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atf2 sirna (Cell Signaling Technology Inc)

Name: atf2 sirna
Brand: Cell Signaling Technology Inc
Rating: 90 (1 reviews)

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Cell Signaling Technology Inc atf2 sirna
Atf2 Sirna, supplied by Cell Signaling Technology Inc, 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/result/atf2 sirna/product/Cell Signaling Technology Inc
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MYBPC1 was negatively associated with grades of laryngeal carcinoma patients. (a) The volcano map of differentially expressed genes for laryngeal carcinoma patients. MYBPC1 is indicated as a blue arrowhead while ATF2 as a red arrowhead respectively. (b) The heat map of differentially expressed genes for laryngeal carcinoma patients. (c) Expression of MYBPC1 and ATF2 in grade I to grade IV laryngeal carcinoma patients detected by qRT-PCR. N = 3, * P < 0.05 compared expression of MYBPC1 in grade I laryngeal carcinoma patients.** P < 0.05 compared expression of ATF2 in grade I laryngeal carcinoma patients. (d) The miR-451a expression in laryngeal carcinoma patients of different grades detected by qRT-PCR.. N = 3, * P < 0.05 compared with grade I. ATF, activating transcription factor; MYBPC1, myosin-binding protein C1; qRT-PCR, quantitative reverse transcription-PCR.

Journal: Anti-Cancer Drugs

Article Title: MYBPC1 is a key regulator for laryngeal carcinoma formation

doi: 10.1097/CAD.0000000000001313

Figure Lengend Snippet: MYBPC1 was negatively associated with grades of laryngeal carcinoma patients. (a) The volcano map of differentially expressed genes for laryngeal carcinoma patients. MYBPC1 is indicated as a blue arrowhead while ATF2 as a red arrowhead respectively. (b) The heat map of differentially expressed genes for laryngeal carcinoma patients. (c) Expression of MYBPC1 and ATF2 in grade I to grade IV laryngeal carcinoma patients detected by qRT-PCR. N = 3, * P < 0.05 compared expression of MYBPC1 in grade I laryngeal carcinoma patients.** P < 0.05 compared expression of ATF2 in grade I laryngeal carcinoma patients. (d) The miR-451a expression in laryngeal carcinoma patients of different grades detected by qRT-PCR.. N = 3, * P < 0.05 compared with grade I. ATF, activating transcription factor; MYBPC1, myosin-binding protein C1; qRT-PCR, quantitative reverse transcription-PCR.

Article Snippet: For siRNA transfection, a specific ATF2 siRNA, a specific MYBPC1 siRNA (50 nmol/l) (OriGene Technologies, Inc.) and a negative control were utilized.

Techniques: Expressing, Quantitative RT-PCR, Binding Assay, Reverse Transcription

MYBPC1 was a indirectly target of miR-451a. (a) Expression of MYBPC1 in different cell lines detected by qRT-PCR. N = 3, * P < 0.05 compared NP69 cells. (b) Western blotting analysis of MYBPC1 and ATF2 expression levels in TU212 cells transfected with negative control (NC), miR-451a mimic or miR-451a inhibitor. (c) Expression of MYBPC1 in TU212 cells transfected with NC, miR-451a mimic or miR-451a inhibitor based on qRT-PCR measurement. N = 3, * P < 0.05 compared NC treatment. (d) Expression of MYBPC1 in TU212 cells transfected with NC, miR-451a mimic, miR-451a mimic and ATF2 plasmid, or MYBPC1 siRNA. N = 3, * P < 0.05 compared NC treatment.. ATF, activating transcription factor; MYBPC1, myosin-binding protein C1; qRT-PCR, quantitative reverse transcription-PCR.

