scholarly journals MicroRNA-200b reduced ZEB1 to inhibit cell proliferation and migration in human gastric cancer

2020 ◽  
Author(s):  
He Chen ◽  
Pengcheng Liu ◽  
Lei Wang ◽  
Yanxia Yu ◽  
Yan Zhao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cyclin D1 ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

Abstract BACKGROUND : Gastric cancer (GC) is one of the most common malignant cancers, with high morbidity and mortality rates worldwide. The present study was to explore whether miR-200b is a tumor suppressor in GC and to unveil the potential mechanisms. METHODS: Levels of c-Myc, Cyclin D1, MMP-3 and MMP-9 expression were detected respectively by qRT-PCR and Western blot assay. BrdU proliferation assay, Cell cycle analysis, Wound-healing and Transwell assays were used to study the role of miR-200b with inhibitor, mimics or ZEB1-RNAi in TGF-β1-treated SGC-7901/DDP cells. The xenograft model with nude mice was established to unveil the role of miR-200b in vivo . RESULTS : Compared with the paracancerous tissues, miR-200b was decreased in GC patients and SGC-7901/DDP cells. Lower level of miR-200b induced by its inhibitor promoted TGF-β1-treated SGC-7901/DDP cells proliferation and migration, and increased the levels of c-Myc, Cyclin D1, MMP-3, MMP-9, β-catenin and APC. Interestingly, miR-200b mimics and ZEB1-RNAi were able to reduce the proliferation and migration of TGF-β1-induced SGC-7901/DDP cells as well as their levels of c-Myc, Cyclin D1, MMP-3 MMP-9, β-catenin and APC. In addition, ZEB1 was indeed the potential target of miR-200b identified by dual luciferase reporter gene assay. Xenograft model also suggested that over-expression of miR-200b suppressed the growth of tumor in vivo. CONCLUSION : Taken together, our findings suggest that miR-200b be likely to play an important role in activating TGF-β1-induced SGC-7901/DDP cells and perform as a tumor suppressor by targeting ZEB1 in GC. What’s more, miR-200b may modulate Wnt/β-catenin signaling pathway in TGF-β1-induced SGC-7901/DDP cells.

scholarly journals MicroRNA-200b reduced ZEB1 to inhibit cell proliferation and migration in human gastric cancer

2020 ◽  
Author(s):  
He Chen ◽  
Pengcheng Liu ◽  
Lei Wang ◽  
Yanxia Yu ◽  
Yan Zhao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cyclin D1 ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

Abstract BACKGROUND: Gastric cancer (GC) is one of the most common malignant cancers, with high morbidity and mortality rates worldwide. The present study was to explore whether miR-200b is a tumor suppressor in GC and to unveil the potential mechanisms. METHODS: Levels of c-Myc, Cyclin D1, MMP-3 and MMP-9 expression were detected respectively by qRT-PCR and Western blot assay. BrdU proliferation assay, Cell cycle analysis, Wound-healing and Transwell assays were used to study the role of miR-200b with inhibitor, mimics or ZEB1-RNAi in TGF-β1-treated SGC-7901/DDP cells. The xenograft model with nude mice was established to unveil the role of miR-200b in vivo.RESULTS: Compared with the paracancerous tissues, miR-200b was decreased in GC patients and SGC-7901/DDP cells. Lower level of miR-200b induced by its inhibitor promoted TGF-β1-treated SGC-7901/DDP cells proliferation and migration, and increased the levels of c-Myc, Cyclin D1, MMP-3, MMP-9, β-catenin and APC. Interestingly, miR-200b mimics and ZEB1-RNAi were able to reduce the proliferation and migration of TGF-β1-induced SGC-7901/DDP cells as well as their levels of c-Myc, Cyclin D1, MMP-3 MMP-9, β-catenin and APC. In addition, ZEB1 was indeed the potential target of miR-200b identified by dual luciferase reporter gene assay. Xenograft model also suggested that over-expression of miR-200b suppressed the growth of tumor in vivo. CONCLUSION: Taken together, our findings suggest that miR-200b be likely to play an important role in activating TGF-β1-induced SGC-7901/DDP cells and perform as a tumor suppressor by targeting ZEB1 in GC. What’s more, miR-200b may modulate Wnt/β-catenin signaling pathway in TGF-β1-induced SGC-7901/DDP cells.

