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pcdna3.1-stat3  (GenScript corporation)

 
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    Structured Review

    GenScript corporation pcdna3.1-stat3
    Pcdna3.1 Stat3, supplied by GenScript corporation, 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/pcdna3%2E1-stat3/pcdna3+1/pm36972141-44-3-12
    Average 90 stars, based on 1 article reviews
    pcdna3.1-stat3 - by Bioz Stars, 2026-10
    90/100 stars

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    Related Articles

    Over Expression:

    Article Title: HOTAIR knockdown impairs metastasis of cervical cancer cells by down-regulating metastasis-related genes.
    Article Snippet: For rescue experiments, pcDNA3.1-STAT3 and pcDNA3.1-Notch1 overexpression vectors were synthesised at GenePharma (GenScript, China) and transfected into cells in various combinations with siHOTAIR using Lipofectamine 3000 Transfection Reagents based on the supplier’s instructions.

    Article Title: KCNQ1OT1 sponges miR-34a to promote malignant progression of malignant melanoma via upregulation of the STAT3/PD-L1 axis.
    Article Snippet: Correspondence Fei Zhu, Department of Plastic Surgery, The First Affiliated Hospital of Anhui Medical University, 218 JiXi Avenue, Hefei 230022, Anhui, People's Republic of China.. Email: hfzfzx@163.com Abstract Background: Malignant melanoma is a leading cause of skin cancer-related death.. In over 30% of cases, the melanoma is invasive and has a metastatic phenotype.

    Transfection:

    Article Title: HOTAIR knockdown impairs metastasis of cervical cancer cells by down-regulating metastasis-related genes.
    Article Snippet: For rescue experiments, pcDNA3.1-STAT3 and pcDNA3.1-Notch1 overexpression vectors were synthesised at GenePharma (GenScript, China) and transfected into cells in various combinations with siHOTAIR using Lipofectamine 3000 Transfection Reagents based on the supplier’s instructions.

    Article Title: KCNQ1OT1 sponges miR-34a to promote malignant progression of malignant melanoma via upregulation of the STAT3/PD-L1 axis.
    Article Snippet: Correspondence Fei Zhu, Department of Plastic Surgery, The First Affiliated Hospital of Anhui Medical University, 218 JiXi Avenue, Hefei 230022, Anhui, People's Republic of China.. Email: hfzfzx@163.com Abstract Background: Malignant melanoma is a leading cause of skin cancer-related death.. In over 30% of cases, the melanoma is invasive and has a metastatic phenotype.



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    <t>STAT3</t> is a target of miR-874-3p. (A) Potential target mRNAs of miR-874-3p predicted by PITA, PicTar, miRanda, microT and miRmap. (B) Underlying downstream mRNAs that could be upregulated in LUAD cells and downregulated by miR-874-3p mimics. (C) RNA pull-down assay was utilized to examine the enrichment of STAT3, TRIB2 and SLC12A5 in miR-874-3p biotin probe. (D) The expression of STAT3 in human normal lung epithelial cell line (BEAS-2B) and LUAD cell lines (PC9, HCC827, A549 and NCI–H23). (E) The interaction between miR-874-3p together with MCF2L-AS1 and STAT3 was determined by RIP assay. (F) The potential binding site between miR-874-3p and STAT3 was predicted through starBase. (G) MiR-874-3p was verified to combine with STAT3 through luciferase reporter assay. (H–I) STAT3 mRNA and protein levels were assessed in LUAD cells transfected with miR-874-3p mimics. (J–K) qRT-PCR and Western blot assays were employed to detect the mRNA and protein levels of STAT3 in MCF2L-AS1 downregulated LUAD cells. **P < 0.01.
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    Image Search Results


    STAT3 is a target of miR-874-3p. (A) Potential target mRNAs of miR-874-3p predicted by PITA, PicTar, miRanda, microT and miRmap. (B) Underlying downstream mRNAs that could be upregulated in LUAD cells and downregulated by miR-874-3p mimics. (C) RNA pull-down assay was utilized to examine the enrichment of STAT3, TRIB2 and SLC12A5 in miR-874-3p biotin probe. (D) The expression of STAT3 in human normal lung epithelial cell line (BEAS-2B) and LUAD cell lines (PC9, HCC827, A549 and NCI–H23). (E) The interaction between miR-874-3p together with MCF2L-AS1 and STAT3 was determined by RIP assay. (F) The potential binding site between miR-874-3p and STAT3 was predicted through starBase. (G) MiR-874-3p was verified to combine with STAT3 through luciferase reporter assay. (H–I) STAT3 mRNA and protein levels were assessed in LUAD cells transfected with miR-874-3p mimics. (J–K) qRT-PCR and Western blot assays were employed to detect the mRNA and protein levels of STAT3 in MCF2L-AS1 downregulated LUAD cells. **P < 0.01.