Journal: Anti-Cancer Drugs

Article Title: MYBPC1 is a key regulator for laryngeal carcinoma formation

doi: 10.1097/CAD.0000000000001313

Figure Lengend Snippet: MYBPC1 was a indirectly target of miR-451a. (a) Expression of MYBPC1 in different cell lines detected by qRT-PCR. N = 3, * P < 0.05 compared NP69 cells. (b) Western blotting analysis of MYBPC1 and ATF2 expression levels in TU212 cells transfected with negative control (NC), miR-451a mimic or miR-451a inhibitor. (c) Expression of MYBPC1 in TU212 cells transfected with NC, miR-451a mimic or miR-451a inhibitor based on qRT-PCR measurement. N = 3, * P < 0.05 compared NC treatment. (d) Expression of MYBPC1 in TU212 cells transfected with NC, miR-451a mimic, miR-451a mimic and ATF2 plasmid, or MYBPC1 siRNA. N = 3, * P < 0.05 compared NC treatment.. ATF, activating transcription factor; MYBPC1, myosin-binding protein C1; qRT-PCR, quantitative reverse transcription-PCR.

Article Snippet: For siRNA transfection, a specific ATF2 siRNA, a specific MYBPC1 siRNA (50 nmol/l) (OriGene Technologies, Inc.) and a negative control were utilized.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Transfection, Negative Control, Plasmid Preparation, Binding Assay, Reverse Transcription

MYBPC1 played a central role in laryngeal carcinoma cell invasion. TU212 cells treated with NC, ATF2 plasmid, or a combination of ATF2 and MYBPC1 plasmids following subsequent colony-forming analysis (a), CCK-8 examination (b), apoptosis measurement (c) as well as cell invasion evaluation (d) respectively. N = 3, * P < 0.05 compared with NC treatment. ATF, activating transcription factor; CCK, Cell Counting Kit; MYBPC1, myosin-binding protein C1.

Journal: Anti-Cancer Drugs

Article Title: MYBPC1 is a key regulator for laryngeal carcinoma formation

doi: 10.1097/CAD.0000000000001313

Figure Lengend Snippet: MYBPC1 played a central role in laryngeal carcinoma cell invasion. TU212 cells treated with NC, ATF2 plasmid, or a combination of ATF2 and MYBPC1 plasmids following subsequent colony-forming analysis (a), CCK-8 examination (b), apoptosis measurement (c) as well as cell invasion evaluation (d) respectively. N = 3, * P < 0.05 compared with NC treatment. ATF, activating transcription factor; CCK, Cell Counting Kit; MYBPC1, myosin-binding protein C1.

Article Snippet: For siRNA transfection, a specific ATF2 siRNA, a specific MYBPC1 siRNA (50 nmol/l) (OriGene Technologies, Inc.) and a negative control were utilized.

Techniques: Plasmid Preparation, CCK-8 Assay, Cell Counting, Binding Assay

Effects of UVA on phosphorylation and protein levels of ATF2/c-Jun ( a ) and MSK1(Thr581/Ser360) ( b ). HDFs were exposed to UVA at the indicated doses in culture and cell lysates prepared at the indicated times post-irradiation were subjected to western blotting as described in the Materials and Methods section. Representative immunoblots from three independent experiments are shown.

Journal: International Journal of Molecular Sciences

Article Title: The Attenuated Secretion of Hyaluronan by UVA-Exposed Human Fibroblasts Is Associated with Up- and Downregulation of HYBID and HAS2 Expression via Activated and Inactivated Signaling of the p38/ATF2 and JAK2/STAT3 Cascades

doi: 10.3390/ijms22042057

Figure Lengend Snippet: Effects of UVA on phosphorylation and protein levels of ATF2/c-Jun ( a ) and MSK1(Thr581/Ser360) ( b ). HDFs were exposed to UVA at the indicated doses in culture and cell lysates prepared at the indicated times post-irradiation were subjected to western blotting as described in the Materials and Methods section. Representative immunoblots from three independent experiments are shown.

