ArticleCancer cell international2021
miR-378d suppresses malignant phenotype of ESCC cells through AKT signaling.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- PDIA6 promotes the cell proliferation of ESCC by enhancing the disulfide bond formation in TRAF4.Cellular & molecular biology letters · 2026Article
- miR-378d suppresses gastric cancer metastasis by targeting METTL4 to inhibit epithelial-mesenchymal transition.Journal of molecular histology · 2025Article
- Article
- Uncovering the role of microRNAs in esophageal cancer: from pathogenesis to clinical applications.Frontiers in pharmacology · 2025Review
- Exploring the Prognosis-Related Genetic Variation in Gastric Cancer Based on mGWAS.International journal of molecular sciences · 2023Article
- LINC00114 stimulates growth and glycolysis of esophageal cancer cells by recruiting EZH2 to enhance H3K27me3 of DLC1.Clinical epigenetics · 2022Article
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Authors and funding
18 authors.
Funding
Abstract
backgroundPost-resistance progress in paclitaxel (PTX) treatment remains a major challenge in tumor treatment. A high dose of PTX was used for cell lines to analyze the changes in molecular expression. The miR-378d was sharply reduced in surviving cells, but the role of miR-378d in Esophageal squamous cell carcinoma (ESCC) remained unclear.
methodsWe analyzed the relationship between miR-378d expression and the clinicopathological features of ESCC. We constructed miR-378d silent expression cell lines to study phenotypes and molecular mechanisms.
resultsThe miR-378d expression was associated with good prognosis in patients with ESCC. miR-378d inhibition promoted chemo-resistance, monoclonal formation, EMT, migration, invasion, stemness, and metastasis of ESCC cells. miR-378d can target downregulated AKT1.
conclusionsTherefore, miR-378d expression is a good prognostic factor of patients with ESCC and regulates the malignant phenotype of tumor cells through AKT.
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