miR-3678-3p Promotes Esophageal Squamous Cell Carcinoma Progression by Regulating Phosphatase and Tensin Homolog
Background/Aims: Esophageal squamous cell carcinoma (ESCC) is a gastrointestinal malignancy characterized by high invasiveness. The current study aimed to evaluate the role of miR-3678-3p in ESCC and its potential mechanisms. Materials and Methods: The study included 109 ESCC patients. The miR-3678-3p expression in ESCC tissues and cells was quantified. The association between miR-3678-3p and ESCC severity and adverse prognosis was evaluated. The target relationship between miR- 3678-3p, phosphatase and tensin homolog (PTEN) was confirmed. The effects of miR 3678-3p and PTEN on ESCC cell function were analyzed. Results: ESCC tissues and cells exhibited elevated expression of miR-3678-3p. Elevated miR-3678-3p expression was significantly associated with malignant clinical features in ESCC, including larger tumor size, advanced tumor-node-metastasis staging, higher lymph node metastasis, and poor tumor differentiation. High miR-3678-3p expression served as a predictor of shorter overall survival. miR-3678-3p targeted and regulated PTEN. miR-3678-3p knockdown significantly suppressed the malignant progression of ESCC cells, whereas silencing of PTEN reversed these effects. miR-3678-3p and PTEN jointly participated in the development of ESCC. Conclusion: miR-3678-3p serves as a promising prognostic marker for predicting the severity and adverse outcomes of ESCC. miR- 3678-3p promotes ESCC progression by targeting PTEN.
Authors
- T T Li
- Jinjun Zhang
- Ci Cheng (ORCID: https://orcid.org/0009-0002-7633-5280)
Institutions
- Tianjin University of Traditional Chinese Medicine (CN)
- Fourth People’s Hospital of Jinan (CN)
- Jinan City People's Hospital (CN)
- Shandong First Medical University (CN)
- Nanjing Polytechnic Institute (CN)
Publication Details
- Journal
- The Turkish Journal of Gastroenterology
- Published
- 2026-04-27
- DOI
- https://doi.org/10.5152/tjg.2026.25836
- Primary Topic
- MicroRNA in disease regulation
- Type
- article
- Field-Weighted Citation Impact
- 0.00