Figure 4.
Transcriptomic analysis reveals TAZ as negative regulator of MYC. GSEA reveals enrichment of apoptotic genes (A) and downregulation of MYC targets (B-C) using the MSigDB Hallmark collection in TAZ-overexpressing KMM1 cells relative to WPI-expressing cells. (D) Table of gene sets enriched in TAZ-expressing KMM1 cells, highlighting the number of genes in each set (n), the normalized enrichment score (NES), and test of statistical significance (false discovery rate [FDR] q value). (E) Expression of TAZ and MYC are anticorrelated in MM patient samples combining data from GSE5900 and GSE2658 using probe sets 202134_s_at (TAZ) and 202431_s_at (MYC). (F) Validation of TAZ targets at the mRNA levels using qPCR. Data are mean ± SD of triplicate samples. **P ≤ .01 using the Student t test. (G) Validation of TAZ targets at the protein level. β-actin was used as a loading control.

Transcriptomic analysis reveals TAZ as negative regulator of MYC. GSEA reveals enrichment of apoptotic genes (A) and downregulation of MYC targets (B-C) using the MSigDB Hallmark collection in TAZ-overexpressing KMM1 cells relative to WPI-expressing cells. (D) Table of gene sets enriched in TAZ-expressing KMM1 cells, highlighting the number of genes in each set (n), the normalized enrichment score (NES), and test of statistical significance (false discovery rate [FDR] q value). (E) Expression of TAZ and MYC are anticorrelated in MM patient samples combining data from GSE5900 and GSE2658 using probe sets 202134_s_at (TAZ) and 202431_s_at (MYC). (F) Validation of TAZ targets at the mRNA levels using qPCR. Data are mean ± SD of triplicate samples. **P ≤ .01 using the Student t test. (G) Validation of TAZ targets at the protein level. β-actin was used as a loading control.

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