srf sirna fragment Search Results


srf fragments  (System Biosciences Inc)
86
System Biosciences Inc srf fragments
List of Primers Used in This Study
Srf Fragments, supplied by System Biosciences Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/srf+sirna+fragment/fragments+srf/pmc07395694-151-0-11
Average 86 stars, based on 1 article reviews
srf fragments - by Bioz Stars, 2026-10
86/100 stars
  Buy from Supplier

Image Search Results


List of Primers Used in This Study

Journal: Cancer Management and Research

Article Title: SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner

doi: 10.2147/CMAR.S257422

Figure Lengend Snippet: List of Primers Used in This Study

Article Snippet: SRF fragments, miR-214 mimic and small interfering RNA (siRNA) targeting PTK6 (System Biosciences, Palo Alto, CA, USA) were cloned into a pmirGLO vector (Promega Corporation, Madison, WI, USA), and the constructed vectors were transfected into cells to establish cells that stably overexpressing SRF, miR-214 or PTK6 deficit.

Techniques: Sequencing

The binding relationship between miR-214 and SRF is identified. ( A ) the transcription factor that regulate miR-214 and the binding promoter sequences predicted by TransmiR and ALGGEN; ( B ) the targeting relationship between SRF and miR-214 verified by a dual-luciferase reporting assay; ( C ) the effect of SRF-NC and SRF-OE on miR-214 promoter validated by ChIP; ( D ) SRF expression in CC and adjacent tissues evaluated by RT-qPCR detection; ( E ) SRF expression in CC cell lines evaluated by RT-qPCR detection; ( F ) SRF expression in CC cell lines overexpressing miR-214 evaluated by RT-qPCR detection; ( G ) SRF expression in CC cell lines overexpressing miR-214 evaluated by RT-qPCR detection. * p < 0.05 according to one-way (panel ( E ) or two-way ANOVA (panel BD, F and G ). Data represent averages of three independent experiments.

Journal: Cancer Management and Research

Article Title: SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner

doi: 10.2147/CMAR.S257422

Figure Lengend Snippet: The binding relationship between miR-214 and SRF is identified. ( A ) the transcription factor that regulate miR-214 and the binding promoter sequences predicted by TransmiR and ALGGEN; ( B ) the targeting relationship between SRF and miR-214 verified by a dual-luciferase reporting assay; ( C ) the effect of SRF-NC and SRF-OE on miR-214 promoter validated by ChIP; ( D ) SRF expression in CC and adjacent tissues evaluated by RT-qPCR detection; ( E ) SRF expression in CC cell lines evaluated by RT-qPCR detection; ( F ) SRF expression in CC cell lines overexpressing miR-214 evaluated by RT-qPCR detection; ( G ) SRF expression in CC cell lines overexpressing miR-214 evaluated by RT-qPCR detection. * p < 0.05 according to one-way (panel ( E ) or two-way ANOVA (panel BD, F and G ). Data represent averages of three independent experiments.

Article Snippet: SRF fragments, miR-214 mimic and small interfering RNA (siRNA) targeting PTK6 (System Biosciences, Palo Alto, CA, USA) were cloned into a pmirGLO vector (Promega Corporation, Madison, WI, USA), and the constructed vectors were transfected into cells to establish cells that stably overexpressing SRF, miR-214 or PTK6 deficit.

Techniques: Binding Assay, Luciferase, Expressing, Quantitative RT-PCR

SRF overexpression rescues the repressive role of miR-214 mimic on CC cell viability. CC cell lines were transfected with SRF-OE or SRF-NC in the presence of miR-214 mimic. ( A ) SRF expression in CC cell lines co-transfected with miR-214 mimic and SRF-OE evaluated by RT-qPCR detection; ( B ) CC cell proliferation determined by EdU staining; ( C ) CC cell migration evaluated by Transwell assays; ( D ) CC cell invasion evaluated by Transwell assays; ( E ) representative tumor images and tumor volume from mice injected with CC cells overexpressing SRF; ( F ), KI67 positive rate of tumors detected by immunohistochemistry; ( G ) changes of pulmonary nodules detected by HE staining. * p < 0.05 according to the two-way ANOVA. Data represent averages of three independent experiments.

Journal: Cancer Management and Research

Article Title: SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner

doi: 10.2147/CMAR.S257422

Figure Lengend Snippet: SRF overexpression rescues the repressive role of miR-214 mimic on CC cell viability. CC cell lines were transfected with SRF-OE or SRF-NC in the presence of miR-214 mimic. ( A ) SRF expression in CC cell lines co-transfected with miR-214 mimic and SRF-OE evaluated by RT-qPCR detection; ( B ) CC cell proliferation determined by EdU staining; ( C ) CC cell migration evaluated by Transwell assays; ( D ) CC cell invasion evaluated by Transwell assays; ( E ) representative tumor images and tumor volume from mice injected with CC cells overexpressing SRF; ( F ), KI67 positive rate of tumors detected by immunohistochemistry; ( G ) changes of pulmonary nodules detected by HE staining. * p < 0.05 according to the two-way ANOVA. Data represent averages of three independent experiments.

Article Snippet: SRF fragments, miR-214 mimic and small interfering RNA (siRNA) targeting PTK6 (System Biosciences, Palo Alto, CA, USA) were cloned into a pmirGLO vector (Promega Corporation, Madison, WI, USA), and the constructed vectors were transfected into cells to establish cells that stably overexpressing SRF, miR-214 or PTK6 deficit.