Article Snippet: On day 1, HDFs were transfected with a control siRNA (MISSION ® siRNA Universal Negative Control, Sigma Aldrich), a c-Fos siRNA (Mission siRNA, Sigma–Aldrich), an ATF2 siRNA (Santa Cruz), or an PTP-MEG2 siRNA (Santa Cruz) using Lipofectamine RNAiMAX Transfection Reagent (Invitrogen, Carlsbad, CA, USA) following the manufacturer’s protocol.

Techniques: Phospho-proteomics, Irradiation, Western Blot

Effects of transfection of c-Fos ( a ) or ATF-2 ( b ) siRNA on the UVA-induced increase in the HYBID protein level in HDFs. ( a ) Effect of transfecting a c-Fos siRNA on the expression of c-Fos and HYBID proteins. ( b ) Effect of transfecting an ATF-2 siRNA on the expression of ATF-2 and HYBID proteins. HDFs were exposed to UVA at the indicated dose in culture and cell lysates prepared at the indicated times post-irradiation were subjected to western blotting as described in the Materials and Methods section. Representative immunoblots from three independent experiments are shown. Data represent means ± SD., n = 3, **: p < 0.01, *: p < 0.05.

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms22042057

Figure Lengend Snippet: Effects of transfection of c-Fos ( a ) or ATF-2 ( b ) siRNA on the UVA-induced increase in the HYBID protein level in HDFs. ( a ) Effect of transfecting a c-Fos siRNA on the expression of c-Fos and HYBID proteins. ( b ) Effect of transfecting an ATF-2 siRNA on the expression of ATF-2 and HYBID proteins. HDFs were exposed to UVA at the indicated dose in culture and cell lysates prepared at the indicated times post-irradiation were subjected to western blotting as described in the Materials and Methods section. Representative immunoblots from three independent experiments are shown. Data represent means ± SD., n = 3, **: p < 0.01, *: p < 0.05.

Techniques: Transfection, Expressing, Irradiation, Western Blot

Effects of the transfection of a protein tyrosine phosphatase (PTPMEG2) siRNA on the UVA-induced decrease in the phosphorylation of STAT3 at Tyr 705 and JAK2 at Tyr 221 in HDFs. ( a ) Effect of transfecting a PTPMEG2 siRNA on the expression level of PTPMEG2 mRNA in UVA- or non-exposed HDFs at 3 h post-irradiation. Cell lysates were prepared at 3 h post-irradiation and were subjected to RT-qPCR analysis as described in the Materials and Methods section. Data represent means ± SD., n = 3, ** p < 0.01. ( b ) Effect of transfecting a PTPMEG2 siRNA on the expression level of PTPMEG2 protein and the phosphorylation level of STAT3 (Tyr705) and ERK in UVA- or non-exposed HDFs at 15 min post-irradiation. ( c ) Effect of transfecting a PTPMEG2 siRNA on the expression level of PTPMEG2 protein and the phosphorylation level of JAK2 (Tyr221) in UVA- or non-exposed HDFs at 5 min post-irradiation. Representative immunoblots from three independent experiments are shown.

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms22042057

Figure Lengend Snippet: Effects of the transfection of a protein tyrosine phosphatase (PTPMEG2) siRNA on the UVA-induced decrease in the phosphorylation of STAT3 at Tyr 705 and JAK2 at Tyr 221 in HDFs. ( a ) Effect of transfecting a PTPMEG2 siRNA on the expression level of PTPMEG2 mRNA in UVA- or non-exposed HDFs at 3 h post-irradiation. Cell lysates were prepared at 3 h post-irradiation and were subjected to RT-qPCR analysis as described in the Materials and Methods section. Data represent means ± SD., n = 3, ** p < 0.01. ( b ) Effect of transfecting a PTPMEG2 siRNA on the expression level of PTPMEG2 protein and the phosphorylation level of STAT3 (Tyr705) and ERK in UVA- or non-exposed HDFs at 15 min post-irradiation. ( c ) Effect of transfecting a PTPMEG2 siRNA on the expression level of PTPMEG2 protein and the phosphorylation level of JAK2 (Tyr221) in UVA- or non-exposed HDFs at 5 min post-irradiation. Representative immunoblots from three independent experiments are shown.

