LncRNA HCP5 promotes malignant cell behaviors in esophageal squamous cell carcinoma via the PI3K/AKT/mTOR signaling
| Autor: | Jianli Ma, Jian Li, Jianyu Xu, Bixi Guan, Songliu Hu, Yan Wang |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Esophageal Neoplasms Biology Phosphatidylinositol 3-Kinases 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Cell Movement Cell Line Tumor Humans MTT assay Viability assay neoplasms Molecular Biology Protein kinase B PI3K/AKT/mTOR pathway Cell Proliferation Competing endogenous RNA Cell growth TOR Serine-Threonine Kinases Cell Biology digestive system diseases MicroRNAs 030104 developmental biology Apoptosis 030220 oncology & carcinogenesis Cancer research RNA Long Noncoding Esophageal Squamous Cell Carcinoma Proto-Oncogene Proteins c-akt Signal Transduction Research Paper Developmental Biology |
| Zdroj: | Cell Cycle |
| ISSN: | 1551-4005 1538-4101 |
| DOI: | 10.1080/15384101.2021.1944512 |
| Popis: | The role of lncRNA HCP5 in esophageal squamous cell carcinoma (ESCC) remains unknown despite its involvement in different malignancies. MTT assay, EdU assay, TUNEL assay, transwell assay, and sphere formation assay were conducted to reveal ESCC cell viability, proliferation, apoptosis, migration, invasion, and stemness characteristics. FISH and subcellular fraction assays were performed to reveal the subcellular location of HCP5 in ESCC cells. Luciferase reporter assay and RIP assay were conducted to explore the downstream axis of HCP5. Our findings revealed that HCP5 expression was at a higher level in ESCC tissues and cells compared to that in control tissues and cells. Additionally, HCP5 promoted ESCC cellular activities by promoting proliferation, migration, invasion ability and stemness characteristics of ESCC cells as well as suppressing cell apoptosis. Furthermore, we found that HCP5 bound with miR-139-5p to upregulate PDE4A via the competing endogenous RNA network in ESCC cells. Importantly, HCP5 was discovered to stimulate the PI3K/AKT/mTOR signaling by regulating the downstream target genes. Finally, rescue assays indicated that HCP5 promoted ESCC cell growth by activating the PDE4A-medaited PI3K/AKT/mTOR pathway. HCP5 promotes ESCC cellular development by modulating the miR-139-5p/PDE4A pathway and stimulating the PI3K/AKT/mTOR signaling pathway, which may be conducive for the improvement of ESCC treatment. |
| Databáze: | OpenAIRE |
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