    Journal: Heliyon

    Article Title: MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance

    doi: 10.1016/j.heliyon.2023.e21342

    Figure Lengend Snippet: STAT3 is a target of miR-874-3p. (A) Potential target mRNAs of miR-874-3p predicted by PITA, PicTar, miRanda, microT and miRmap. (B) Underlying downstream mRNAs that could be upregulated in LUAD cells and downregulated by miR-874-3p mimics. (C) RNA pull-down assay was utilized to examine the enrichment of STAT3, TRIB2 and SLC12A5 in miR-874-3p biotin probe. (D) The expression of STAT3 in human normal lung epithelial cell line (BEAS-2B) and LUAD cell lines (PC9, HCC827, A549 and NCI–H23). (E) The interaction between miR-874-3p together with MCF2L-AS1 and STAT3 was determined by RIP assay. (F) The potential binding site between miR-874-3p and STAT3 was predicted through starBase. (G) MiR-874-3p was verified to combine with STAT3 through luciferase reporter assay. (H–I) STAT3 mRNA and protein levels were assessed in LUAD cells transfected with miR-874-3p mimics. (J–K) qRT-PCR and Western blot assays were employed to detect the mRNA and protein levels of STAT3 in MCF2L-AS1 downregulated LUAD cells. **P < 0.01.

    Article Snippet: The MCF2L-AS1 or STAT3-specific shRNAs (sh-MCF2L-AS1#1/2, sh-STAT3#1/2) and control (sh-NC), the pcDNA3.1/STAT3 and control (pcDNA3.1) were procured from Genepharma (Shanghai, China) for plasmid transfection.

    Techniques: Pull Down Assay, Expressing, Binding Assay, Luciferase, Reporter Assay, Transfection, Quantitative RT-PCR, Western Blot

    MCF2L-AS1 facilitate LUAD cell growth by targeting miR-874-3p/STAT3. (A) Expressions of miR-874-3p and STAT3 were tested by separately transfecting miR-874-3p inhibitor and sh-STAT3. (B–D) The proliferative capacity of MCF2L-AS1 silenced cells was estimated after transfecting NC inhibitor, miR-874-3p inhibitor, miR-874-3p inhibitor plus sh-STAT3. (E–F) NC inhibitor, miR-874-3p inhibitor, miR-874-3p inhibitor plus sh-STAT3 were transfected into MCF2L-AS1 downregulated cells to observe cell apoptosis. (G) Cell migration was evaluated after transfecting above appointed plasmids in sh-MCF2L-AS1 transfected cells. (H) Above appointed plasmids were transfected into MCF2L-AS1 downregulated cells to detect cell invasion. **P < 0.01.

    Journal: Heliyon

    Article Title: MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance

    doi: 10.1016/j.heliyon.2023.e21342

    Figure Lengend Snippet: MCF2L-AS1 facilitate LUAD cell growth by targeting miR-874-3p/STAT3. (A) Expressions of miR-874-3p and STAT3 were tested by separately transfecting miR-874-3p inhibitor and sh-STAT3. (B–D) The proliferative capacity of MCF2L-AS1 silenced cells was estimated after transfecting NC inhibitor, miR-874-3p inhibitor, miR-874-3p inhibitor plus sh-STAT3. (E–F) NC inhibitor, miR-874-3p inhibitor, miR-874-3p inhibitor plus sh-STAT3 were transfected into MCF2L-AS1 downregulated cells to observe cell apoptosis. (G) Cell migration was evaluated after transfecting above appointed plasmids in sh-MCF2L-AS1 transfected cells. (H) Above appointed plasmids were transfected into MCF2L-AS1 downregulated cells to detect cell invasion. **P < 0.01.

    Article Snippet: The MCF2L-AS1 or STAT3-specific shRNAs (sh-MCF2L-AS1#1/2, sh-STAT3#1/2) and control (sh-NC), the pcDNA3.1/STAT3 and control (pcDNA3.1) were procured from Genepharma (Shanghai, China) for plasmid transfection.

    Techniques: Transfection, Migration

    STAT3 binds to MCF2L-AS1 promoter. (A–B) The overexpression efficiency of STAT3 was detected in LUAD cells. (C) MCF2L-AS1 expression in STAT3 overexpressed LUAD cells. (D) The effect of STAT3 knockdown on MCF2L-AS1 expression. (E) The binding sites between STAT3 and MCF2L-AS1 promoter. (F) ChIP assay was performed to determine the interaction between STAT3 and MCF2L-AS1 promoter. (G) Luciferase reporter assay was utilized to measure the combination of STAT3 in MCF2L-AS1 promoter. **P < 0.01.

    Journal: Heliyon

    Article Title: MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance

    doi: 10.1016/j.heliyon.2023.e21342

    Figure Lengend Snippet: STAT3 binds to MCF2L-AS1 promoter. (A–B) The overexpression efficiency of STAT3 was detected in LUAD cells. (C) MCF2L-AS1 expression in STAT3 overexpressed LUAD cells. (D) The effect of STAT3 knockdown on MCF2L-AS1 expression. (E) The binding sites between STAT3 and MCF2L-AS1 promoter. (F) ChIP assay was performed to determine the interaction between STAT3 and MCF2L-AS1 promoter. (G) Luciferase reporter assay was utilized to measure the combination of STAT3 in MCF2L-AS1 promoter. **P < 0.01.

    Article Snippet: The MCF2L-AS1 or STAT3-specific shRNAs (sh-MCF2L-AS1#1/2, sh-STAT3#1/2) and control (sh-NC), the pcDNA3.1/STAT3 and control (pcDNA3.1) were procured from Genepharma (Shanghai, China) for plasmid transfection.

    Techniques: Over Expression, Expressing, Binding Assay, Luciferase, Reporter Assay