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Tretyakova, N.

Publications and source records attributed to Tretyakova, N..

2 recordsLinked to original sources

Bivalent Inhibitor Development for a Dynamic Epigenetic Tandem Reader Protein Using a Combinatorial Histone Code

Epigenetic readers are a class of proteins that recognize specific chemical modifications on histones to differentially regulate gene expression. Aberrant expression of readers can drive the progression of many diseases and cancers, making this protein class viable therapeutic targets. Understanding the landscape of histone modifications recognized by reader domains, and the structural mechanisms that drive these molecular recognition events, is crucial for guiding the design of pharmaceutically relevant chemical probes. BPTF contains a plant homeodomain (PHD) finger and tandem bromodomain (BRD). Here, we expand upon previous studies that found the BPTF BRD can engage acetyllysine modifications on the N-terminus of histone H3. We uncover H3K4me3K14ac as the specific modifications recognized by the PHD BRD cassette, which is confirmed by crystallography. Using orthogonal methods, our work explores how these modifications can be read cooperatively, including in cis. We report the first experimental evidence proposing a ligand-induced conformational change between the two reader domains of BPTF, supporting previous computational approaches that have predicted a macromolecular rearrangement. We leverage these structural insights to rationally design a peptide-small molecule conjugate MJ-1 that inhibits both domains of BPTF and overcomes ligandability challenges associated with PHD-finger-containing proteins. The results presented here elucidate the molecular basis of the bivalent recognition of multiply modified histone H3 by BPTF and provide structural insight for developing compounds targeting the PHD finger of BPTF for therapeutic applications.

biochemistry↗

TET1 Functions as a Tumor Suppressor in Lung Adenocarcinoma Through Epigenetic Remodeling and Immune Modulation

Ten-Eleven Translocation (TET1-3) dioxygenases oxidize 5-methylcytosine (5mC) in DNA to generate 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC), initiating DNA demethylation. The three proteins share significant sequence homology and catalyze the same chemical reaction utilizing alpha-ketoglutarate cofactor and non-heme iron to oxidize the methyl group of 5mC. Since their discovery in 2009, there have been contradictory reports regarding the roles of TET proteins in cancer. TET genes have been characterized as tumor suppressor genes because their expression levels are reduced in many human cancers including lymphoma, prostate, and pancreas, and TET2 gene mutations are common in hematological cancers. However, TET1 was recently reported to be overexpressed in triple negative breast cancer and to act as a protooncogene in lung cancer. In the present study, we employed genetic approaches to directly address the function of TET1 protein in lung adenocarcinoma. We found that overexpression of TET1 in human lung adenocarcinoma (H441) cells decreased their proliferation and inhibited colony formation, cell migration, and 3D spheroid tumorigenesis. In contrast, TET1 knockout in lung adenocarcinoma accelerated cell growth and promoted colony formation, cell migration, and 3D spheroid tumorigenesis. Transcriptomics and proteomics analyses revealed that TET1 overexpression was associated with overexpression of immune markers, primarily via activation of TNF and NF-kB signaling pathways. TET1 knockout in lung adenocarcinoma cells induces the expression of genes involved in cellular metabolism and cell growth. Our results are consistent with a tumor suppressor role of TET1 gene in lung adenocarcinoma and reveal its role in activating antitumor immunity.

cancer biology↗