scholarly journals MicroRNA-200b reduced ZEB1 to inhibit cell proliferation and migration in human gastric cancer

2020 ◽  
Author(s):  
He Chen ◽  
Pengcheng Liu ◽  
Lei Wang ◽  
Yanxia Yu ◽  
Yan Zhao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cyclin D1 ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

Abstract BACKGROUND: Gastric cancer (GC) is one of the most common malignant cancers, with high morbidity and mortality rates worldwide. The present study was to explore whether miR-200b is a tumor suppressor in GC and to unveil the potential mechanisms. METHODS: Levels of c-Myc, Cyclin D1, MMP-3 and MMP-9 expression were detected respectively by qRT-PCR and Western blot assay. BrdU proliferation assay, Cell cycle analysis, Wound-healing and Transwell assays were used to study the role of miR-200b with inhibitor, mimics or ZEB1-RNAi in TGF-β1-treated SGC-7901/DDP cells. The xenograft model with nude mice was established to unveil the role of miR-200b in vivo.RESULTS: Compared with the paracancerous tissues, miR-200b was decreased in GC patients and SGC-7901/DDP cells. Lower level of miR-200b induced by its inhibitor promoted TGF-β1-treated SGC-7901/DDP cells proliferation and migration, and increased the levels of c-Myc, Cyclin D1, MMP-3, MMP-9, β-catenin and APC. Interestingly, miR-200b mimics and ZEB1-RNAi were able to reduce the proliferation and migration of TGF-β1-induced SGC-7901/DDP cells as well as their levels of c-Myc, Cyclin D1, MMP-3 MMP-9, β-catenin and APC. In addition, ZEB1 was indeed the potential target of miR-200b identified by dual luciferase reporter gene assay. Xenograft model also suggested that over-expression of miR-200b suppressed the growth of tumor in vivo. CONCLUSION: Taken together, our findings suggest that miR-200b be likely to play an important role in activating TGF-β1-induced SGC-7901/DDP cells and perform as a tumor suppressor by targeting ZEB1 in GC. What’s more, miR-200b may modulate Wnt/β-catenin signaling pathway in TGF-β1-induced SGC-7901/DDP cells.

scholarly journals MicroRNA-200b reduced ZEB1 to inhibit cell proliferation and migration in human gastric cancer

2019 ◽  
Author(s):  
He Chen ◽  
Pengcheng Liu ◽  
Lei Wang ◽  
Yanxia Yu ◽  
Yan Zhao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cyclin D1 ◽  
Luciferase Reporter ◽  
High Morbidity ◽  
Human Gastric Cancer ◽  
Luciferase Reporter Gene ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

Abstract BACKGROUND Gastric cancer (GC) is one of the most common malignant cancers, with high morbidity and mortality rates worldwide. The present study was to explore whether miR-200b is a tumor suppressor in GC and to unveil the potential mechanisms.METHODS Levels of c-Myc, Cyclin D1, MMP-3 and MMP-9 expression were detected respectively by q-PCR and Western blot assay. BrdU proliferation assay, Cell cycle analysis and Wound-healing were used to study the role of miR-200b with inhibitor, mimics or ZEB1-RNAi in TGF-β1-treated SGC-7901/DDP cells.RESULTS Compared with the paracancerous tissues, miR-200b was decreased in GC patients and SGC-7901/DDP cells. Lower level of miR-200b induced by its inhibitor promoted TGF-β1-treated SGC-7901/DDP cells proliferation and migration, and increased the levels of c-Myc, Cyclin D1, MMP-3, and MMP-9. Interestingly, miR-200b mimics and ZEB1-RNAi were able to reduce the proliferation and migration of TGF-β1-induced SGC-7901/DDP cells as well as their levels of c-Myc, Cyclin D1, MMP-3 and MMP-9. In addition, ZEB1 was indeed the potential target of miR-200b identified by dual luciferase reporter gene assay.CONCLUSION Taken together, our findings suggest that miR-200b be likely to play an important role in activating TGF-β1-induced SGC-7901/DDP cells and perform as a tumor suppressor by targeting ZEB1 in GC.

