RESUMO
The article "The carcinogenic complex lncRNA FOXP4-AS1/EZH2/LSD1 accelerates proliferation, migration and invasion of gastric cancer, by R.-Y. Chen, Q. Ju, L.-M. Feng, Q. Yuan, L. Zhang, published in Eur Rev Med Pharmacol Sci 2019; 23 (19): 8371-8376-DOI: 10.26355/eurrev_201910_19148-PMID: 31646567" has been retracted by the authors. After publication, the authors raised concerns about the reliability of the data used to conduct the study by stating that some data cannot be repeated by further research. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19148.
Assuntos
Neoplasias do Endométrio , Pólipos , Doenças Uterinas , Neoplasias Uterinas , Procedimentos Clínicos , Neoplasias do Endométrio/diagnóstico , Neoplasias do Endométrio/cirurgia , Feminino , Humanos , Histeroscopia , Pólipos/diagnóstico , Pólipos/cirurgia , Gravidez , Estudos Retrospectivos , Doenças Uterinas/diagnósticoRESUMO
OBJECTIVE: To clarify the role of lncRNA FOX4-AS1 in the progression of gastric cancer (GC) via interacting with EZH2/LSD1. PATIENTS AND METHODS: Relative level of FOXP4-AS1 in GC tissues and adjacent normal tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The potential influences of FOXP4-AS1 on cellular behaviors of GC cells were evaluated via a series of functional experiments. Bioinformatics prediction, RNA immunoprecipitation (RIP) assay, and Western blot were conducted to verify the potential of EZH2/LSD1 as a target of FOXP4-AS1. RESULTS: FOXP4-AS1 was upregulated in GC tissues relative to controls. Its level was higher in GC patients with stage III-IV than those with stage I-II. The survival rate was lower in GC patients presenting the high expression of FOXP4-AS1 compared with those presenting low expression. Transfection of sh-FOXP4-AS1 1# or sh-FOXP4-AS1 2# attenuated proliferative, migratory, and invasive abilities of AGS and BGC7901 cells. FOXP4-AS1 could bind to LSD1 and EZH2, and positively regulated their expression levels. Transfection of sh-LSD1 or sh-EZH2 reduced the proliferative ability of GC cells. CONCLUSIONS: FOXP4-AS1 binds to EZH2/LSD1 to form a carcinogenic complex, thus accelerating GC cells to proliferate, migrate and invade.
Assuntos
Proteína Potenciadora do Homólogo 2 de Zeste/metabolismo , Fatores de Transcrição Forkhead/metabolismo , Histona Desmetilases/metabolismo , RNA Longo não Codificante/metabolismo , Neoplasias Gástricas/metabolismo , Movimento Celular , Proliferação de Células , Sobrevivência Celular , Proteína Potenciadora do Homólogo 2 de Zeste/genética , Fatores de Transcrição Forkhead/genética , Histona Desmetilases/genética , Humanos , RNA Longo não Codificante/genética , Neoplasias Gástricas/genética , Neoplasias Gástricas/patologia , Células Tumorais CultivadasRESUMO
OBJECTIVE: To investigate the effect and clinical significance of long non-coding RNA 00673 (lncRNA00673) in the occurrence and development of colorectal cancer (CRC) through the research on the expression level, biological effect and clinical significance of lncRNA00673 in CRC. PATIENTS AND METHODS: The relative expression of lncRNA00673 in 71 pairs of CRC tissues and cells was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The correlation of the relative expression of lncRNA00673 with the clinicopathological features of CRC patients was analyzed. The lncRNA00673 interference sequence was designed and synthesized, and its transfection efficiency was detected by qRT-PCR assays. 3-(4,5-Dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay and clone formation experiments were performed to investigate the effect of lncRNA00673 on the proliferation ability of CRC cells. RESULTS: In CRC tissues of 71 patients, there were 51 patients whose lncRNA00673 level was up-regulated compared with that of cancer-adjacent tissues. The highly expressed lncRNA00673 was positively correlated with tumor, node and metastasis (TNM) staging, regional lymph node metastasis, distant metastasis and tumor size in CRC patients. Cox proportional-hazards regression model showed that the highly expressed lncRNA00673 was an independent risk factor for the overall survival of CRC patients. Kaplan-Meier curve analysis showed that highly expressed lncRNA00673 was significantly associated with the relatively lower overall survival (OS). MTT and clone formation experiments showed that knockdown of lncRNA0673 could inhibit the proliferation of CRC cells. CONCLUSIONS: The expression level of lncRNA00673 is up-regulated in CRC tissues and cells, which is related to the degree of malignancy and poor prognosis. LncRNA00673 can be used as a potential molecular marker for the prognosis of CRC.