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cat# sc-376654, lot#h0416  (Santa Cruz Biotechnology)
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MiR‐612 inhibitor abolished circSMOC1 knockdown‐caused <t>CCL28</t> downregulation in NSCLC. (A) Schematic representation of the binding sites between miR‐612 and WT or Mut CCL28 3′UTR. (B) Analysis of luciferase activities of WT or Mut CCL28 3′UTR after co‐transfection with miR‐612 mimics and WT or Mut CCL28 3′UTR in PC‐9 and 95D cells. (C, D) RT‐qPCR and Western blotting analysis of the expression levels of CCL28 after co‐transfection with sh‐circSMOC1 and miR‐612 inhibitor in PC‐9 and 95D cells. (E, F) Colony formation and transwell analysis of the cell colonies and invasion capabilities after co‐transfection with si‐CCL28 and miR‐612 inhibitor in PC‐9 and 95D cells. Data shown are the mean ± SEM of three experiments. Data shown are the mean ± SEM of three experiments. * p < 0.05, ** p < 0.01, *** p < 0.001.
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si- ccl28  (Shanghai GenePharma)
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MiR‐612 inhibitor abolished circSMOC1 knockdown‐caused <t>CCL28</t> downregulation in NSCLC. (A) Schematic representation of the binding sites between miR‐612 and WT or Mut CCL28 3′UTR. (B) Analysis of luciferase activities of WT or Mut CCL28 3′UTR after co‐transfection with miR‐612 mimics and WT or Mut CCL28 3′UTR in PC‐9 and 95D cells. (C, D) RT‐qPCR and Western blotting analysis of the expression levels of CCL28 after co‐transfection with sh‐circSMOC1 and miR‐612 inhibitor in PC‐9 and 95D cells. (E, F) Colony formation and transwell analysis of the cell colonies and invasion capabilities after co‐transfection with si‐CCL28 and miR‐612 inhibitor in PC‐9 and 95D cells. Data shown are the mean ± SEM of three experiments. Data shown are the mean ± SEM of three experiments. * p < 0.05, ** p < 0.01, *** p < 0.001.
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anti- ccl28  (GeneTex)
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MiR‐612 inhibitor abolished circSMOC1 knockdown‐caused <t>CCL28</t> downregulation in NSCLC. (A) Schematic representation of the binding sites between miR‐612 and WT or Mut CCL28 3′UTR. (B) Analysis of luciferase activities of WT or Mut CCL28 3′UTR after co‐transfection with miR‐612 mimics and WT or Mut CCL28 3′UTR in PC‐9 and 95D cells. (C, D) RT‐qPCR and Western blotting analysis of the expression levels of CCL28 after co‐transfection with sh‐circSMOC1 and miR‐612 inhibitor in PC‐9 and 95D cells. (E, F) Colony formation and transwell analysis of the cell colonies and invasion capabilities after co‐transfection with si‐CCL28 and miR‐612 inhibitor in PC‐9 and 95D cells. Data shown are the mean ± SEM of three experiments. Data shown are the mean ± SEM of three experiments. * p < 0.05, ** p < 0.01, *** p < 0.001.
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MiR‐612 inhibitor abolished circSMOC1 knockdown‐caused <t>CCL28</t> downregulation in NSCLC. (A) Schematic representation of the binding sites between miR‐612 and WT or Mut CCL28 3′UTR. (B) Analysis of luciferase activities of WT or Mut CCL28 3′UTR after co‐transfection with miR‐612 mimics and WT or Mut CCL28 3′UTR in PC‐9 and 95D cells. (C, D) RT‐qPCR and Western blotting analysis of the expression levels of CCL28 after co‐transfection with sh‐circSMOC1 and miR‐612 inhibitor in PC‐9 and 95D cells. (E, F) Colony formation and transwell analysis of the cell colonies and invasion capabilities after co‐transfection with si‐CCL28 and miR‐612 inhibitor in PC‐9 and 95D cells. Data shown are the mean ± SEM of three experiments. Data shown are the mean ± SEM of three experiments. * p < 0.05, ** p < 0.01, *** p < 0.001.
Ccl28 Pa5–28821, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ccl28 df7045 antibody  (Affinity Biosciences)
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MiR‐612 inhibitor abolished circSMOC1 knockdown‐caused <t>CCL28</t> downregulation in NSCLC. (A) Schematic representation of the binding sites between miR‐612 and WT or Mut CCL28 3′UTR. (B) Analysis of luciferase activities of WT or Mut CCL28 3′UTR after co‐transfection with miR‐612 mimics and WT or Mut CCL28 3′UTR in PC‐9 and 95D cells. (C, D) RT‐qPCR and Western blotting analysis of the expression levels of CCL28 after co‐transfection with sh‐circSMOC1 and miR‐612 inhibitor in PC‐9 and 95D cells. (E, F) Colony formation and transwell analysis of the cell colonies and invasion capabilities after co‐transfection with si‐CCL28 and miR‐612 inhibitor in PC‐9 and 95D cells. Data shown are the mean ± SEM of three experiments. Data shown are the mean ± SEM of three experiments. * p < 0.05, ** p < 0.01, *** p < 0.001.
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MiR‐612 inhibitor abolished circSMOC1 knockdown‐caused CCL28 downregulation in NSCLC. (A) Schematic representation of the binding sites between miR‐612 and WT or Mut CCL28 3′UTR. (B) Analysis of luciferase activities of WT or Mut CCL28 3′UTR after co‐transfection with miR‐612 mimics and WT or Mut CCL28 3′UTR in PC‐9 and 95D cells. (C, D) RT‐qPCR and Western blotting analysis of the expression levels of CCL28 after co‐transfection with sh‐circSMOC1 and miR‐612 inhibitor in PC‐9 and 95D cells. (E, F) Colony formation and transwell analysis of the cell colonies and invasion capabilities after co‐transfection with si‐CCL28 and miR‐612 inhibitor in PC‐9 and 95D cells. Data shown are the mean ± SEM of three experiments. Data shown are the mean ± SEM of three experiments. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WTAP ‐Mediated m 6 A Modification of circSMOC1 Accelerates the Tumorigenesis of Non‐Small Cell Lung Cancer by Regulating miR ‐612/ CCL28 Axis