scholarly journals MicroRNA-200b reduced ZEB1 to inhibit cell proliferation and migration in human gastric cancer

2020 ◽  
Author(s):  
He Chen ◽  
Pengcheng Liu ◽  
Lei Wang ◽  
Yanxia Yu ◽  
Yan Zhao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cyclin D1 ◽  
Luciferase Reporter ◽  
High Morbidity ◽  
Human Gastric Cancer ◽  
Gene Assay ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

Abstract BACKGROUND : Gastric cancer (GC) is one of the most common malignant cancers, with high morbidity and mortality rates worldwide. The present study was to explore whether miR-200b is a tumor suppressor in GC and to unveil the potential mechanisms. METHODS: Levels of c-Myc, Cyclin D1, MMP-3 and MMP-9 expression were detected respectively by qRT-PCR and Western blot assay. BrdU proliferation assay, Cell cycle analysis, Wound-healing and Transwell assays were used to study the role of miR-200b with inhibitor, mimics or ZEB1-RNAi in TGF-β1-treated SGC-7901/DDP cells. RESULTS : Compared with the paracancerous tissues, miR-200b was decreased in GC patients and SGC-7901/DDP cells. Lower level of miR-200b induced by its inhibitor promoted TGF-β1-treated SGC-7901/DDP cells proliferation and migration, and increased the levels of c-Myc, Cyclin D1, MMP-3, MMP-9, β-catenin and APC. Interestingly, miR-200b mimics and ZEB1-RNAi were able to reduce the proliferation and migration of TGF-β1-induced SGC-7901/DDP cells as well as their levels of c-Myc, Cyclin D1, MMP-3 MMP-9, β-catenin and APC. In addition, ZEB1 was indeed the potential target of miR-200b identified by dual luciferase reporter gene assay. CONCLUSION : Taken together, our findings suggest that miR-200b be likely to play an important role in activating TGF-β1-induced SGC-7901/DDP cells and perform as a tumor suppressor by targeting ZEB1 in GC. What’s more, miR-200b may modulate Wnt/β-catenin signaling pathway in TGF-β1-induced SGC-7901/DDP cells.

scholarly journals MicroRNA-200b reduced ZEB1 to inhibit cell proliferation and migration in human gastric cancer

2020 ◽  
Author(s):  
He Chen ◽  
Pengcheng Liu ◽  
Lei Wang ◽  
Yanxia Yu ◽  
Yan Zhao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Cyclin D1 ◽  
Luciferase Reporter ◽  
High Morbidity ◽  
Human Gastric Cancer ◽  
Gene Assay ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

Abstract BACKGROUND : Gastric cancer (GC) is one of the most common malignant cancers, with high morbidity and mortality rates worldwide. The present study was to explore whether miR-200b is a tumor suppressor in GC and to unveil the potential mechanisms. METHODS: Levels of c-Myc, Cyclin D1, MMP-3 and MMP-9 expression were detected respectively by qRT-PCR and Western blot assay. BrdU proliferation assay, Cell cycle analysis, Wound-healing and Transwell assays were used to study the role of miR-200b with inhibitor, mimics or ZEB1-RNAi in TGF-β1-treated SGC-7901/DDP cells. RESULTS : Compared with the paracancerous tissues, miR-200b was decreased in GC patients and SGC-7901/DDP cells. Lower level of miR-200b induced by its inhibitor promoted TGF-β1-treated SGC-7901/DDP cells proliferation and migration, and increased the levels of c-Myc, Cyclin D1, MMP-3, MMP-9, β-catenin and APC. Interestingly, miR-200b mimics and ZEB1-RNAi were able to reduce the proliferation and migration of TGF-β1-induced SGC-7901/DDP cells as well as their levels of c-Myc, Cyclin D1, MMP-3 MMP-9, β-catenin and APC. In addition, ZEB1 was indeed the potential target of miR-200b identified by dual luciferase reporter gene assay. CONCLUSION : Taken together, our findings suggest that miR-200b be likely to play an important role in activating TGF-β1-induced SGC-7901/DDP cells and perform as a tumor suppressor by targeting ZEB1 in GC. What’s more, miR-200b may modulate Wnt/β-catenin signaling pathway in TGF-β1-induced SGC-7901/DDP cells.

