scholarly journals miR-301-3p directly regulates Cx43 to mediate the development of gastric cancer

2021 ◽  
Vol 49 (9) ◽  
pp. 030006052110331
Author(s):  
Shasha Liu ◽  
Yang Zhao ◽  
Huan Liu ◽  
Xing Zhao ◽  
Xingbin Shen
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Clinical Prognosis ◽  
Expression Levels ◽  
Reporter Assays ◽  
Cx43 Mrna ◽  
Development Of Gastric Cancer

Objective Identifying novel biomarkers involved in the development of gastric cancer (GC) can provide potential therapeutic strategies and improve clinical prognosis. miR-301-3p and Cx43 are reportedly dysregulated in GC. miR-301-3p and Cx43 interaction, and their functions in GC progression, are still poorly understood. Methods The expression levels of miR-301-3p and Cx43 in GC tissues and cell lines with various differentiation degrees were evaluated by RT-qPCR. The interaction between miR-301-3p and Cx43 was assessed by dual-luciferase reporter assays. CCK8 and Transwell assays were employed to assess the effects of the miR-301-3p- Cx43 axis on GC cell proliferation, migration, and invasion. Results Cx43 was significantly downregulated in GC tissues and cell lines, while miR-301-3p expression was negatively correlated with Cx43 mRNA levels. The expression levels of Cx43 and miR-301-3p were closely associated with the differentiation, TNM stage, vascular invasion, and lymph node metastasis status of GC patients. Cx43 overexpression could suppress the proliferation, migration, and invasion of GC cells. Cx43 mRNA is a direct target of miR-301-3p, and transfection of an miR-301-3p mimic could reverse the inhibitory effects of Cx43. Conclusion The miR-301-3p- Cx43 axis is involved in the development and progression of GC by affecting the proliferation, migration, and invasion of GC cells.

scholarly journals H19/miR-194/E2F3 regulating loop promotes gastric cancer growth and metastasis

2020 ◽  
Author(s):  
Wanxiang Qin ◽  
Ying Shi ◽  
Dan Zhu ◽  
Yaohua Chen ◽  
Yuping Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Competitive Binding ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Ags Cells ◽  
Qrt Pcr ◽  
Gene Assay

Abstract 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.

scholarly journals MiR-541-3p suppresses gastric cancer via negative regulation of HSF1

2021 ◽  
Vol 20 (11) ◽  
pp. 2293-2298
Author(s):  
Zihan Zheng ◽  
Peng Zhou ◽  
Yangyang Xiao ◽  
Qian Liu ◽  
Tao Wan
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Caspase 3 ◽  
Target Prediction ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Microrna Target ◽  
Gastric Cancer Cells

Purpose: To explore the effects of miR-541-3P on the expression of heat shock transcription factor 1 (HSF1) in gastric cancer cells (GC).Methods: The MicroRNA Target Prediction Database was used to predict whether miR-541-3p interacts with HSF1. Interaction was assessed by dual-luciferase reporter assays. Furthermore, miR-541-3p mRNA levels in GC cell lines were determined by qRT-PCR. Human GC cell lines MKN45 and NCI-N87 were transfected with miR-541-3p mimic. Cell apoptosis, proliferation, invasion, and migration were evaluated using flow cytometry, apoptosis assays, Edu assays, CCK-8 assays, and transwell assays, respectively. Caspase-3, Bcl-2, and cleaved caspase-3 expression levels were determined by western blot.Results: Expression of miR-541-3p was significantly down-regulated in GC cells. Functionally, miR-541-3p mimic inhibited GC cell proliferation, migration, and invasion and induced apoptosis in vitro (p <0.01). Mechanistically, miR-541-3p interacted with HSF1 and inhibited its expression. Overexpression of HSF1 counteracted the effects of miR-541-3p mimic in GC cells.Conclusion: These results indicate that miR-541-3p suppresses the development of GC by targeting HSF1 and thus, is a possible strategy for for the management of GC.

scholarly journals H19/miR-194/E2F3 regulating loop promotes gastric cancer growth and metastasis

2020 ◽  
Author(s):  
Wanxiang Qin ◽  
Ying Shi ◽  
Dan Zhu ◽  
Yaohua Chen ◽  
Yuping Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Competitive Binding ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Ags Cells ◽  
Qrt Pcr ◽  
Gene Assay

Abstract 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.

