C/D-Box Snord105b Promotes Tumorigenesis in Gastric Cancer via ALDOA/C-Myc Pathway

2018 ◽  
Vol 45 (6) ◽  
pp. 2471-2482 ◽  
Author(s):  
Cong Zhang ◽  
Lian-mei Zhao ◽  
Hao Wu ◽  
Guo Tian ◽  
Su-li Dai ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Tumor Development ◽  
Migration And Invasion ◽  
Small Nucleolar Rnas ◽  
Wound Healing Assay ◽  
Qrt Pcr ◽  
New Biomarkers ◽  
Nucleolar Rnas

Background/Aims: Small nucleolar RNAs (snoRNAs) play an important role in carcinogenesis. In this study, we identified a C/D box snoRNA, snord105b, and further investigated the function and mechanism of the snord105b in gastric cancer (GC). Methods: The expression level of snord105b in GC tissures, sera and cell lines were detected by qRT-PCR. Cell viability was assessed using MTS assay. Transwell and wound healing assay were performed to evaluate migration and invasion, and protein expression was examined by western blotting. ChIRP and MS analysis was used to seek for the special binding protein of snord105b. Results: The snord105b was upregulated and associated with tumor size, differentiation, and pathological stage in GC. Snord105b affected proliferation, migration and invasion in multiple GC cell lines. The oncoqenic activity of snord105b was also confirmed with in vivo data. Mechanistically, snord105b specifically bound to ALDOA and affected C-myc, which plays a key role in carcinogenesis and tumor development. Conclusion: Snord105b appears to be a novel oncogene and is clinically and functionally involved in the development of GC. Targeting snord105b and its pathway may provide new biomarkers or potential treatments for patients with GC.

scholarly journals MiR-223 Promotes Tumor Progression via Targeting RhoB in Gastric Cancer

2022 ◽  
Vol 2022 ◽  
pp. 1-10
Author(s):  
You Hu ◽  
Bin Yi ◽  
Xin Chen ◽  
Lu Xu ◽  
Xiaojun Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Progression ◽  
Cancer Progression ◽  
Tumor Development ◽  
Migration And Invasion ◽  
Cellular Mechanisms ◽  
Borrmann Type ◽  
Potential Biomarker

Gastric cancer (GC) is among the most prevalent causes of cancer-related death globally. MiR-223 has been implicated in a variety of cellular mechanisms linked to cancer progression. However, the miR-223 expressions and its function in GC are unknown. We discovered that miR-223 expression was raised in GC tissues in comparison with nearby normal tissues in this investigation. Additionally, multiplied miR-223 expression was strongly linked with TNM stage ( p = 0.022 ), live metastasis ( p = 0.004 ),lymph node metastasis ( p = 0.004 ),and Borrmann type and was associated with an unfavorable prognostic for patients with GC. Furthermore, suppressing miR-223 significantly increased cell death and prevented cell migration and invasion in vitro. Additionally, miR-223 silencing decreased tumor development in vivo. Additionally, we discovered that miR-223 enhanced GC development by specifically targeting RhoB. In summary, our findings reveal that miR-223 increases tumor progression in GC by targeting RhoB, suggesting that it could serve to be a potential biomarker for the prediction of the disease.

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 HOTAIR contributes to the carcinogenesis of gastric cancer via modulating cellular and exosomal miRNAs level

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Jie Zhang ◽  
Wei-qing Qiu ◽  
Hongyi Zhu ◽  
Hua Liu ◽  
Jian-hua Sun ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Noncoding Rna ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Tissue Samples ◽  
Capillary Formation ◽  
Qrt Pcr ◽  
Exosomal Mirnas ◽  
New Biomarkers

Abstract Gastric cancer (GC) is one of the most leading malignancies. Long noncoding RNA is related to GC. In this study, 11 miRNAs in the exosomes and six lncRNAs in the tissues was examined by qRT-PCR. Correlation analysis was used to analyze the relationship between miRNAs in exosome and lncRNAs in the tissues. Four miRNAs level in GC tissues were examined by qRT-PCR. MTT was used to determine cell viability. Flow cytometry was used to quantify the apoptotic cells. Transwell assay was used to examine the migration and invasion capacity. Dual-luciferase assay was used to examine the interaction between HOTAIR and miR-30a or -b. Capillary formation was used to determine the capillary formation capacity. Weak negative correlations were found between HOTAIR and miR-30a or -b in GC tissue samples. Interestingly, strong negative correlations were identified between the HOTAIR level in GC tissue samples and the miR-30a or -b levels in plasma exosomes. HOTAIR knockdown GC cells exhibited decreased migration, invasion, proliferation, and upregulated apoptosis, which released more miR-30a and -b into the exosomes. KRAS was upregulated when co-cultured with exosomes from HOTAIR overexpressed cells, and promoted GC cells proliferation, migration, and invasion. Meanwhile, HUVEC cells expressed increased VEGF-A and formatted more capillaries. Subsequently, we identified a 10mer target site of miR-30a or -b in HOTAIR sequence, and the overexpression of HOTAIR induced the degradation of miR-30a or -b, indicating a ceRNA role of HOTAIR. We report the negative correlation between the plasma miRNAs level and GC tissue HOTAIR expression for the first time and unveiled the ceRNA role of HOTAIR in GC. HOTAIR functions as an onco-lncRNA regulating the level of miR-30a and -b in both GC cells and exosomes. These findings may give insight into understanding the mechanism of GC pathogenesis and provide new biomarkers for clinical diagnosis.

