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Characterization of Overlap66 genes.

Journal: Cancers

Article Title: Prognostic and Therapeutic Potential of the OIP5 Network in Papillary Renal Cell Carcinoma

doi: 10.3390/cancers13174483

Figure Lengend Snippet: Characterization of Overlap66 genes.

Article Snippet: OIP5 (1:50, Sigma-Aldrich), Anti-Phospho-Histone H3 (Ser 10) (1:200, Upstate Biotechnology Inc., Lake Placid, NY, USA), CDK2 (1:200, Santa Cruz, Dallas, TX, USA), and PLK1 (1:300, Novus Biologicals, Toronto, ON, Canada) antibodies were used in the analyses for the xenograft tumors.

Techniques:

PLK1 inhibitor reduces OIP5-mediated pRCC tumorigenesis. ( A , B ) RNA-seq and real-time PCR analyses of PLK1 expression in ACHN EV and ACHN OIP5 tumors. RNA-seq was performed in 3 each from ACHN EV and ACHN OIP5 tumors. ( C ) ACHN EV and ACHN OIP5 cells were treated with DMSO (−) or the PLK1 inhibitor (BI2536) in 40 nM PLK1 inhibitor for 72 h, followed by quantification of cell cycle distributions. Experiments were repeated 3 times; means ± SEMs are graphed. **: p < 0.01, ***: p < 0.001, ****: p < 0.0001 in the indicated comparisons by 2-tailed Student’s test. ( D – G ) Mice bearing ACHN EV or ACHN OIP5 tumors were treated with vehicle or BI2536 (50 mg/kg) intravenously. The overall profiles of tumor growth in the vehicle treated setting ( D ); tumor volumes were recorded following treatments ( E – G ). Statistical analyses were performed using 2-tailed Student’s t -test; *: p < 0.05, ***: p < 0.001. ( H ) Kaplan Meier curve for the indicated mice reaching endpoints. Statistical analysis was performed using logrank test.

Journal: Cancers

Article Title: Prognostic and Therapeutic Potential of the OIP5 Network in Papillary Renal Cell Carcinoma

doi: 10.3390/cancers13174483

Figure Lengend Snippet: PLK1 inhibitor reduces OIP5-mediated pRCC tumorigenesis. ( A , B ) RNA-seq and real-time PCR analyses of PLK1 expression in ACHN EV and ACHN OIP5 tumors. RNA-seq was performed in 3 each from ACHN EV and ACHN OIP5 tumors. ( C ) ACHN EV and ACHN OIP5 cells were treated with DMSO (−) or the PLK1 inhibitor (BI2536) in 40 nM PLK1 inhibitor for 72 h, followed by quantification of cell cycle distributions. Experiments were repeated 3 times; means ± SEMs are graphed. **: p < 0.01, ***: p < 0.001, ****: p < 0.0001 in the indicated comparisons by 2-tailed Student’s test. ( D – G ) Mice bearing ACHN EV or ACHN OIP5 tumors were treated with vehicle or BI2536 (50 mg/kg) intravenously. The overall profiles of tumor growth in the vehicle treated setting ( D ); tumor volumes were recorded following treatments ( E – G ). Statistical analyses were performed using 2-tailed Student’s t -test; *: p < 0.05, ***: p < 0.001. ( H ) Kaplan Meier curve for the indicated mice reaching endpoints. Statistical analysis was performed using logrank test.

Article Snippet: OIP5 (1:50, Sigma-Aldrich), Anti-Phospho-Histone H3 (Ser 10) (1:200, Upstate Biotechnology Inc., Lake Placid, NY, USA), CDK2 (1:200, Santa Cruz, Dallas, TX, USA), and PLK1 (1:300, Novus Biologicals, Toronto, ON, Canada) antibodies were used in the analyses for the xenograft tumors.

Techniques: RNA Sequencing, Real-time Polymerase Chain Reaction, Expressing