scholarly journals MicroRNA-224 Promotes Pancreatic Cancer Cell Proliferation and Migration by Targeting the TXNIP-Mediated HIF1α Pathway

2018 ◽  
Vol 48 (4) ◽  
pp. 1735-1746 ◽  
Author(s):  
Guanghui Zhu ◽  
Lianming Zhou ◽  
Haijun Liu ◽  
Yuanzhou Shan ◽  
Xueli Zhang
Keyword(s):  
Cell Proliferation ◽  
Nuclear Export ◽  
Xenograft Model ◽  
Ductal Adenocarcinoma ◽  
Luciferase Reporter ◽  
Mouse Xenograft Model ◽  
And Migration ◽  
Proliferation And Migration

Background/Aims: MicroRNAs (miRNAs) have been shown to participate in the development of pancreatic ductal adenocarcinoma (PDAC) by modulating multiple cellular processes. Increased miR-224 expression enhances proliferation and metastasis in human cancers. This study aimed to investigate the role of miR-224 and its underlying mechanism of action in PDAC. Methods: BrdU, MTT, and cell migration assays were performed to determine cell proliferation, viability, and migration, respectively. The binding sites of miR-224 were identified using a luciferase reporter system, whereas protein expression of target genes was determined by immunoblotting and immunofluorescence analyses. A BALB/c nude mouse xenograft model was used to evaluate the role of miR-224 in vivo. Results: We demonstrated that miR-224 expression was enhanced in PDAC cells and tissues, and was related to migration and proliferation. Noticeably, miR-224 overexpression promoted the proliferation, migration, and metastasis of Panc1 cells, while miR-224 inhibition had the reverse effect on PDAC cells. Moreover, we found that thioredoxin-interacting protein (TXNIP) is a target of miR-224. The results also indicated that miR-224 inversely regulated TXNIP by binding directly to its 3′-untranslated region, which resulted in the activation of hypoxia-inducible factor 1α (HIF1α). Further, either TXNIP re-expression or HIF1α depletion abolished the effects of miR-224 on the proliferation and migration of PDAC cells in vitro and in vivo. Regarding the relationship of TXNIP and HIF1α, we found that TXNIP mediated the nuclear export of HIF1α and its degradation by forming a complex with HIF1α. Conclusion: The miR-224-TXNIP-HIF1α axis may be useful in developing novel therapies for PDAC.

scholarly journals Circular RNA hsa_circ_0004872 inhibits gastric cancer progression via the miR-224/Smad4/ADAR1 successive regulatory circuit

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Cunying Ma ◽  
Xiaoying Wang ◽  
Fenghua Yang ◽  
Yichen Zang ◽  
Jiansong Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Nude Mice ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Invasion And Migration ◽  
Potential Biomarker ◽  
And Migration