Techniques: Transfection, Phospho-proteomics, Expressing, Irradiation, Quantitative RT-PCR, Western Blot

Effect of knockdown of ATF2 on growth and tumourigenesis of MCF7 and TAMR (MCF7-derived tamoxifen-resistant) cell lines. MCF7 ( a ) and TAMR ( b ) cells were transfected with negative control siRNA (siControl), ATF2-siRNA1 and ATF2-siRNA2. Protein lysates were prepared and immunoblotting was carried out for ATF2 with β-actin as a loading control. c Densitometry analysis of knockdown efficiency relative to untransfected cells. SRB growth assay for MCF7 ( d ) and TAMR ( e ) indicated a significant growth reduction in TAMR cells after ATF2 silencing ( n = 3). f Graph indicating the percentage of growth at day 5 relative to untransfected cells. g The effect of ATF2 knockdown on tumourigenesis was determined by anchorage-independent colony formation. Although there was a reduction of colonies in the MCF7 cells after ATF2 silencing, this reduction was more profound in the TAMRs ( n = 3). Asterisks indicate statistically significant (* p < 0.05, ** p < 0.005) difference from untransfected cells

Journal: Breast Cancer Research : BCR

Article Title: Activating transcription factor-2 (ATF2) is a key determinant of resistance to endocrine treatment in an in vitro model of breast cancer

doi: 10.1186/s13058-020-01359-7

Figure Lengend Snippet: Effect of knockdown of ATF2 on growth and tumourigenesis of MCF7 and TAMR (MCF7-derived tamoxifen-resistant) cell lines. MCF7 ( a ) and TAMR ( b ) cells were transfected with negative control siRNA (siControl), ATF2-siRNA1 and ATF2-siRNA2. Protein lysates were prepared and immunoblotting was carried out for ATF2 with β-actin as a loading control. c Densitometry analysis of knockdown efficiency relative to untransfected cells. SRB growth assay for MCF7 ( d ) and TAMR ( e ) indicated a significant growth reduction in TAMR cells after ATF2 silencing ( n = 3). f Graph indicating the percentage of growth at day 5 relative to untransfected cells. g The effect of ATF2 knockdown on tumourigenesis was determined by anchorage-independent colony formation. Although there was a reduction of colonies in the MCF7 cells after ATF2 silencing, this reduction was more profound in the TAMRs ( n = 3). Asterisks indicate statistically significant (* p < 0.05, ** p < 0.005) difference from untransfected cells

Article Snippet: Two small interfering RNA (siRNA) duplexes for ATF2 mRNA depletion (S3492 and S3493) and the non-targeting siRNA (NT-siControl) (Silencer® Negative Control: AM4635) were used in our experiments (Thermofisher Scientific, Paisley, UK).

Techniques: Knockdown, Derivative Assay, Transfection, Negative Control, Western Blot, Control, Growth Assay

Effect of knockdown of ATF2 on migration of MCF7 and MCF7 derived tamoxifen-resistant cell line (TAMR). MCF7 ( a , c , e , and g ) and TAMR ( b , d , f , and h ) cells transfected with negative control siRNA (siControl), ATF2-siRNA1 and ATF2-siRNA2. Chemotaxis assay (migration) was carried out and migrated cells were counted relative to vehicle control ( n = 3). ATF2 knockdown inhibited the migratory ability of TAMR ( b , d ) cells but not of the MCF7 ( a , c ). Similarly, knockdown of ATF2 reduced the migratory ability of TAMR ( f , h ) cells in an in vitro wound healing scratch assay but did not affect the MCF7 ( e , g ) cells. Asterisks indicate statistically significant (* p < 0.05, ** p < 0.005) difference from vehicle control

