# Long Noncoding RNA Lnc-MTPAP-1 Overexpressed by Particulate Matter Suppresses Apoptosis in Non-Small Cell Lung Cancer (NSCLC) Cells

## TL;DR

This study shows that a specific long noncoding RNA, lnc-MTPAP-1, is increased by pollution and helps lung cancer cells avoid dying.

## Contribution

The novel contribution is identifying lnc-MTPAP-1 as a pollution-responsive lncRNA that suppresses apoptosis in lung cancer cells.

## Key findings

- lnc-MTPAP-1 is significantly up-regulated in lung cancer cells exposed to particulate matter.
- Silencing lnc-MTPAP-1 increases apoptosis in multiple lung cancer cell lines.
- Knockdown of lnc-MTPAP-1 alters expression of apoptosis-related genes like TNS4, MyD88, and IL6R.

## Abstract

Lung cancer remains one of the most common and lethal malignancies worldwide, with poor prognosis largely due to late-stage diagnosis and resistance to therapy. Emerging evidence indicates that long non-coding RNAs (lncRNAs) play critical roles in cancer development, metastasis, and treatment resistance. Particulate matter (PM), a major environmental pollutant and recognized Group 1 carcinogen, has been linked to lung cancer through mechanisms that may involve dysregulation of lncRNA expression. This study aimed to identify PM-responsive lncRNAs in lung cancer, and investigate their potential functional roles. Microarray analysis of lung cancer cell lines A549, H358, H292, and HCC827, exposed to PM10, revealed significant up-regulation of lnc-MTPAP-1. TUNEL staining confirmed that silencing of lnc-MTPAP-1 via siRNA resulted in increased apoptosis across all tested lines. Transcriptome analysis using next-generation sequencing showed that knockdown of lnc-MTPAP-1 altered the expression of apoptosis-related genes, with up-regulation of TNS4, MyD88, and IL6R, and down-regulation of CLPTM1L and EI24. These findings suggest that lnc-MTPAP-1 may exert anti-apoptotic effects in lung cancer cells, and be involved in pollution-induced cancer progression. Further research should explore the therapeutic potential of targeting lnc-MTPAP-1, and better understand the molecular impact of PM exposure on lung cancer pathogenesis.