# Nit1 is upregulated in non-small cell lung cancer and promotes cancer cell proliferation and invasion and regulates EMT-related molecules and cyclins

## TL;DR

Nit1 is overactive in non-small cell lung cancer and helps cancer cells grow and spread by affecting specific proteins.

## Contribution

Nit1's role in promoting cancer progression through EMT and cyclin regulation is newly identified in non-small cell lung cancer.

## Key findings

- Nit1 is overexpressed in non-small cell lung cancer tissues and cell lines.
- Nit1 overexpression increases cancer cell proliferation and invasion.
- Nit1 modulates EMT-related molecules and cyclins like MMP3, Slug, snail, cyclin D1, D3, and E.

## Abstract

Nitrilase homolog 1 (Nit1) is a member of the carbon-nitrogen hydrolase family whose function in human cancer is largely unknown. In this study we investigated the expression and function of Nit1 in non-small cell lung cancer (NSCLC) in vivo and vitro. Immunohistochemistry study shows that expression of Nit1 was elevated in non-small cell lung cancer compared to normal lung epithelial cells including submucosal glands and bronchial epithelial cells (p<0.05). Expression of Nit1 was significantly associated with advanced TNM stages, lymph node metastasis and poor clinical outcome of the patients (60.70 ±5.48 vs 30.83 ± 4.88) (p<0.05). Western blot also shows elevated expression of Nit1 in cancer tissues compared to adjacent normal lung tissues (p<0.05). We detected Nit1 expression using Western blot in lung cancer cell lines including A549, H460, H661, H1299, LK2, PC9, and SK, and bronchial epithelial cell line HBE. Immunofluorescent staining shows that Nit1 was located in cytoplasm in HBE, A549, H1299, H460 and PC9 cells. Overexpression of Nit1 in H1299 cells significantly promoted cancer cell proliferation and invasion in vitro (p<0.05). Western blot study confirmed that overexpression of Nit1 in H1299 cells significantly upregulated EMT-related molecules including MMP3, Slug, snail, and cyclins including cyclin D1, cyclin D3 and cyclin E, and downregulated EMT-related molecule E-cadherin. These results indicate that Nit1 expression was upregulated in non-small cell lung cancer and may contribute to the malignant phenotype through regulating EMT-related molecules and cyclins.