Journal: Breast Cancer Research : BCR

Article Title: Activating transcription factor-2 (ATF2) is a key determinant of resistance to endocrine treatment in an in vitro model of breast cancer

doi: 10.1186/s13058-020-01359-7

Figure Lengend Snippet: Effect of knockdown of ATF2 on migration of MCF7 and MCF7 derived tamoxifen-resistant cell line (TAMR). MCF7 ( a , c , e , and g ) and TAMR ( b , d , f , and h ) cells transfected with negative control siRNA (siControl), ATF2-siRNA1 and ATF2-siRNA2. Chemotaxis assay (migration) was carried out and migrated cells were counted relative to vehicle control ( n = 3). ATF2 knockdown inhibited the migratory ability of TAMR ( b , d ) cells but not of the MCF7 ( a , c ). Similarly, knockdown of ATF2 reduced the migratory ability of TAMR ( f , h ) cells in an in vitro wound healing scratch assay but did not affect the MCF7 ( e , g ) cells. Asterisks indicate statistically significant (* p < 0.05, ** p < 0.005) difference from vehicle control

Techniques: Knockdown, Migration, Derivative Assay, Transfection, Negative Control, Chemotaxis Assay, Control, In Vitro, Wound Healing Assay

Differential gene expression analysis in basal MCF7 versus TAMR cell lines revealed an ATF2-enriched transcription factor network. a Heatmap of genes that were differentially expressed in MCF7 (blue) relative to TAMR (red) cells at basal level. This analysis identified 3260 upregulated and 4423 downregulated genes in TAMR cells relative to MCF7. b Enrichment analysis identified a shift from the ER (ESR1)-enriched transcription factor network present on MCF7 (blue) towards an ATF2-enriched transcription factor network on TAMR (red). c KEGG enrichment also identified a shift from the oestrogen and progesterone pathways to TGF-β and metabolic pathways

Journal: Breast Cancer Research : BCR

Article Title: Activating transcription factor-2 (ATF2) is a key determinant of resistance to endocrine treatment in an in vitro model of breast cancer

doi: 10.1186/s13058-020-01359-7

Figure Lengend Snippet: Differential gene expression analysis in basal MCF7 versus TAMR cell lines revealed an ATF2-enriched transcription factor network. a Heatmap of genes that were differentially expressed in MCF7 (blue) relative to TAMR (red) cells at basal level. This analysis identified 3260 upregulated and 4423 downregulated genes in TAMR cells relative to MCF7. b Enrichment analysis identified a shift from the ER (ESR1)-enriched transcription factor network present on MCF7 (blue) towards an ATF2-enriched transcription factor network on TAMR (red). c KEGG enrichment also identified a shift from the oestrogen and progesterone pathways to TGF-β and metabolic pathways

Techniques: Gene Expression

Differential gene expression analysis after ATF2 silencing revealed ER-responsive genes and pathways regulated by ATF2 in TAMR. Heatmaps of genes that were a upregulated and b downregulated in TAMRs (red) cells after ATF2 silencing relative to MCF7 (blue). c Enrichment analysis revealed ATF2 silencing in TAMR cells leads to the reintroduction of the ER signalling network and a reduction in MYC. Venn diagrams of differentially regulated genes in TAMRs after ATF2 silencing. A total of 543 upregulated ( d ) and 483 downregulated ( e ) genes were commonly identified after both ATF2-siRNA knockdown (si1 and si2 vs siNT)

Journal: Breast Cancer Research : BCR

Article Title: Activating transcription factor-2 (ATF2) is a key determinant of resistance to endocrine treatment in an in vitro model of breast cancer

doi: 10.1186/s13058-020-01359-7

Figure Lengend Snippet: Differential gene expression analysis after ATF2 silencing revealed ER-responsive genes and pathways regulated by ATF2 in TAMR. Heatmaps of genes that were a upregulated and b downregulated in TAMRs (red) cells after ATF2 silencing relative to MCF7 (blue). c Enrichment analysis revealed ATF2 silencing in TAMR cells leads to the reintroduction of the ER signalling network and a reduction in MYC. Venn diagrams of differentially regulated genes in TAMRs after ATF2 silencing. A total of 543 upregulated ( d ) and 483 downregulated ( e ) genes were commonly identified after both ATF2-siRNA knockdown (si1 and si2 vs siNT)