Abstract Background Emerging evidence has shown that circular RNAs (circRNAs) play a crucial regulatory role in the occurrence and development of cancer. Exploring the roles and mechanisms of circRNAs in tumorigenesis and progression may help to identify new diagnostic markers and therapeutic targets. In the present study, we investigated the role and regulatory mechanism of hsa_circ_0004872 in gastric cancer (GC). Methods qRT-PCR was used to determine the expression of hsa_circ_0004872 in GC tissues and cells. EdU, CCK-8, transwell and scratch wound healing assays were used to assess the role of hsa_circ_0004872 in GC cell proliferation, invasion and migration, respectively. Subcutaneous and tail vein tumor injections in nude mice were used to assess the role of hsa_circ_0004872 in vivo. RIP assay, biotin-coupled probe pull-down assay, FISH and luciferase reporter assay were performed to confirm the relationship between hsa_circ_0004872 and the identified miRNA. ChIP assay, luciferase reporter assay and western blot were used to determine the direct binding of Smad4 to the promoter of the ADAR1 gene. Results In this study, we found that hsa_circ_0004872 was dramatically downregulated in GC tissues compared with adjacent noncancerous tissues. The expression level of hsa_circ_0004872 was associated with tumor size and local lymph node metastasis. Enforced expression of hsa_circ_0004872 inhibited the proliferation, invasion and migration of GC cells, whereas knockdown of hsa_circ_0004872 had the opposite effects. Nude mice experiments showed that ectopic expression of hsa_circ_0004872 dramatically inhibited tumor growth and metastasis in vivo. Moreover, we demonstrated that hsa_circ_0004872 acted as a “molecular sponge” for miR-224 to upregulate the expression of the miR-224 downstream targets p21 and Smad4. Importantly, we found that the RNA-editing enzyme ADAR1 inhibited hsa_circ_0004872 expression and further led to the upregulation of miR-224. Smad4, the downstream target of miR-224, could further affect hsa_circ_0004872 levels by directly binding to the promoter region of ADAR1 to inhibit ADAR1 expression. Conclusions Our findings showed that hsa_circ_0004872 acted as a tumor suppressor in GC by forming a negative regulatory loop consisting of hsa_circ_0004872/miR-224/Smad4/ADAR1. Thus, hsa_circ_0004872 may serve as a potential biomarker and therapeutic target for GC.

scholarly journals Knockdown of Kremen2 Inhibits Tumor Growth and Migration in Gastric Cancer

2021 ◽  
Vol 10 ◽  
Author(s):  
Beibei Chen ◽  
Sai-Qi Wang ◽  
Jinxi Huang ◽  
Weifeng Xu ◽  
Huifang Lv ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Xenograft Model ◽  
Gastric Cancer Cells ◽  
And Migration ◽  
Induced Apoptosis ◽  
Gastric Cancer Patients

Kremen2 (Krm2) plays an important role in embryonic development, bone formation, and tumorigenesis as a crucial regulator of classical Wnt/β-catenin signaling pathway. However, the role of Krm2 in gastric cancer is not clear. The aim of this study was to explore the regulatory role of Krm2 in the tumorigenesis and metastasis of gastric cancer. It was demonstrated that, compared to para-cancerous tissues, Krm2 was significantly up-regulated in gastric cancer tissues and was positively correlated with the pathological grade of gastric cancer patients. Given that Krm2 is abundantly expressed in most tested gastric cancer cell lines, Krm2 knockdown cell models were established and further used to construct mice xenograft model. After knocking down Krm2, both the cell survival in vitro and tumorigenesis in vivo of gastric cancer cells were inhibited. At the same time, knockdown of Krm2 induced apoptosis, cell cycle arrest at G2/M phase and repression of migration in gastric cancer cells in vitro. Mechanistically, we found that knockdown of Krm2 suppressed PI3K/Akt pathway. Therefore, we revealed the novel role and the molecular mechanism of Krm2 in promoting the tumorigenesis and metastasis in gastric cancer. Krm2 can be a potent candidate for designing of targeted therapy.

scholarly journals Knockdown of lncRNA BDNF-AS inhibited the progression of multiple myeloma by targeting the miR-125a/b-5p-BCL2 axis

2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Min Chu ◽  
Yingchao Fan ◽  
Liting Wu ◽  
Xiaoyan Ma ◽  
Jinfeng Sao ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Luciferase Reporter ◽  
Expression Levels ◽  
And Migration ◽  
Related Proteins ◽  
Proliferation And Migration