scholarly journals Circular RNA hsa_circ_0001829 promotes gastric cancer progression through miR-155-5p/SMAD2 axis

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Qiuling Niu ◽  
Zhijie Dong ◽  
Min Liang ◽  
Yuanwei Luo ◽  
Hai Lin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Progression ◽  
Cell Cycle Progression ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Gain Of Function

Abstract Background Accumulating evidences have shown that circular RNAs (circRNAs) play important roles in regulating the pathogenesis of cancer. However, the role of circRNAs in gastric cancer (GC) remains largely unclear. Methods In this study, we identified a novel upregulated circRNA, hsa_circ_0001829, in chemically induced malignant transformed human gastric epithelial cells using RNA-seq. Subsequent qRT-PCR and ISH assays were performed to detect the expression level of hsa_circ_0001829 in GC cell lines and tissues. Functional roles of hsa_circ_0001829 in GC were then explored by loss- and gain-of- function assays. Bioinformatic prediction and luciferase assay were used to investigate potential mechanisms of hsa_circ_0001829. Finally, the mice xenograft and metastasis models were constructed to assess the function of hsa_circ_0001829 in vivo. Results We found that hsa_circ_0001829 was significantly upregulated in GC tissues and cell lines. Loss- and gain-of- function assays showed that hsa_circ_0001829 promotes GC cells proliferation, migration and invasion, and the affected cell cycle progression and apoptosis rates may account for the effect of hsa_circ_0001829 on GC proliferation. In addition, bioinformatic prediction and luciferase assay showed that hsa_circ_0001829 acts as a molecular sponge for miR-155-5p and that SMAD2 was a target gene of miR-155-5p; moreover, hsa_circ_0001829 sponges miR-155-5p to regulate SMAD2 expression and hsa_circ_0001829 promotes GC progression through the miR-155-5p–SMAD2 pathway. Finally, suppression of hsa_circ_0001829 expression inhibited tumor growth and aggressiveness in vivo. Conclusion Taken together, our findings firstly demonstrated a novel oncogenic role of hsa_circ_0001829 in GC progression through miR-155-5p–SMAD2 axis, and our study may offer novel biomarkers and therapeutic targets 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 Adenosine interaction with adenosine receptor A2a promotes gastric cancer metastasis by enhancing PI3K–AKT–mTOR signaling

2019 ◽  
Vol 30 (19) ◽  
pp. 2527-2534 ◽  
Author(s):  
Linsen Shi ◽  
Zhaoying Wu ◽  
Ji Miao ◽  
Shangce Du ◽  
Shichao Ai ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Mesenchymal Transition ◽  
Poor Outcomes

The accumulation of adenosine in the tumor microenvironment is associated with tumor progression in many cancers. However, whether adenosine is involved in gastric cancer (GC) metastasis and progression, and the underlying molecular mechanism, is largely unclear. In this study, we find that GC tissues and cell lines had higher A2aR levels than nontumor gastric tissues and cell lines. A2aR expression correlated positively with TNMstage, and associated with poor outcomes. Adenosine enhanced the expression of the stemness and epithelial–mesenchymal transition-associated genes by binding to A2aR. A2aR expression on GC cells promoted metastasis in vivo. The PI3K-AKT-mTOR signaling pathway was involved in adenosine-stimulated GC cell migration and invasion. Our results indicate that adenosine promotes GC cell invasion and metastasis by interacting with A2aR to enhance PI3K–AKT–mTOR pathway signaling.

scholarly journals MicroRNA-491-5p inhibit gastric cancer development by targeting EMT, cell adhesion genes and IFITM2

