# Mechanisms of RNA turnover during the epithelial-mesenchymal transition

> **NIH NIH R35** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2023 · $403,750

## Abstract

Project Summary/Abstract
 Cells alter their gene expression landscape to change their cellular state. The ability of cells to quickly
transit between cell states is essential for many processes in biology—from development to wound healing and
regeneration, processes which often go awry in pathological conditions like cancer or fibrosis. Thus, there is a
biomedical need to understand the basic mechanisms driving these rapid cellular transitions. The epithelial-
mesenchymal transition (EMT) is one such cellular transition that has reiterative roles in human health and
disease. While much is known about the transcriptional programs that promote EMT, there are additional levels
of gene expression control that impact cell state transitions and by extension EMT. The role of post-
transcriptional regulation, and how it drives and contributes to a spectrum of EMT states, is not well
understood. Here, we examine the role of post-transcriptional regulation, with emphasis on transcript turnover,
during EMT. Neural crest cells undergo a tightly regulated EMT and offer a tractable model system in which to
investigate the basic mechanisms of RNA turnover during EMT.
 We hypothesize that, in addition to pro-EMT transcriptional activation, transcripts that inhibit EMT (anti-
EMT) or serve to maintain a previous cellular state must be degraded to drive EMT and cell state transitions.
Using neural crest EMT as a model system, we seek to test this hypothesis by answering the following
questions: 1) How are anti-EMT and residual transcripts targeted for turnover; and 2) What are the targets of
RNA turnover during EMT and how does specific RNA turnover contribute to hybrid EMT states? To answer
these questions, we will: 1) Apply a combination of unbiased multi-omic and candidate gene approaches to
identify the RNA-binding proteins that promote RNA turnover during EMT; and 2) Apply RNA-sequencing
approaches to broadly identify the targets of RNA turnover, the mechanism of how they are turned over, and
how this contributes to hybrid EMT states.
 This Proposal seeks to understand the mechanisms of RNA turnover during EMT. The results of these
studies will greatly advance current understanding of the basic cellular mechanisms driving EMT, providing
novel targets for modulating EMT in human health and disease.

## Key facts

- **NIH application ID:** 10714965
- **Project number:** 1R35GM150763-01
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Erica Hutchins
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $403,750
- **Award type:** 1
- **Project period:** 2023-08-01 → 2028-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10714965

## Citation

> US National Institutes of Health, RePORTER application 10714965, Mechanisms of RNA turnover during the epithelial-mesenchymal transition (1R35GM150763-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10714965. Licensed CC0.

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