# A novel lncRNA RP11-544M22.13 enhances glycolysis-induced cisplatin resistance in non-small cell lung cancer

## TL;DR

This study identifies a new lncRNA that promotes cisplatin resistance in lung cancer by enhancing glycolysis, offering a potential new treatment target.

## Contribution

The study reveals a novel lncRNA mechanism involving miR-1291 and SLC2A1 in cisplatin resistance in non-small cell lung cancer.

## Key findings

- RP11-544M22.13 is elevated in cisplatin-resistant NSCLC tissues and cells.
- The lncRNA promotes resistance by acting as a miR-1291 sponge and upregulating SLC2A1.
- This mechanism supports malignant behavior and chemoresistance in NSCLC.

## Abstract

LncRNAs and glycolysis play integral roles in the advancement and development of different types of cancer, such as non-small cell lung cancer (NSCLC). This particular study aims to delve into the specific function and potential mechanism of RP11-544M22.13, a newly identified lncRNA, in NSCLC. We utilized qRT-PCR to measure RP11-544M22.13, miR-1291, and SLC2A1 expression levels. The MTT assay assessed NSCLC cell chemoresistance. RP11-544M22.13 was highly elevated in diamminedichloroplatinum (DDP)-resistant NSCLC tissues and cells, promoting both DDP resistance and malignant behavior. Its mechanism involved targeting SLC2A1, suppressing miR-1291, and subsequently upregulating SLC2A1 expression via direct interaction with SLC2A1 mRNA. RP11-544M22.13 acts as a miR-1291 sponge, boosting SLC2A1 expression and promoting DDP resistance and malignancy in NSCLC cells. This presents a potential treatment target for NSCLC and aids in developing small-molecule drugs for combined chemotherapy in late-stage, chemoresistant NSCLC patients.