# LncRNA SOX21‐AS1 Promotes the Progression of Pancreatic Cancer by Sponging miR‐9‐3p and Upregulating YOD1

## TL;DR

This study shows that the long noncoding RNA SOX21-AS1 promotes pancreatic cancer progression by interacting with miR-9-3p and increasing YOD1 levels, which activates a cancer-related signaling pathway.

## Contribution

The novel contribution is identifying the SOX21-AS1/miR-9-3p/YOD1 axis as a new mechanism driving pancreatic cancer progression.

## Key findings

- SOX21-AS1 is highly expressed in pancreatic cancer tissues and correlates with poor prognosis.
- Knockdown of SOX21-AS1 reduces cancer cell proliferation, migration, and tumor growth in mice.
- SOX21-AS1 promotes YOD1 upregulation by sponging miR-9-3p, activating the TGF-β/Smad pathway.

## Abstract

Pancreatic cancer (PC) is a highly aggressive malignancy of the digestive system. Recent studies have indicated that the long noncoding RNA SOX21‐AS1 is significantly upregulated in PC tissue samples. This study aims to elucidate the biological role and underlying molecular mechanisms of SOX21‐AS1 in PC progression. Quantitative real‐time PCR (qRT‐PCR) and western blot analyses were employed to assess RNA and protein expression levels, respectively. The subcellular localization of SOX21‐AS1 was determined using subcellular fractionation assays. PC cell viability, migratory capacity, and apoptosis were evaluated through CCK‐8 assays, wound healing assays, and flow cytometry. Dual‐luciferase reporter and RNA pull‐down assays were conducted to confirm the interactions between miR‐9‐3p and either SOX21‐AS1 or YOD1. Additionally, a xenograft mouse model was established to investigate the in vivo effects of SOX21‐AS1. The findings revealed that SOX21‐AS1 is highly expressed in PC tissues and cell lines, with its upregulation correlating with poor patient prognosis. Functional assays demonstrated that knockdown of SOX21‐AS1 suppressed PC cell proliferation and migration, induced apoptosis in vitro, and reduced tumor growth in vivo. Mechanistically, SOX21‐AS1 competitively interacted with miR‐9‐3p to upregulate YOD1, consequently activating the TGF‐β/Smad signaling pathway. Furthermore, overexpression of YOD1 reversed the tumor‐suppressive effects observed after SOX21‐AS1 knockdown. In conclusion, SOX21‐AS1 promotes PC cell malignancy through the miR‐9‐3p/YOD1 axis and subsequent activation of TGF‐β/Smad signaling.