mutation), and SW480G12V (KRAS G12V mutation) were all obtained from American Type Culture Collection.

    Techniques: Over Expression, Plasmid Preparation, MTT Assay, Transfection, Mutagenesis

    Overexpressing KRAS in KRAS wild-type CRC cells leads to oxaliplatin sensitivity and ERCC1 downregulation. (A) KRAS G13D -DDK-myc-COLO320DM cells were more sensitive to oxaliplatin, but have the same sensitivity to irinotecan, 5FU, and doxorubicin than parental COLO320DM cells, as demonstrated by MTT assay. (B) The protein level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G13D mutant vector. (C) The mRNA level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G13D mutant vector. **: p

    Journal: PLoS ONE

    Article Title: KRAS Mutation Is a Predictor of Oxaliplatin Sensitivity in Colon Cancer Cells

    doi: 10.1371/journal.pone.0050701

    Figure Lengend Snippet: Overexpressing KRAS in KRAS wild-type CRC cells leads to oxaliplatin sensitivity and ERCC1 downregulation. (A) KRAS G13D -DDK-myc-COLO320DM cells were more sensitive to oxaliplatin, but have the same sensitivity to irinotecan, 5FU, and doxorubicin than parental COLO320DM cells, as demonstrated by MTT assay. (B) The protein level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G13D mutant vector. (C) The mRNA level of ERCC1, but not those of TOPO1 or TS, was downregulated after COLO320DM cells were transfected by the KRAS G13D mutant vector. **: p

    Article Snippet: Cell Culture and Reagents Human CRC cell lines COLO320DM (KRAS-wild-type), DLD-1G13D (KRAS G13D mutation), and SW480G12V (KRAS G12V mutation) were all obtained from American Type Culture Collection.

    Techniques: MTT Assay, Transfection, Mutagenesis, Plasmid Preparation