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Background: Gastric cancer (GC) is one of the most frequent malignant digestive tumors and second fatal cancer. This study was to investigate whether lncRNA-H19 can regulate E2F3 expression through competitive binding to microRNA-194 (miR-194), thus regulating GC growth and metastasis.
Methods: H19, miR-194, and E2F3 expression levels in GC tissues and cell lines were investigated using quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR). Meanwhile, the mRNA levels of H19 and E2F3 in gastric cancer tissues were also analyzed through the GEPIA web tool. The binding condition of miR-194 with H19 and E2F3 was investigated using a dual-luciferase reporter gene assay. The regulatory effects of H19 on proliferative, migratory, and invasive abilities of AGS cells and SGC-7901 cells were detected by transwell assay and cell counting kit-8 (CCK-8). Genes involved in proliferation, migration, and invasion (PCNA, Vimentin, and N-cadherin) were determined using QRT-PCR and western blot. The regulatory interaction between H19 and miR-194, miR-194, and E2F3 were investigated using rescue experiments.
Results: The results revealed that H19 was highly expressed in GC tissues and cell lines than those of controls. Downregulated H19 decreased the proliferation, migration, and invasion of AGS cells and SGC-7901 cells. H19 was demonstrated that being the molecular sponge of miR-194 in regulating the growth of the GC cells. The level of E2F3 expression was also found significantly higher in GC tissues and cell lines than those of controls. And then, the mimics of miR-194 inhibited the expression of E2F3 in the GC cells. CCK-8 assay showed decreased proliferative ability induced by miR-194 mimics were reversed by E2F3 overexpression. Transwell assays showed decreased migratory and invasive ability induced by miR-194 mimics were reversed by E2F3 overexpression.
Conclusions: This study demonstrates that H19 promotes GC growth and metastasis by regulating E2F3 via competitive binding to miRNA-194.
Keywords
LncRNA, H19, MicroRNA, CeRNA, MiR-194, E2F3, Gastric cancer
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research article
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 6
Posted 30 Mar, 2020
No community comments so far
No comments provided
No comments provided
No comments provided
No comments provided
No comments provided
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cancer Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Gastric cancer (GC) is one of the most frequent malignant digestive tumors and second fatal cancer. This study was to investigate whether lncRNA-H19 can regulate E2F3 expression through competitive binding to microRNA-194 (miR-194), thus regulating GC growth and metastasis.
Methods: H19, miR-194, and E2F3 expression levels in GC tissues and cell lines were investigated using quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR). Meanwhile, the mRNA levels of H19 and E2F3 in gastric cancer tissues were also analyzed through the GEPIA web tool. The binding condition of miR-194 with H19 and E2F3 was investigated using a dual-luciferase reporter gene assay. The regulatory effects of H19 on proliferative, migratory, and invasive abilities of AGS cells and SGC-7901 cells were detected by transwell assay and cell counting kit-8 (CCK-8). Genes involved in proliferation, migration, and invasion (PCNA, Vimentin, and N-cadherin) were determined using QRT-PCR and western blot. The regulatory interaction between H19 and miR-194, miR-194, and E2F3 were investigated using rescue experiments.
Results: The results revealed that H19 was highly expressed in GC tissues and cell lines than those of controls. Downregulated H19 decreased the proliferation, migration, and invasion of AGS cells and SGC-7901 cells. H19 was demonstrated that being the molecular sponge of miR-194 in regulating the growth of the GC cells. The level of E2F3 expression was also found significantly higher in GC tissues and cell lines than those of controls. And then, the mimics of miR-194 inhibited the expression of E2F3 in the GC cells. CCK-8 assay showed decreased proliferative ability induced by miR-194 mimics were reversed by E2F3 overexpression. Transwell assays showed decreased migratory and invasive ability induced by miR-194 mimics were reversed by E2F3 overexpression.
Conclusions: This study demonstrates that H19 promotes GC growth and metastasis by regulating E2F3 via competitive binding to miRNA-194.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
This is a list of supplementary files associated with this preprint. Click to download.
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