eIF6 affects the occurrence and development of esophageal cancer.

Authors

Cong-Gai Huang, Xin Zhou, Ran Huang, Hui-Ling Zhang, Chen-Xi Li, Fei Du, Hong Lei, Qiong Dai, Zhi-Hui Yang

Published in

Molecular biology reports. Volume 53. Issue 1. Aug 06, 2026. Epub Aug 06, 2026.

Abstract

Esophageal cancer (EC) ranks 11th in incidence and 7th in mortality among malignancies globally. The role of eukaryotic translation initiation factor 6 (eIF6) in esophageal squamous cell carcinoma (ESCA) progression, including its involvement in tumor development, invasion, and epithelial-mesenchymal transition (EMT), remains to be fully characterized.
Bioinformatic and immunohistochemistry (IHC) analyses of 114 ESCA cases demonstrated eIF6 upregulation, which was associated with lower tumor differentiation. Elevated eIF6 expression in ESCA cell lines (KYSE150, TE-1) relative to normal esophageal epithelial cells (HEEC) was verified by reverse transcription-quantitative PCR and western blotting. eIF6 silencing via short hairpin RNA (shRNA) attenuated ESCA cell proliferation, migration, and colony formation in vitro, as assessed by Cell Counting Kit-8, wound healing, and Transwell assays.
Bioinformatic analysis and IHC results showed that eIF6 protein was up-regulated in ESCC, and its expression level was inversely correlated with tumor differentiation degree. eIF6 knockdown was associated with reduced proliferation, migration, and colony formation of ESCC cells, accompanied by shifts in EMT markers, including increased E-cadherin and decreased N-cadherin and Vimentin levels. In addition, eIF6 depletion was accompanied by decreased phosphorylation of AKT (p-AKT^Ser473) and mTOR (p-mTOR), both key components of the PI3K/AKT/mTOR pathway.
These findings indicate an association between eIF6 upregulation and ESCA aggressiveness, along with concomitant changes in the PI3K/AKT/mTOR signaling pathway.

PMID:
42560586
Bibliographic data and abstract were imported from PubMed on 06 Aug 2026.

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