2020 ◽  
Author(s):  
Zhijian Wei ◽  
Lixiang Zhang ◽  
Angqing Li ◽  
Chuanhong Li ◽  
Wenxiu Han ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Adhesion ◽  
Tumor Suppressor ◽  
Tumor Development ◽  
Migration And Invasion ◽  
Different Types ◽  
High Level

Abstract Gastric cancer (GC) is one of the deadliest cancers in China. And, it can be regulated by MicroRNAs (miRNAs) generally. miR-491-5p function as a tumor suppressor in different types of cancer, but we still don’t know the role of miR-491-5p in gastric cancer. In this study, we found that high level of miR-491-5p caused a weak cell proliferation, migration and invasion abilities. In order to explore the role of miR-491-5p in vivo, we set a xenograft mouse model, and also found that high level of miR-491-5p suppressed tumor growth. Moreover, we found that miR-491-5p regulate the tumor development thought regulate the expression of EMT, cell adhesion genes and IFITM2. These data show that miR-491-5p function as a tumor suppressor in GC both in vitro and in vivo .

scholarly journals Overexpression of long noncoding RNA GAS5 suppresses tumorigenesis and development of gastric cancer by sponging miR-106a-5p through the Akt/mToR pathway

2019 ◽  
Author(s):  
Shuaijun Dong ◽  
Xiefu Zhang ◽  
Dechun Liu
Keyword(s):  
Gastric Cancer ◽  
Noncoding Rna ◽  
Mtor Pathway ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Qrt Pcr ◽  
Non Coding Rnas ◽  
Development Of Gastric Cancer

AbstractLong non-coding RNAs (lncRNAs) have emerged as important regulators of human cancers. LncRNA GAS5 (GAS5) is identified tumor suppressor involved in several cancers. However, the roles of GAS5 and the mechanisms responsible for its functions in gastric cancer (GC) have not been well undocumented. Herein, the decreased GAS5 and increased miRNA-106a-5p levels were observed in GC and cell lines. GAS5 expression level was significantly inversely correlated with miRNA-106a-5p level in GC tissues. Moreover, luciferase reporter and qRT-PCR assays showed that GAS5 bound to miRNA-106a-5p and negatively regulated its expression in GC cells. Functional experiments showed that GAS5 overexpression suppressed GC cell proliferation, migration, and invasion capabilities and promoted apoptosis, while miRNA-106a-5p overexpression inversed the functional effects induced by GAS5 overexpression. In vivo, GAS5 overexpression inhibited tumor growth by negatively regulating miRNA-106a-5p expression. Mechanistic investigations revealed that GAS5 overexpression inactivating the Akt/mToR pathway by suppressing miRNA-106a-5p expression in vitro and in vivo. Taken together, our findings conclude the GAS5 overexpression suppresses tumorigenesis and development of gastric cancer by sponging miR-106a-5p through the Akt/mToR pathway.

scholarly journals The Interaction Between Long Non-Coding RNA LINC01564 and POU2F1 Promotes the Proliferation and Metastasis of Gastric Cancer

2021 ◽  
Author(s):  
Jixu Wang ◽  
Futao Hou ◽  
Lusheng Tang ◽  
Ke Xiao ◽  
Tengfei Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Transcription Factor ◽  
Tumor Development ◽  
Transcription Activation ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Proliferation And Metastasis ◽  
And Migration

Abstract Background: An increasing number of studies have demonstrated that long non-coding RNAs (lncRNAs) serve as key regulators in tumor development and progression. However, only a few lncRNAs have been functionally characterized in gastric cancer (GC). Methods: Bioinformatics analysis was conducted to find lncRNAs that are associated with GC metastasis. RNA FISH, RIP, and RNA pull down assays were used to study the complementary binding of LINC01564 complementary to the 3’UTR of transcription factor POU2F1. The transcription activation of LINC01564 by POU2F1 as a transcription factor was examined by ChIP assay. In vitro assays such as MTT, cell invasion assay, and clonogenic assay were conducted to examined the impacts of LINC01564 and POU2F1 on GC cell proliferation and invasion. Experiments in vivo were performed to access the impacts of LINC01564 and POU2F1 on GC metastasis. Results: The results showed that LINC01564 complementary bound to the 3’UTR of POU2F1 to form an RNA duplex, whereby stabilizing POU2F1 mRNA and increasing the enrichment in cells. The level of LINC01564 was also increased by POU2F1 through transcription activation. In vitro assays showed that LINC01564 promoted the proliferation, invasion and migration of GC cells through increasing POU2F1. In vivo experiments indicate the promotion of GC proliferation and metastasis by the interaction between LINC01564 and POU2F1. Conclusion: Taken together, our results indicate that the interaction between LINC01564 and POU2F1 promotes 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.

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