lncRNA-MIAT regulates cell biological behaviors in gastric cancer through a mechanism involving the miR-29a-3p/HDAC4 axis

Li, Yanfeng; Wang, Kuan; Yin, Wei; Yao, Qiang; Zhang, Qifan; Qu, Huamin; Zhu, Guanyu

doi:10.3892/or.2017.6020

Cited by 44 publications

(34 citation statements)

References 21 publications

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“…It is well known that lncRNAs act as ceRNA to regulate functional gene expression via sponging miRNAs . In the previous studies, MIAT was reported to function as ceRNA in ccRCC, colorectal cancer, breast cancer, gastric cancer and non‐small‐cell lung cancer . Therefore, we speculated that MIAT might function as an oncogene through a ceRNA manner.…”

Section: Discussionmentioning

confidence: 90%

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

et al. 2019

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The aberrant expression of long non‐coding RNAs (lncRNAs) has been involved in the progression of many human tumors including osteosarcoma (OS). However, the biological function and the underlying mechanism of the lncRNA myocardial infarction‐associated transcript (MIAT) in OS remain unclear. In the present study, we found that lncRNA MIAT was significantly up‐regulated in both OS tissues and cell lines, and high expression of MIAT was positively associated with tumor size and lymph node metastasis of OS patients. In addition, knockdown of MIAT inhibited proliferation, migration, invasion and promoted apoptosis of OS cells in vitro. Moreover, the expression of MIAT was negatively associated with miR‐128‐3p but positively correlated with vascular endothelial growth factor C (VEGFC) in OS. Further mechanistic study revealed that lncRNA MIAT promoted OS progression by up‐regulating VEGFC via sponging miR‐128‐3p in vitro. Taken together, our results suggest that MIAT/miR‐128‐3p/VEGFC axis contributes to OS progression and may be used as a novel therapeutic target for OS. © 2019 IUBMB Life, 9999(9999):1–9, 2019

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Section: Discussionmentioning

confidence: 90%

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

et al. 2019

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“…The human HDAC4 gene, located on chromosome 2q37.3, has been found to be involved in initiation and development of various cancers, and functions as an oncogene in many cancers [32][33][34][35][36]. A previous study confirmed HDAC4 as a target of miR-29b-3p in MM cells [25].…”

Section: Discussionmentioning

confidence: 94%

Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

2019

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Background: Long non-coding RNA taurine up-regulated gene 1 (TUG1) was reportedly involved in initiation and development of several cancers. However, its function and molecular mechanisms in multiple myeloma (MM) are still unclear. The present study aimed to determine the expression status, biological function, and potential mechanisms of TUG1 in the progression of MM. Materials and methods: The expression levels of TUG1 were examined in MM samples and cell lines by real-time quantitative PCR. The effects of TUG1 on MM cells proliferation and apoptosis were assessed using Cell Counting Kit-8 assay and flow cytometry respectively. MiRNAs-targeted sites in TUG1 were screened by Starbase2.0 and were identified by RNA immunoprecipitation assay combined with luciferase reporter assay. Results: The expression levels of TUG1 were markedly increased in MM samples and cell lines. Knockdown of TUG1 significantly suppressed the proliferation, induced cell cycle arrest at G1/G0 phase, and promoted apoptosis of MM cells. In exploring the regulatory mechanism, miR-29b-3p was confirmed to be a direct target of TUG1, and repression of miR-29b-3p could partially rescue the effect TUG1 knockdown on MM cell proliferation, cycle, and apoptosis. In addition, TUG1 positively modulated histone deacetylases 4 (HDAC4, a target of miR-29b-3p) expression through sponging of miR-29b-3p in MM cells. Conclusion: These findings suggested that TUG1 exerted an oncogenic role in MM by acting as a competing endogenous RNA of miR-29b-3p, and implied the potential application of TUG1 in treatment for MM.

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“…22,23 HDAC4, a member of the HDAC family, is overexpressed in GC, and plays multiple roles in the malignant characteristics of GC cells in vitro and in vivo. [33][34][35] Understanding the newly identified RGMB-AS1-miR-574-HDAC4 regulatory network can clarify the oncogenic activities of RGMB-AS1 in GC and may point to promising therapeutic regimens for patients with GC.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Noncoding RNA <em>RGMB-AS1</em> Acts as a microRNA-574 Sponge Thereby Enhancing the Aggressiveness of Gastric Cancer via HDAC4 Upregulation</p>

Wang¹,

Chen²,

Tian³

et al. 2020

OTT

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Purpose: The long noncoding RNA RGMB-AS1 plays an important part in the genesis and progression of multiple human cancers. Nonetheless, little is known regarding its expression, roles, and mechanisms of action in gastric cancer (GC). This study was aimed at investigating the relationship between RGMB-AS1 and GC and illustrating the mechanisms of action of RGMB-AS1 therein. Methods: RGMB-AS1 expression in GC was measured via reverse-transcription quantitative PCR. A series of experiments including Cell Counting Kit-8 assay, flow-cytometric analysis of apoptosis, Transwell migration and invasion assays, and in vivo tumorigenesis experiment were conducted to test the effects of RGMB-AS1 on the malignant phenotype of GC cells. The molecular events behind the oncogenic actions of RGMB-AS1 in GC were elucidated through subcellular fractionation, RNA immunoprecipitation assay, bioinformatics analysis and luciferase reporter assay. Results: RGMB-AS1 upregulation was confirmed in GC tissues and cell lines. Higher RGMB-AS1 expression was associated with adverse clinical parameters and negatively correlated with patient overall survival. RGMB-AS1 knockdown inhibited GC cell proliferation, facilitated apoptosis, and reduced migration and invasion in vitro. Further experiments revealed that RGMB-AS1 knockdown decreased the tumor growth of GC cells in vivo. Mechanistically, RGMB-AS1 functioned as a competing endogenous RNA upregulating histone deacetylase 4 (HDAC4) by sponging . Rescue experiments indicated that miR-574 inhibition and HDAC4 reintroduction reversed the effects of the RGMB-AS1 knockdown on GC cells. Conclusion: The RGMB-AS1-miR-574-HDAC4 regulatory network contributes to the malignancy of GC, thereby offering a novel target for the diagnosis, prognosis, and/or treatment of GC.

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lncRNA-MIAT regulates cell biological behaviors in gastric cancer through a mechanism involving the miR-29a-3p/HDAC4 axis

Cited by 44 publications

References 21 publications

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

<p>Long Noncoding RNA <em>RGMB-AS1</em> Acts as a microRNA-574 Sponge Thereby Enhancing the Aggressiveness of Gastric Cancer via HDAC4 Upregulation</p>

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