Techniques: Gene Expression, Knockdown

Pathways that are differentially regulated in MCF7 versus TAMR and in TAMR after ATF2 silencing. Commonly identified pathways dysregulated between MCF7 and TAMRs and re-instated after ATF2 knockdown. The complete list of KEGG and REACTOME pathways are presented in Supplementary files <xref ref-type=

1 (MCF7 vs TAMR) and 2 (TAMRs after siATF2 knockout)" width="100%" height="100%">

Journal: Breast Cancer Research : BCR

Article Title: Activating transcription factor-2 (ATF2) is a key determinant of resistance to endocrine treatment in an in vitro model of breast cancer

doi: 10.1186/s13058-020-01359-7

Figure Lengend Snippet: Pathways that are differentially regulated in MCF7 versus TAMR and in TAMR after ATF2 silencing. Commonly identified pathways dysregulated between MCF7 and TAMRs and re-instated after ATF2 knockdown. The complete list of KEGG and REACTOME pathways are presented in Supplementary files 1 (MCF7 vs TAMR) and 2 (TAMRs after siATF2 knockout)

Techniques: Knockdown, Knock-Out, Gene Expression, Membrane

Validation of genes identified using microarray. MCF7 and TAMR cells were transfected with silencer negative control siRNA, ATF2 siRNA1 and ATF2 siRNA2. qRT-PCR was carried out using Taqman primers for the genes indicated. Data analysis for each cell line was carried out relative to the siControl ( n = 3) and asterisks indicate the genes that were significantly changed after ATF2 knockdown (* p < 0.05, ** p < 0.005)

Journal: Breast Cancer Research : BCR

Article Title: Activating transcription factor-2 (ATF2) is a key determinant of resistance to endocrine treatment in an in vitro model of breast cancer

doi: 10.1186/s13058-020-01359-7

Figure Lengend Snippet: Validation of genes identified using microarray. MCF7 and TAMR cells were transfected with silencer negative control siRNA, ATF2 siRNA1 and ATF2 siRNA2. qRT-PCR was carried out using Taqman primers for the genes indicated. Data analysis for each cell line was carried out relative to the siControl ( n = 3) and asterisks indicate the genes that were significantly changed after ATF2 knockdown (* p < 0.05, ** p < 0.005)

Techniques: Biomarker Discovery, Microarray, Transfection, Negative Control, Quantitative RT-PCR, Knockdown

Effect of knockdown of ATF2 on ER and ER-regulated genes and proposed model of resistance. a – f MCF7 (left bars) and TAMR (right bars) cells were transfected with ATF2 siRNA and qRT-PCR was carried for ATF2 ( a ), ERα ( ESR1 ) ( b ), TFF1 ( c ), GREB1 ( d ), PGR ( e ) and NCOA3 ( f ) using TaqMan primers. GAPDH was used as the housekeeping gene and changes in mRNA levels after ATF2 knockdown were calculated relative to the control. Asterisks indicate the genes that were significantly changed after ATF2 knockdown (* p < 0.05, ** p < 0.005). g Protein lysates were also prepared in triplicates of three independent experiments and immunoblotting was carried out using the antibodies indicated. ATF2 knockdown had no effect on the ER and ER-regulated genes on the tamoxifen-sensitive MCF7 cells but affected their expression both on the mRNA and protein levels on the tamoxifen-resistant TAMRs. The following model of resistance is proposed: h In endocrine-sensitive cells, gene transcription is ER-dependent and endocrine therapy is able to stop their growth and proliferation. However, endocrine-resistant cells have a shift from ER-dependent to an ER-independent ATF2-dependent transcriptional program and therefore, they are not responding to endocrine treatment. i Targeting the ATF-2 transcription factor in endocrine-resistant cells represents a new mechanism to revert resistance and enhance endocrine sensitivity. The genes shown in this model ( h , i ) such as TFF1, GREB1 and NCOA3 are examples of resistance candidates only, since their biological function to endocrine resistance has not been validated in animal models in this study

