# Expression of NOTCH1 Is Correlated with Expression of Cancer Stem Cell Markers and miR-150 in Oral Epithelial Dysplasia

## TL;DR

This study shows that NOTCH1 expression is linked to cancer stem cell markers and miR-150 in early oral cancer development.

## Contribution

The study reveals a novel correlation between NOTCH1 and stem cell markers in oral epithelial dysplasia, a pre-cancerous condition.

## Key findings

- NOTCH1 mRNA levels were significantly higher in OAD compared to normal mucosa.
- NOTCH1 positively correlated with stem cell markers and miR-150 in OAD.
- NOTCH1 expression patterns varied in OAD and normal mucosa by immunohistochemistry.

## Abstract

NOTCH1 is associated with various tumors, including oral squamous cell carcinoma (OSCC), with a complex role depending on cellular contexts. Our aim was to analyze the expression of NOTCH1, several stem cell markers, and selected microRNAs in preneoplastic lesion of the oral cavity, oral epithelial dysplasia (OAD). Our study included formalin-fixed paraffin-embedded biopsy samples of 36 cases of OAD and 15 cases of normal oral mucosa. Expression of NOTCH1, stem cell markers (AGR2, KLF4, NANOG, OCT4, SOX2), and miR-27a, miR-34a, miR-128, miR-145, miR-150, and miR-335 was analyzed by quantitative PCR (qPCR). Expression of NOTCH1 protein was analyzed by immunohistochemistry. In OAD compared to normal mucosa, we found a significant increase in mRNA levels of NOTCH1, stem cell markers AGR2, NANOG, OCT4, and SOX2, and miR-150 and miR-128. NOTCH1 mRNA positively correlated with all five stem cell markers’ mRNA levels and miR-150. Immunohistochemistry showed variable expression patterns of NOTCH1 in OAD and normal mucosa. Our results support the role of NOTCH1 in early phases of OSCC development, with a potential contributory role in stemness, in association with AGR2, NANOG, OCT4, and SOX2, miR-150 and miR-128. These results support a complex role of NOTCH1 in carcinoma development, i.e., from oncogenic to tumor suppressor roles and stemness maintenance, not only in invasive OSCC but also in its precursor—OED.