doi: 10.1111/jcmm.70207

Figure Lengend Snippet: MiR‐612 inhibitor abolished circSMOC1 knockdown‐caused CCL28 downregulation in NSCLC. (A) Schematic representation of the binding sites between miR‐612 and WT or Mut CCL28 3′UTR. (B) Analysis of luciferase activities of WT or Mut CCL28 3′UTR after co‐transfection with miR‐612 mimics and WT or Mut CCL28 3′UTR in PC‐9 and 95D cells. (C, D) RT‐qPCR and Western blotting analysis of the expression levels of CCL28 after co‐transfection with sh‐circSMOC1 and miR‐612 inhibitor in PC‐9 and 95D cells. (E, F) Colony formation and transwell analysis of the cell colonies and invasion capabilities after co‐transfection with si‐CCL28 and miR‐612 inhibitor in PC‐9 and 95D cells. Data shown are the mean ± SEM of three experiments. Data shown are the mean ± SEM of three experiments. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The supernatants were resolved in SDS‐PAGE and transferred onto polyvinylidene fluoride (PVDF) membranes (Millipore), incubated with anti‐WTAP (10200‐1‐AP, Proteintech), anti‐caspase‐9 (AF6348, Affinity), anti‐cleaved caspase‐9 (AF5240, Affinity), anti‐caspase‐7 (DF6441, Affinity), anti‐cleaved caspase‐7 (AF4023, Affinity), anti‐caspase‐3 (DF6020, Affinity), anti‐cleaved caspase‐3 (AF7022, Affinity), anti‐CCL28 (N3C3, GeneTex) and anti‐GAPDH (AB‐P‐R 001) overnight at 4°C.

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

Knockdown of circSMOC1 suppressed in vivo NSCLC tumorigenesis. (A) Representative photographs of the subcutaneous xenograft tumours between sh‐circSMOC1 and sh‐NC groups. (B) Comparison of the tumour growth curve after treatment with sh‐circSMOC1 or sh‐NC transfected PC‐9 cells. (C) Comparison of the tumour volume and tumour weight between circSMOC1 and sh‐NC groups. (D) IHC analysis of the Ki‐67 levels and CCL28 protein expression between circSMOC1 and sh‐NC groups.

Journal: Journal of Cellular and Molecular Medicine

Article Title: WTAP ‐Mediated m 6 A Modification of circSMOC1 Accelerates the Tumorigenesis of Non‐Small Cell Lung Cancer by Regulating miR ‐612/ CCL28 Axis

doi: 10.1111/jcmm.70207

Figure Lengend Snippet: Knockdown of circSMOC1 suppressed in vivo NSCLC tumorigenesis. (A) Representative photographs of the subcutaneous xenograft tumours between sh‐circSMOC1 and sh‐NC groups. (B) Comparison of the tumour growth curve after treatment with sh‐circSMOC1 or sh‐NC transfected PC‐9 cells. (C) Comparison of the tumour volume and tumour weight between circSMOC1 and sh‐NC groups. (D) IHC analysis of the Ki‐67 levels and CCL28 protein expression between circSMOC1 and sh‐NC groups.

Article Snippet: The supernatants were resolved in SDS‐PAGE and transferred onto polyvinylidene fluoride (PVDF) membranes (Millipore), incubated with anti‐WTAP (10200‐1‐AP, Proteintech), anti‐caspase‐9 (AF6348, Affinity), anti‐cleaved caspase‐9 (AF5240, Affinity), anti‐caspase‐7 (DF6441, Affinity), anti‐cleaved caspase‐7 (AF4023, Affinity), anti‐caspase‐3 (DF6020, Affinity), anti‐cleaved caspase‐3 (AF7022, Affinity), anti‐CCL28 (N3C3, GeneTex) and anti‐GAPDH (AB‐P‐R 001) overnight at 4°C.

Techniques: Knockdown, In Vivo, Comparison, Transfection, Expressing