Journal: Breast Cancer Research : BCR

Article Title: Activating transcription factor-2 (ATF2) is a key determinant of resistance to endocrine treatment in an in vitro model of breast cancer

doi: 10.1186/s13058-020-01359-7

Figure Lengend Snippet: Effect of knockdown of ATF2 on ER and ER-regulated genes and proposed model of resistance. a – f MCF7 (left bars) and TAMR (right bars) cells were transfected with ATF2 siRNA and qRT-PCR was carried for ATF2 ( a ), ERα ( ESR1 ) ( b ), TFF1 ( c ), GREB1 ( d ), PGR ( e ) and NCOA3 ( f ) using TaqMan primers. GAPDH was used as the housekeeping gene and changes in mRNA levels after ATF2 knockdown were calculated relative to the control. Asterisks indicate the genes that were significantly changed after ATF2 knockdown (* p < 0.05, ** p < 0.005). g Protein lysates were also prepared in triplicates of three independent experiments and immunoblotting was carried out using the antibodies indicated. ATF2 knockdown had no effect on the ER and ER-regulated genes on the tamoxifen-sensitive MCF7 cells but affected their expression both on the mRNA and protein levels on the tamoxifen-resistant TAMRs. The following model of resistance is proposed: h In endocrine-sensitive cells, gene transcription is ER-dependent and endocrine therapy is able to stop their growth and proliferation. However, endocrine-resistant cells have a shift from ER-dependent to an ER-independent ATF2-dependent transcriptional program and therefore, they are not responding to endocrine treatment. i Targeting the ATF-2 transcription factor in endocrine-resistant cells represents a new mechanism to revert resistance and enhance endocrine sensitivity. The genes shown in this model ( h , i ) such as TFF1, GREB1 and NCOA3 are examples of resistance candidates only, since their biological function to endocrine resistance has not been validated in animal models in this study

Techniques: Knockdown, Transfection, Quantitative RT-PCR, Control, Western Blot, Expressing

Effects of MAAs on intracellular signaling cascades of p38 (A), ERK (B), JNK (C), ATF2 (D), MSK1(Thr-581/Ser-360/Ser-376) (E–G), c-Jun (H), NF-κB (Ser-276/Ser-536) (I and J), IκB (K), CREB (L), and c-Fos (M) in HDFs. HDFs were incubated with MAAs or with IL-1α at the indicated concentrations and were harvested at 15 and 30 min or 2 h post-treatment and then immunoblotted with antibodies to β-actin and to phosphorylated or nonphosphorylated signaling factors. K: β-actin was used as a loading control because of undetectable levels of nonphosphorylated IκB protein in IL-1α–treated cells. Representative immunoblots from three independent experiments are shown. Data represent means ± S.D., n = 3; *, p < 0.05; **, p < 0.01 versus control (0 μg/ml).

Journal: The Journal of Biological Chemistry

Article Title: Mycosporine-like amino acids stimulate hyaluronan secretion by up-regulating hyaluronan synthase 2 via activation of the p38/MSK1/CREB/c-Fos/AP-1 axis

doi: 10.1074/jbc.RA119.011139

Figure Lengend Snippet: Effects of MAAs on intracellular signaling cascades of p38 (A), ERK (B), JNK (C), ATF2 (D), MSK1(Thr-581/Ser-360/Ser-376) (E–G), c-Jun (H), NF-κB (Ser-276/Ser-536) (I and J), IκB (K), CREB (L), and c-Fos (M) in HDFs. HDFs were incubated with MAAs or with IL-1α at the indicated concentrations and were harvested at 15 and 30 min or 2 h post-treatment and then immunoblotted with antibodies to β-actin and to phosphorylated or nonphosphorylated signaling factors. K: β-actin was used as a loading control because of undetectable levels of nonphosphorylated IκB protein in IL-1α–treated cells. Representative immunoblots from three independent experiments are shown. Data represent means ± S.D., n = 3; *, p < 0.05; **, p < 0.01 versus control (0 μg/ml).

