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Updated: Feb 11, 2026

Establishment and Histological Analysis of Esophageal Organoids Modeling the Progression from Normal to Cancerous Tissues
Published on: May 30, 2025
LncRNA GHET1 Overexpression Facilitates Cancer Progression and Is an Unfavorable Prognosis Factor in Esophageal
1Department of Thoracic Surgery, Shaanxi Provincial People's Hospital, Xi'An 710068, China.
Aim:
This research sought to estimate the prognostic performance and cellular behaviors of lncRNA GHET1 (gastric carcinoma highly expressed transcript 1) in sufferers of esophageal cancer.
Method:
GHET1 expression was measured in esophageal cancer through quantitative real-time polymerase chain reaction (qRT-PCR) method. The prognostic performance of GHET1 level was estimated by Kaplan-Meier and Cox regression analyses. The cellular activities of GHET1 on esophageal cancer cells were estimated by transfecting siRNA.
Results:
The relative abundance of GHET1 was notably elevated in esophageal cancer tissues and cells in respective order (P < 0.001). Abnormal GHET1 expression was notably in relation to differentiation (P = 0.049), LNM (lymph node metastasis, P = 0.002) and TNM (tumor node metastasis, P = 0.015). Moreover, relative to low GHET1 expression group, a poorer overall survival and relapse-free survival time existed in patients expressing high GHET1 expression (log-rank, P < 0.001). Multivariable analysis illustrated that GHET1 levels could be an independent index for the prognosis of patients diagnosed with esophageal cancer (P < 0.001, HR = 3.659, 95%CI: 2.208-6.061). Furthermore, GHET1 was found to bind directly with miR-105-3p, displaying an inverse correlation (r = -0.3790,P < 0.001). Experimental biological studies revealed silencing GHET1 could impede cell growth through the modulation of miR-105-3p (P < 0.001), which was rescued via transfecting miR-105-3p inhibitor in esophageal cancer.
Conclusion:
GHET1 emerges as a promising prognostic biomarker and tumor promoter in esophageal cancer, functioning through the modulation of miR-105-3p.
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