scholarly journals Long Non-Coding RNA RP11-789C1.1 Suppresses Epithelial to Mesenchymal Transition in Gastric Cancer Through the RP11-789C1.1/MiR-5003/E-Cadherin Axis

2018 ◽  
Vol 47 (6) ◽  
pp. 2432-2444 ◽  
Author(s):  
Zehong Chen ◽  
Jialin Wu ◽  
Wensheng Huang ◽  
Jianjun Peng ◽  
Jinning Ye ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Epithelial To Mesenchymal Transition ◽  
Cellular Level ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Reporter Assays ◽  
E Cadherin

Background/Aims: Gastric cancer (GC) is a common malignancy with a global incidence that ranks fourth among all tumor types. Epithelial-to-mesenchymal transition (EMT) is a tumor biological process with a role in GC cell metastasis. Long non-coding RNAs (lncRNAs) and microRNAs possess important regulatory functions at the cellular level and in diverse pathophysiological processes. This study was conducted to investigate whether lncRNA RP11-789C1.1 regulates EMT in GC by mediating the miR-5003/E-cadherin pathway. Methods: RP11-789C1.1 and miR-5003 expression was detected in GC specimens and cell lines by quantitative real-time PCR. Western blotting and immunohistochemistry were performed to detect EMT markers in GC. Cell Counting Kit 8 assays were carried out to explore cell proliferation. Wound healing and Transwell assays were conducted to determine the migration and invasion of GC cells. To clarify the correlation between RP11-789C1.1, miR-5003, and E-cadherin, dual-luciferase reporter assays were applied. Results: LncRNA RP11-789C1.1 was significantly down-regulated in GC patients and cell lines, along with the concomitant up-regulation of miR-5003. Silencing RP11-789C1.1 and over-expressing miR-5003 significantly promoted the tumor behavior of GC cells. Dual-luciferase reporter assays confirmed that miR-5003 was the target of both RP11-789C1.1 and E-cadherin. Furthermore, at both the mRNA and protein level, silencing RP11-789C1.1 remarkably reduced the expression of E-cadherin and promoted EMT, which were reversed by knocking down miR-5003. Conclusions: LncRNA RP11-789C1.1 inhibited EMT in GC through the RP11-789C1.1/miR-5003/E-cadherin axis, which could be a promising therapeutic target for GC.

scholarly journals H19/miR-194/E2F3 regulating loop promotes gastric cancer growth and metastasis

2020 ◽  
Author(s):  
Wanxiang Qin ◽  
Ying Shi ◽  
Dan Zhu ◽  
Yaohua Chen ◽  
Yuping Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Competitive Binding ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Ags Cells ◽  
Qrt Pcr ◽  
Gene Assay

Abstract 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.

scholarly journals H19/miR-194/E2F3 regulating loop promotes gastric cancer growth and metastasis

2020 ◽  
Author(s):  
Wanxiang Qin ◽  
Ying Shi ◽  
Dan Zhu ◽  
Yaohua Chen ◽  
Yuping Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Competitive Binding ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Ags Cells ◽  
Qrt Pcr ◽  
Gene Assay

Abstract 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.

scholarly journals H19/miR-194/E2F3 regulating loop promotes gastric cancer growth and metastasis

2019 ◽  
Author(s):  
Wanxiang Qin ◽  
Ying Shi ◽  
Dan Zhu ◽  
Yaohua Chen ◽  
Yuping Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Competitive Binding ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Ags Cells ◽  
Qrt Pcr ◽  
Gene Assay

Abstract 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. 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.

scholarly journals H19/miR-194/E2F3 regulating loop promotes gastric cancer growth and metastasis

2019 ◽  
Author(s):  
Wanxiang Qin ◽  
Ying Shi ◽  
Dan Zhu ◽  
Yaohua Chen ◽  
Yuping Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Competitive Binding ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Ags Cells ◽  
Binding Condition ◽  
Gene Assay

Abstract 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 though the GEPIA web tool. The binding condition of miR-194 with H19 and E2F3 were 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). 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.

scholarly journals TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
You Shuai ◽  
Zhonghua Ma ◽  
Weitao Liu ◽  
Tao Yu ◽  
Changsheng Yan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Mechanistic Model ◽  
Ectopic Expression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Tissue Samples ◽  
Reporter Assays