Article Snippet: On day 1, HDFs were transfected with a control siRNA (MISSION® siRNA Universal Negative Control, Sigma), an ATF2 siRNA or a c-Fos siRNA (Mission siRNA, Sigma), and an HAS2 siRNA using Lipofectamine RNAiMAX transfection reagent (Invitrogen) following the manufacturer's protocol.

Techniques: Incubation, Western Blot

Effects of transfecting an ATF2 siRNA or a c-Fos siRNA. A: effect of transfecting an ATF2 siRNA on the expression of ATF2 protein and its phosphorylation. HDFs were incubated with or without MAAs at 25 μg/ml. Lysates were harvested at 15 min post-treatment and were immunoblotted with antibodies to β-actin and to phosphorylated or nonphosphorylated ATF2. Representative immunoblots from three independent experiments are shown. Data represent means ± S.D., n = 3; **, p < 0.01. B: effect of transfection of a c-Fos siRNA on the MAA-stimulated expressions of c-Fos protein. HDFs were incubated with or without MAAs at 25 μg/ml. Lysates were harvested at 2 h post-treatment and were immunoblotted with antibodies to β-actin and c-Fos. Representative immunoblots from three independent experiments are shown. Data represent means ± S.D., n = 3; *, p < 0.05; **, p < 0.01. C: effects of transfection of an ATF2 siRNA or a c-Fos siRNA on MAA-increased gene expression of HAS2 in HDFs. After transfection of an ATF2 siRNA or a c-Fos siRNA, HDFs were cultured in the presence or absence of MAAs at 25 μg/ml for 3 h and then were subjected to RT-PCR analysis for mRNA levels of HAS2. Data represent means ± S.D., n = 3; *, p < 0.05; **, p < 0.01.

Journal: The Journal of Biological Chemistry

Article Title: Mycosporine-like amino acids stimulate hyaluronan secretion by up-regulating hyaluronan synthase 2 via activation of the p38/MSK1/CREB/c-Fos/AP-1 axis

doi: 10.1074/jbc.RA119.011139

Figure Lengend Snippet: Effects of transfecting an ATF2 siRNA or a c-Fos siRNA. A: effect of transfecting an ATF2 siRNA on the expression of ATF2 protein and its phosphorylation. HDFs were incubated with or without MAAs at 25 μg/ml. Lysates were harvested at 15 min post-treatment and were immunoblotted with antibodies to β-actin and to phosphorylated or nonphosphorylated ATF2. Representative immunoblots from three independent experiments are shown. Data represent means ± S.D., n = 3; **, p < 0.01. B: effect of transfection of a c-Fos siRNA on the MAA-stimulated expressions of c-Fos protein. HDFs were incubated with or without MAAs at 25 μg/ml. Lysates were harvested at 2 h post-treatment and were immunoblotted with antibodies to β-actin and c-Fos. Representative immunoblots from three independent experiments are shown. Data represent means ± S.D., n = 3; *, p < 0.05; **, p < 0.01. C: effects of transfection of an ATF2 siRNA or a c-Fos siRNA on MAA-increased gene expression of HAS2 in HDFs. After transfection of an ATF2 siRNA or a c-Fos siRNA, HDFs were cultured in the presence or absence of MAAs at 25 μg/ml for 3 h and then were subjected to RT-PCR analysis for mRNA levels of HAS2. Data represent means ± S.D., n = 3; *, p < 0.05; **, p < 0.01.

Techniques: Expressing, Incubation, Western Blot, Transfection, Cell Culture, Reverse Transcription Polymerase Chain Reaction

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