LncRNA PAPAS aggravates the progression of gastric cancer through regulating miRNA-188-5p.

Since this paper presents several inaccuracies and mistakes, the article "LncRNA PAPAS aggravates the progression of gastric cancer through regulating miRNA-188-5p, by X. Shi, X. You, W.-C. Zeng, Y.-J. Deng, H.-L. Hong, O.-X. Huang, M.-F. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (24): 10761-10768-DOI: 10.26355/eurrev_201912_19778-PMID: 31858543" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19778.

LncRNA PAPAS aggravates the progression of gastric cancer through regulating miRNA-188-5p.

OBJECTIVE: To uncover the biological effect of long non-coding RNA (lncRNA) PAPAS on the progression of gastric cancer (GC) by mediating microRNA-188-5p (miRNA-188-5p) level. PATIENTS AND METHODS: The relative level of PAPAS was determined in GC tissues and cell lines by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The Kaplan-Meier method was introduced to assess the prognostic potential of PAPAS in the overall survival of GC patients. Regulatory effects of PAPAS on proliferative, migratory, and invasive abilities of HGC-27 and AGS cells were detected by cell counting kit-8 (CCK-8), transwell, and wound closure assay, respectively. Subsequently, the binding relation between PAPAS and miRNA-188-5p was verified by the Dual-luciferase reporter gene assay. Correlation between expression levels of PAPAS and miRNA-188-5p in GC tissues was explored. Finally, rescue experiments were conducted to uncover the role of PAPAS/miRNA-188-5p axis in the progression of GC. RESULTS: PAPAS was upregulated in GC tissues and cell lines compared to controls. GC patients expressing a high level of PAPAS suffered worse prognosis relative to those with low level. The silence of PAPAS remarkably attenuated proliferative, migratory, and invasive abilities of HGC-27 cells. Overexpression of PAPAS in AGS cells obtained the opposite trends. MiRNA-188-5p was the direct target of PAPAS, which was negatively regulated by PAPAS. MiRNA-188-5p was able to reverse the regulatory effects of PA-PAS on proliferative, migratory, and invasive abilities of GC cells. CONCLUSIONS: LncRNA PAPAS is upregulated in GC and closely related to lymphatic metastasis, distant metastasis, and poor prognosis of GC patients. PAPAS aggravate the malignant progression of GC by negatively regulating the miRNA-188-5p level.

Knockdown of LINC00461 inhibits cell proliferation and induces apoptosis in gastric cancer by targeting LSD1.

OBJECTIVE: To uncover the function of LINC00461 in regulating cellular behaviors of gastric cancer (GC) via targeting LSD1. PATIENTS AND METHODS: LINC00461 level in GC tissues with different tumor node metastasis (TNM) staging and lymphatic metastasis statues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). In vitro influences of LINC00461 on proliferative and apoptotic rates were evaluated in AGS and SGC-7901 cells. The interaction between LINC00461 and LSD1 was explored by RNA immunoprecipitation (RIP) assay and qRT-PCR. Finally, the potential role of LSD1 in the proliferative ability of GC cells mediated by LINC00461 was assessed. RESULTS: LINC00461 level was higher in GC tissues relative to matched control ones. It was positively correlated to TNM staging and lymphatic metastasis of GC. Knockdown of LINC00461 markedly attenuated viability and the proliferative ability of AGS and SGC-7901 cells, but induced apoptosis. RIP assay demonstrated the interaction between LINC00461 and LSD1. Moreover, LSD1 could reverse the regulatory effect of LINC00461 on the proliferative ability of GC cells. CONCLUSIONS: LINC00461 is upregulated in GC, which is positively related to TNM staging and lymphatic metastasis. LINC00461 mediates proliferation and apoptosis of GC cells, thereafter aggravating the progression of GC.