MicroRNA-23a-3p influences the molecular mechanism of gastric cancer cells via CCL22/PI3K/Akt axis
| Autor: | Zhipeng Jiang, Min Su, Hua Chen, Limian Wu, Xinpei Yu, Zichuan Liu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
Cell Survival Down-Regulation Mice Nude Bioengineering Applied Microbiology and Biotechnology Phosphatidylinositol 3-Kinases Stomach Neoplasms Cell Line Tumor Animals Humans Neoplasm Metastasis Chemokine CCL22 PI3K/AKT Mice Inbred BALB C Base Sequence gastric cancer General Medicine Middle Aged Prognosis Gene Expression Regulation Neoplastic MicroRNAs miR-23a-3p Disease Progression Female molecular mechanism Proto-Oncogene Proteins c-akt TP248.13-248.65 Biotechnology Research Article Research Paper Signal Transduction |
| Zdroj: | Bioengineered article-version (VoR) Version of Record Bioengineered, Vol 12, Iss 2, Pp 11277-11287 (2021) |
| ISSN: | 2165-5987 2165-5979 |
| Popis: | A great many microRNAs (miRNAs) have been reported to play different roles in human cancers, including gastric cancer (GC). However, the specific character of miR-23a-3p in GC has not been elucidated. This study was to explore the function of miR-23a-3p in GC. The results manifested that miR-23a-3p was down-regulated in GC and patients with reduced miR-23a-3p had poor prognosis. Functional experiments assured that elevated miR-23a-3p refrained GC proliferation, invasion, migration, PIK3/Akt phosphorylation and apoptosis, while knockdown miR-23a-3p accelerated the growth of GC. Double luciferase report experiments manifested that miR-23a-3p targeted CCL22 expression. Functional rescue experiments affirmed that the repression of elevated miR-23a-3p on GC was reversed by simultaneous augmented CCL22. In vivo, elevated miR-23a-3p restrained the volume and tumor of GC and reduced the expression of CCL22 and phosphorylated PIK3/Akt, while knockdown miR-23a-3p motivated tumor growth. In conclusion, the results of this study indicate that miR-23a-3p plays a repressive role in GC, and affects the progression of GC via down-regulating CCL22 and blocking PI3K/AKT signal transduction pathway, which may offer a new molecular target for clinical treatment of GC. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|