Techniques: Over Expression, Transfection, Expressing, Quantitative RT-PCR, Staining, Migration, Injection, Immunohistochemistry

The binding relationship between miR-214 and PTK6 is identified. ( A ) the targeting relationship between PTK6 and miR-214 predicted by bioinformatic analysis and verified by a dual-luciferase reporting assay; ( B) no direct targeting relationship between PTK6 and SRF verified by a dual-luciferase reporting assay; ( C ) PTK6 expression in CC and adjacent tissues evaluated by RT-qPCR detection; ( D ) PTK6 expression in CC cell lines evaluated by RT-qPCR detection; ( E ) PTK6 expression in CC cell lines overexpressing miR-214 or SRF evaluated by RT-qPCR detection; ( F ) PTK6 expression in CC cell lines with PTK6 knockdown evaluated by RT-qPCR detection. * p < 0.05 according to one-way (panel ( D ) or two-way ANOVA (panel AC, E and F ). Data represent averages of three independent experiments.

Journal: Cancer Management and Research

Article Title: SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner

doi: 10.2147/CMAR.S257422

Figure Lengend Snippet: The binding relationship between miR-214 and PTK6 is identified. ( A ) the targeting relationship between PTK6 and miR-214 predicted by bioinformatic analysis and verified by a dual-luciferase reporting assay; ( B) no direct targeting relationship between PTK6 and SRF verified by a dual-luciferase reporting assay; ( C ) PTK6 expression in CC and adjacent tissues evaluated by RT-qPCR detection; ( D ) PTK6 expression in CC cell lines evaluated by RT-qPCR detection; ( E ) PTK6 expression in CC cell lines overexpressing miR-214 or SRF evaluated by RT-qPCR detection; ( F ) PTK6 expression in CC cell lines with PTK6 knockdown evaluated by RT-qPCR detection. * p < 0.05 according to one-way (panel ( D ) or two-way ANOVA (panel AC, E and F ). Data represent averages of three independent experiments.

Article Snippet: SRF fragments, miR-214 mimic and small interfering RNA (siRNA) targeting PTK6 (System Biosciences, Palo Alto, CA, USA) were cloned into a pmirGLO vector (Promega Corporation, Madison, WI, USA), and the constructed vectors were transfected into cells to establish cells that stably overexpressing SRF, miR-214 or PTK6 deficit.

Techniques: Binding Assay, Luciferase, Expressing, Quantitative RT-PCR, Knockdown

The JAK2/STAT3 pathway is regulated by the SRF/miR-214/PTK6 axis. The JAK2 and STAT3 protein expression and phosphorylation in LOVO ( A ) and SW620 ( B ) cells transfected with SRF-NC, SRF-OE, miR-214 control, miR-214 mimic, miR-214 mimic + SRF-NC, miR-214 mimic + SRF-OE, PTK6-NC or si-PTK6. * p < 0.05 according to the two-way ANOVA. Data represent averages of three independent experiments.

Journal: Cancer Management and Research

Article Title: SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner

doi: 10.2147/CMAR.S257422

Figure Lengend Snippet: The JAK2/STAT3 pathway is regulated by the SRF/miR-214/PTK6 axis. The JAK2 and STAT3 protein expression and phosphorylation in LOVO ( A ) and SW620 ( B ) cells transfected with SRF-NC, SRF-OE, miR-214 control, miR-214 mimic, miR-214 mimic + SRF-NC, miR-214 mimic + SRF-OE, PTK6-NC or si-PTK6. * p < 0.05 according to the two-way ANOVA. Data represent averages of three independent experiments.

Article Snippet: SRF fragments, miR-214 mimic and small interfering RNA (siRNA) targeting PTK6 (System Biosciences, Palo Alto, CA, USA) were cloned into a pmirGLO vector (Promega Corporation, Madison, WI, USA), and the constructed vectors were transfected into cells to establish cells that stably overexpressing SRF, miR-214 or PTK6 deficit.

Techniques: Expressing, Phospho-proteomics, Transfection, Control

The model for miR-214 regulation upon CC cell progression. SRF could bind to the miR-214 promoter region, located on chromosome 1 q24.3, and repress its expression. The restoration of miR-214 lowers the expression PTK6, thereby inhibiting the activity of the JAK2/STAT3 pathway, which in turn inhibits CC cell proliferation, migration, invasion, tumorigenesis, and metastasis.

Journal: Cancer Management and Research

Article Title: SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner

doi: 10.2147/CMAR.S257422

Figure Lengend Snippet: The model for miR-214 regulation upon CC cell progression. SRF could bind to the miR-214 promoter region, located on chromosome 1 q24.3, and repress its expression. The restoration of miR-214 lowers the expression PTK6, thereby inhibiting the activity of the JAK2/STAT3 pathway, which in turn inhibits CC cell proliferation, migration, invasion, tumorigenesis, and metastasis.

Article Snippet: SRF fragments, miR-214 mimic and small interfering RNA (siRNA) targeting PTK6 (System Biosciences, Palo Alto, CA, USA) were cloned into a pmirGLO vector (Promega Corporation, Madison, WI, USA), and the constructed vectors were transfected into cells to establish cells that stably overexpressing SRF, miR-214 or PTK6 deficit.

Techniques: Expressing, Activity Assay, Migration