# FEZF1-AS1 drives autophagy-mediated progression of colon cancer and reduces chemosensitivity through inhabiting the PI3K/AKT/mTOR signaling pathway

## TL;DR

This paper shows that FEZF1-AS1, a non-coding RNA, promotes colon cancer growth and resistance to chemotherapy by affecting a key signaling pathway.

## Contribution

The study identifies FEZF1-AS1 as a novel driver of colon cancer progression and chemoresistance via autophagy and the PI3K/AKT/mTOR pathway.

## Key findings

- FEZF1-AS1 is highly expressed in colon cancer and may serve as a diagnostic biomarker.
- FEZF1-AS1 promotes cancer cell proliferation, invasion, and chemoresistance to oxaliplatin.
- FEZF1-AS1 reduces chemosensitivity by inhibiting the PI3K/AKT/mTOR signaling pathway.

## Abstract

The pathogenesis and chemoresistance mechanisms of colon cancer (CC) are still unclear. Here, we find that a long non-coding RNA (lncRNA), FEZ family zinc finger 1-antisense RNA 1 (FEZF1-AS1), is highly expressed in CC, which may be caused by the amplification mutation of FEZF1-AS1 at the gene level through bioinformatic analysis. FEZF1-AS1 has the potential to be a biomarker in the diagnosis of CC. Functionally, FEZF1-AS1 promotes the proliferation, invasion, metastasis, and survival of CC cells and reduces the sensitivity of CC cells to oxaliplatin. Mechanistically, FEZF1-AS1 drives autophagy-mediated development of CC and reduces chemosensitivity to oxaliplatin through inhabiting the PI3K/AKT/mTOR signaling pathway. In summary, our data suggest that FEZF1-AS1 may be a key driver of CC progression and chemotherapy resistance, and targeting FEZF1-AS1 may be a potential strategy for the diagnosis and treatment of CC.