miR-221 is a prognostic marker and promotes the proliferation and migration of esophageal squamous cell carcinoma by inhibiting autophagy.

Abstract

Purpose: Esophageal squamous cell carcinoma (ESCC) is a globally prevalent malignancy with high mortality rates. Elucidating the underlying pathophysiological mechanisms of ESCC tumorigenesis is critical for advancing its diagnosis and treatment. MicroRNAs (miRNAs) are pivotal regulators of tumor progression, exerting their effects by binding to target mRNAs and modulating mRNA translation as well as downstream signaling pathways. While the functional roles of numerous miRNAs in ESCC remain incompletely understood, existing studies have implicated autophagy deficiency in aging, cancer, and neurodegenerative diseases. Despite these insights, the relationship between miRNAs and autophagy in ESCC has been insufficiently explored. This study investigates the role of miRNA-221 (miR-221) in ESCC and its interaction with autophagy.

Methods: Bioinformatics analysis was employed to determine the biological relevance of miR-221 in ESCC. RT-qPCR was utilized to quantify miR-221 expression in ESCC tissues and cell lines. The effects of miR-221 overexpression or knockdown on cell proliferation and migration were assessed using Cell Counting Kit-8 (CCK8), EdU, and Transwell assays. Western blot analysis was conducted to evaluate autophagy-related changes in ESCC cell lines.

Results: The findings demonstrate that elevated miR-221 expression in tissues from patients with ESCC is a potential independent prognostic marker. Overexpression of miR-221 enhances tumorigenic and metastatic capabilities in ESCC cell lines by suppressing autophagy. Notably, rapamycin-induced autophagy activation partially mitigated the tumor-promoting effects of miR-221 on proliferation and migration.

Conclusion: The interaction between miR-221 and autophagy presents a promising therapeutic target for ESCC management.