# The Involvement of Epithelial-Mesenchymal Transition in Squamous Cell Carcinoma in vivo

> **NIH NIH F31** · ROCKEFELLER UNIVERSITY · 2020 · $45,520

## Abstract

Project Summary
I have been developing my thesis project on the heterogeneity of cancer progression. To date, most studies use
cancer models that result in tumors stemming from a homogenous origin and then analyze the phenotype or
downstream molecular consequences. However, cancer is a heterogeneous disease and even within a single
tumor, the cancer cells vary in their proliferative potential due to heterogeneity in the tumor microenvironment as
well as genome instability. I plan to exploit these variabilities to gain new insights into cancer.
The skin as the body's largest and most external organ is highly susceptible to mutagenic, toxic, and pathogenic
insults. A deleterious result of this cellular damage is the development of squamous cell carcinoma, which arises
from the squamous epithelial cells of the epidermis. The vast majority of squamous cell carcinomas can be cured
if detected early; however, upon poor prognosis squamous cell carcinoma metastasizes becoming ever more
lethal. Epithelial mesenchymal transition (EMT), a process by which epithelial cells develop a mesenchymal
phenotype through the loss of polarity and adhesion in exchange gaining mobility and stemness. The
physiological significance of EMT is not only to the important developmental events such as gastrulation and
neural crest formation, but also to physiologic responses such wound healing and pathologic processes such as
organ fibrosis and cancer. It has been implicated in converting stationary epithelial tumor cells into motile
malignant mesenchymal cells leading to invasion and metastasis.
A subset of tumor-initiating SCC cells receive a TGFβ signal. These cells become invasive and undergo an EMT.
I hypothesize that at this stage these TGFβ-responding EMT-transitioning cells have a unique “molecular
signature” that is distinct from earlier stages in tumorigenesis, and holds clues to their invasive, potentially
metastatic properties. Identifying these transcriptional changes could lead to novel drug targets that reduce the
severity of SCCs by inhibiting cancer cell invasion. In this proposal, I outline a plan to: (1) Define the
transcriptional changes downstream of TGFβ signaling as benign tumor-initiating cells progress to SCC cancer
stem cells. (2) Develop an EMT-specific reporter that will allow me to monitor invasive SCC tumor cells as they
undergo an EMT and define the transcriptional signature that distinguishes this process. (3) Devise and exploit
CRISR/CAS-mediated technology to selectively target the ablation of EMT candidate genes in tumor-initiating
cells and determine whether I can block SCC progression and/or metastasis as a consequence. If successful,
my research will elucidate the components of EMT that are required for invasiveness and reveal potential
therapeutic targets for the treatment or prevention of this malignant state of cancer.

## Key facts

- **NIH application ID:** 9840455
- **Project number:** 5F31CA210485-03
- **Recipient organization:** ROCKEFELLER UNIVERSITY
- **Principal Investigator:** Shaopeng Yuan
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $45,520
- **Award type:** 5
- **Project period:** 2018-02-01 → 2021-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9840455

## Citation

> US National Institutes of Health, RePORTER application 9840455, The Involvement of Epithelial-Mesenchymal Transition in Squamous Cell Carcinoma in vivo (5F31CA210485-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9840455. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*