Abstract Background Gastric cancer (GC) is the third leading cause of cancer-related mortality globally. Long noncoding RNAs (lncRNAs) are dysregulated in obvious malignancies including GC and exploring the regulatory mechanisms underlying their expression is an attractive research area. However, these molecular mechanisms require further clarification, especially upstream mechanisms. Methods LncRNA MNX1-AS1 expression in GC tissue samples was investigated via microarray analysis and further determined in a cohort of GC tissues via quantitative reverse transcription polymerase chain reaction (qRT-PCR) assays. Cell proliferation and flow cytometry assays were performed to confirm the roles of MNX1-AS1 in GC proliferation, cell cycle regulation, and apoptosis. The influence of MNX1-AS1 on GC cell migration and invasion was explored with Transwell assays. A xenograft tumour model was established to verify the effects of MNX1-AS1 on in vivo tumourigenesis. The TEAD4-involved upstream regulatory mechanism of MNX1-AS1 was explored through ChIP and luciferase reporter assays. The mechanistic model of MNX1-AS1 in regulating gene expression was further detected by subcellular fractionation, FISH, RIP, ChIP and luciferase reporter assays. Results It was found that MNX1-AS1 displayed obvious upregulation in GC tissue samples and cell lines, and ectopic expression of MNX1-AS1 predicted poor clinical outcomes for patients with GC. Overexpressed MNX1-AS1 expression promoted proliferation, migration and invasion of GC cells markedly, whereas decreased MNX1-AS1 expression elicited the opposite effects. Consistent with the in vitro results, MNX1-AS1 depletion effectively inhibited the growth of xenograft tumour in vivo. Mechanistically, TEAD4 directly bound the promoter region of MNX1-AS1 and stimulated the transcription of MNX1-AS1. Furthermore, MNX1-AS1 can sponge miR-6785-5p to upregulate the expression of BCL2 in GC cells. Meanwhile, MNX1-AS1 suppressed the transcription of BTG2 by recruiting polycomb repressive complex 2 to BTG2 promoter regions. Conclusions Our findings demonstrate that MNX1-AS1 may be able to serve as a prognostic indicator in GC patients and that TEAD4-activatd MNX1-AS1 can promote GC progression through EZH2/BTG2 and miR-6785-5p/BCL2 axes, implicating it as a novel and potent target for the treatment of GC.

scholarly journals MicroRNA-219-5p Represses the Proliferation, Migration, and Invasion of Gastric Cancer Cells by Targeting the LRH-1/Wnt/β-Catenin Signaling Pathway

2017 ◽  
Vol 25 (4) ◽  
pp. 617-627 ◽  
Author(s):  
Chunsheng Li ◽  
Jingrong Dong ◽  
Zhenqi Han ◽  
Kai Zhang
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Human Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cancer Tissues

MicroRNAs (miRNAs) are reportedly involved in gastric cancer development and progression. In particular, miR-219-5p has been reported to be a tumor-associated miRNA in human cancer. However, the role of miR-219-5p in gastric cancer remains unclear. In this study, we investigated for the first time the potential role and underlying mechanism of miR-219-5p in the proliferation, migration, and invasion of human gastric cancer cells. miR-219-5p was found to be markedly decreased in gastric cancer tissues and cell lines compared with adjacent tissues and normal gastric epithelial cells. miR-219-5p mimics or anti-miR-219-5p was transfected into gastric cancer cell lines to overexpress or suppress miR-219-5p expression, respectively. Results showed that miR-219-5p overexpression significantly decreased the proliferation, migration, and invasion of gastric cancer cells. Conversely, miR-219-5p suppression demonstrated a completely opposite effect. Bioinformatics and luciferase reporter assays indicated that miR-219-5p targeted the 3′-untranslated region of the liver receptor homolog-1 (LRH-1), a well-characterized oncogene. Furthermore, miR-219-5p inhibited the mRNA and protein levels of LRH-1. LRH-1 mRNA expression was inversely correlated with miR-219-5p expression in gastric cancer tissues. miR-219-5p overexpression significantly decreased the Wnt/β-catenin signaling pathway in gastric cancer cells. Additionally, LRH-1 restoration can markedly reverse miR-219-5p-mediated tumor suppressive effects. Our study suggests that miR-219-5p regulated the proliferation, migration, and invasion of human gastric cancer cells by suppressing LRH-1. miR-219-5p may be a potential target for gastric cancer therapy.

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