Soto-Feliciano Laboratory

Principal Investigator Yadira Soto-Feliciano is the Howard S. (1953) and Linda B. Stern
Career Development Professor.

The Soto-Feliciano Laboratory studies chromatin — the DNA-protein complex that packages our genetic material inside our cells — as well as the epigenetic mechanisms that regulate gene expression during normal and cancer development.

Precise regulation of chromatin states is critical to many vital cellular processes, including differentiation and proliferation. Chromatin dysregulation and epigenetic reprogramming have been directly linked to cancer evolution and metastasis. The Soto-Feliciano group is studying the mechanisms by which genomic access is controlled at the level of chromatin. The overarching goal of this work is to determine how cellular phenotypes are established and maintained, and how these processes are altered in disease.

The group combines genomics and epigenomics tools with more classical biochemical approaches to study how chromatin adaptor proteins coordinate multi-protein complexes to transduce chromatin signals into transcriptional outputs. Using this multi-tiered approach, the researchers have identified combinatorial histone modifications and transcription factors, as well as delineated their biological relationships with the chromatin adaptor Menin and how they contribute to its genomic localization and chromatin-based functions. The Soto-Feliciano laboratory is also studying how recurrent MEN1 mutations affect Menin’s ability to target and shape the chromatin landscape, as well as affect gene expression program during tumorigenesis. The laboratory is working to identify the cellular and organismal phenotypes elicited by endogenous expression of MEN1 mutant alleles in novel mouse models of neuroendocrine tumors (NETs). These studies will provide new knowledge on how Menin regulates chromatin biology and transcription and a greater understanding of the mechanisms by which disease-associated mutant Menin proteins promote cancer progression and metastasis. Such knowledge could yield novel insights into the roles of chromatin and epigenetic regulators in normal physiology and cancer.

We now appreciate that mutations affecting the epigenome and/or regulation of the chromatin structure are associated with many human disorders, and some have been causally implicated in their pathology. However, our understanding of these chromatin/epigenetic-associated mechanisms remains in its infancy. Studies from our group will provide mechanistic insights into chromatin and epigenetic regulatory processes, and have the potential to inform the development of novel therapeutic strategies that can impact a plethora of human cancers.

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