Abstract Purpose This study aimed to explore the role of long non-coding RNA (lncRNA) BDNF-AS in the progression of multiple myeloma (MM). Methods The expression of BDNF-AS, miR-125a-5p, and miR-125b-5p in MM serum and cell lines were detected by quantitative reverse transcriptase PCR (qRT-PCR). The binding relationships between miR-125a/b-5p and BDNF-AS or Bcl-2 were predicted by Starbase and verified by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2′-deoxyuridine (EdU) staining assay. Cell migration was evaluated by wound healing assay. The expression levels of apoptosis-related proteins were evaluated by Western blot analysis. The role of BDNF-AS was also investigated in a xenograft tumor model in vivo. Results BDNF-AS was significantly upregulated, while miR-125a-5p and miR-125b-5p were downregulated in MM serum and corresponding cancer cell lines. Knockdown of BDNF-AS effectively inhibited the proliferation and migration of MM.1S and U266 cells, and co-transfection of miR-125a-5p or miR-125b-5p inhibitor and sh-BDNF-AS enhanced cell proliferation and migration compared with that in sh-BDNF-AS group. Knockdown of miR-125a-5p or miR-125b-5p significantly enhanced the proliferation and migration of MM.1S and U266 cells, and co-transfection of sh-Bcl-2 and miR-125a/b-5p inhibitor inhibited cell proliferation compared with that in miR-125a/b-5p inhibitor group. Moreover, knockdown of BDNF-AS increased the expression levels of apoptosis-related proteins (cleaved caspase 3 and cleaved PARP), while knockdown of miR-125a-5p or miR-125b-5p reduced the expression levels of these apoptosis-related proteins compared with knockdown of BDNF-AS. Furthermore, knockdown of BDNF-AS effectively suppressed MM tumor growth in vivo. Conclusion Our findings revealed that knockdown of BDNF-AS inhibited the progression of MM by targeting the miR-125a/b-5p-Bcl-2 axis, indicating that BDNF-AS might serve as a novel drug target for MM.

scholarly journals Assessing the Regulatory Functions of LncRNA SNHG11 in Gastric Cancer Cell Proliferation and Migration

2021 ◽  
Vol 9 ◽  
Author(s):  
Danyi Zhao ◽  
Huawei Chen ◽  
Bing Wang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Luciferase Reporter ◽  
Cell Proliferation And Migration ◽  
Gastric Cancer Cell Proliferation ◽  
And Migration ◽  
Migration Capacity ◽  
Regulatory Functions ◽  
Proliferation And Migration

The aim of this study was to assess the regulatory functions of SNHG11 in gastric cancer (GC) cell proliferation and migration. Dual-luciferase reporter assay and bioinformatics prediction [starBase (http://starbase.sysu.edu.cn/) and TargetScan (http://www.targetscan.org)] indicated that SNHG11 functions as a miR-184 sponge that can directly act on CDC25A. Compared with normal healthy gastric tissue and mucosal epithelial cell GES-1, SNHG11 and CDC25A expressions were dramatically increased in GC samples and cell lines, whereas microRNA-184 (miR-184) levels were reduced. SNHG11 silencing led to increased miR-184 and reduced CDC25A, whereas miR-184 downregulation recovered the expression of CDC25A. Additionally, miR-184 upregulation also played a role in regulating CDC25A ablation. Then, SNHG11 was silenced or miR-184 was upregulated in two GC cells (SGC-7901 and MKN-28). SNHG11 silencing and miR-184 upregulation caused a notable decrease in GC cell growth and proliferation and increased the apoptotic level of GC cells. Furthermore, SNHG11 silencing and miR-184 upregulation contributed to a decreased migration capacity of GC cells. Downregulated miR-184 expression in SNHG11 silenced GC cells showed that miR-184 inhibition reversed the effect of SNHG11 silencing on the growth, proliferation, apoptosis, and migration of GC cells. Moreover, in vivo xenograft experiments demonstrated that SNHG11 knockdown can inhibit tumor growth. These observations confirmed that SNHG11 acts as an oncogene, whereas miR-194 served as a tumor suppressor in GC development. SNHG11 may provide a new biomarker for GC diagnosis, treatment, and prognosis.

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