Authors
Suchismita Raha, Qiong Zhang, Devon Farrar, Charles Tseng, Rachel G Mendoza, Rabha M Younis, Kayla A Rodriguez, Samyukta Iyer, Mark A Subler, Jolene J Windle, Zhao Lai, Mikhail Dozmorov, Jamy C Peng, Devanand Sarkar
Published in
The Journal of biological chemistry. Pages 113581. Sep 18, 2026. Epub Sep 18, 2026.
Abstract
The oncogenes MYC and TAF2 (TATA-box binding protein associated factor 2) are frequently overexpressed and co-amplified in many cancers, including Hepatocellular Carcinoma (HCC). We recently demonstrated that overexpression of TAF2 in mouse liver markedly augmented MYC overexpression-induced HCC. MYC is a transcription factor. TAF2 is a component of transcription factor IID (TFIID) and functions as a transcription co-factor. We hypothesized that TAF2 modulates gene regulation by MYC, contributing to augmentation of MYC's oncogenic activity. To test this hypothesis, we generated stable HepG2 cell lines overexpressing TAF2, MYC, or both. Combined overexpression of TAF2 and MYC significantly augmented in vitro proliferation, migration and invasion, compared to the overexpression of each gene alone. We performed RNA-sequencing and CUT&RUN (cleavage under targets & release using nuclease) to identify MYC-regulated genes that are induced only by TAF2 overexpression. RASGEF1A (RasGEF domain family member 1A), a guanine exchange factor activating Ras, was significantly induced by TAF2 and MYC overexpression. Consequently, the MEK/ERK pathway was robustly activated in cells co-overexpressing TAF2 and MYC, rendering them uniquely sensitive to MEK inhibitor Trametinib. These findings suggest that HCC patients with TAF2 and MYC overexpression might benefit from targeted treatment with MEK inhibitors.
PMID:
42759661
Bibliographic data and abstract were imported from PubMed on 19 Sep 2026.
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