RESUMEN
Gastric cancer (GC) is one of the malignant tumors with both high morbidity and mortality in China. Immunotherapy is expected to improve its prognosis. Molecular classification of GC based on multiple levels of assessment such as genes and tumor immune microenvironment (TiME), which can precisely screen the population with potential benefit from immunotherapy. It is helpful to make the treatment decision-making, and to further improve the efficacy of immunotherapy.
Asunto(s)
Neoplasias Gástricas , China , Humanos , Inmunoterapia , Pronóstico , Neoplasias Gástricas/genética , Neoplasias Gástricas/terapia , Microambiente TumoralRESUMEN
Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long non-coding RNA DLX6-AS1 acts as an oncogene by targeting miR-613 in ovarian cancer, by Q. You, H.-Y. Shi, C.-F. Gong, X.-Y. Tian, S. Li, published in Eur Rev Med Pharmacol Sci 2019;23 (15): 6429-6435-DOI: 10.26355/eurrev_201908_18524-PMID: 31378881" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18524.
RESUMEN
OBJECTIVE: Recently, long non-coding RNAs (lncRNAs) have been extensively studied for their role in tumor progression. This work explored the role of lncRNA DLX6-AS1 in mediating the development of ovarian cancer (OC). PATIENTS AND METHODS: DLX6-AS1 expression was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) in OC tissues. Moreover, wound healing assay and transwell assay were performed to detect the effect of DLX6-AS1 on the metastasis of OC. Furthermore, the underlying mechanism of DLX6-AS1 in mediating the progression of OC was explored through the Dual-Luciferase reporter gene assay and RNA immunoprecipitation assay (RIP). RESULTS: DLX6-AS1 expression was higher in OC samples than that in the adjacent ones. Moreover, cell migration and invasion were suppressed after DLX6-AS1 knockdown in vitro. Conversely, cell migration and invasion were promoted by overexpressed DLX6-AS1. Moreover, the expression of microRNA-613 (miR-613) was upregulated via knockdown of DLX6-AS1, but was downregulated after overexpression of DLX6-AS1. Furthermore, the Luciferase reporter gene assay and RIP assay showed that miR-613 was a direct target of MIAT in DLX6-AS1 in OC tissues. CONCLUSIONS: DLX6-AS1 could enhance migration and invasion of OC cells via targeting miR-613, which might serve as a potential therapeutic target in OC.