LINC00052 regulates the expression of NTRK3 by miR-128 and miR-485-3p to strengthen HCC cells invasion and migration

Xiong, Dongmei; Sheng, Yanrui; Ding, Shijia; Chen, Juan; Tan, Xixi; Zeng, Tao; Qin, Dongdong; Zhū, Lìyǐng; Huang, Aiping; Tang, Hua

doi:10.18632/oncotarget.10250

Cited by 63 publications

(63 citation statements)

References 29 publications

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“…A noncoding small RNA is also called as microRNA (miRNA), which generally includes about 20 nucleotides and has the ability to modulate some target genes . In recent years, several miRNAs have been clarified in human diseases, and some existing researches have implied that miRNAs were correlated with the development of HCC, such as miR‐128, miR‐485‐3p, and miR‐221 . As one of the miRNAs, miR‐124‐3p belongs to the miR‐124 family, and was proved to be related with different kinds of human diseases, including nasopharyngeal carcinoma, gastric cancer, and glioblastoma .…”

Section: Introductionmentioning

confidence: 99%

Midazolam inhibits proliferation and accelerates apoptosis of hepatocellular carcinoma cells by elevating microRNA‐124‐3p and suppressing PIM‐1

Qi¹,

Yao²,

Du³

2019

IUBMB Life

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Objective Recently, the impact of microRNAs (miRNAs) has been identified in hepatocellular carcinoma (HCC), this study was designed to assess the effects of miR‐124‐3p and midazolam (MDZ) in HCC with the involvement of PIM‐1. Methods HepG2 human HCC cells were selected for our study, which were treated with different concentrations of MDZ. The gain‐ and loss‐of‐function experiments were performed to elucidate the migration, invasion, proliferation, colony formation ability, cell cycle, and apoptosis of HepG2 cells upon treatment of MDZ, miR‐124‐3p mimics, or miR‐124‐3p inhibitor. The expression levels of miR‐124‐3p, PIM‐1, Bax, Bcl‐2, P21, and Ki‐67 in HepG2 cells were assessed by reverse transcription quantitative polymerase chain reaction and western blot analysis. Moreover, HepG2 cell growth in vivo was measured by subcutaneous tumorigenesis in nude mice, and the target relation between miR‐124‐3p and PIM‐1 was evaluated using dual luciferase reporter gene assay. Results We have found that after treated with overexpression of miR‐124‐3p and MDZ, there exhibited elevated miR‐124‐3p, declined expression of PIM‐1, attenuated migration, invasion, proliferation and colony formation ability, and promoted apoptosis of HepG2 cells. Additionally, it could be observed that the tumor volume and weight were all reduced upon treatment of overexpression of miR‐124‐3p and MDZ. Meanwhile, the results in the HepG2 cells that treated with down‐regulated miR‐124‐3p were the opposite. Furthermore, PIM‐1 was found to be a target gene of miR‐124‐3p. Conclusion Our study found that MDZ could inhibit proliferation and accelerate apoptosis of HCC cells by elevation of miR‐124‐3p and suppressing PIM‐1, which may be an effective method in the treatment of HCC.

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Section: Introductionmentioning

confidence: 99%

Midazolam inhibits proliferation and accelerates apoptosis of hepatocellular carcinoma cells by elevating microRNA‐124‐3p and suppressing PIM‐1

Qi¹,

Yao²,

Du³

2019

IUBMB Life

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“…Our previous studies found that lncRNAs could modulate the biological behaviors of HCC cells through their neighboring mRNAs [15,19]. The neighboring mRNA of CRNDE was IRX5 (Fig.…”

Section: Discussionmentioning

confidence: 91%

“…Accumulating evidence showed that lncRNA might be a competing ceRNA or a molecular sponge in inflecting the expression and biological functions of miRNA [15]. Using a bioinformatics databases (Starbase, RNAhybrid), miR-136-5P is a putative target of CRNDE in several miRNAs (Table 2).…”

Section: Reciprocal Repression Between Crnde and Mir-136-5pmentioning

confidence: 99%

Long-Noncoding RNA Colorectal Neoplasia Differentially Expressed Gene as a Potential Target to Upregulate the Expression of IRX5 by miR-136-5P to Promote Oncogenic Properties in Hepatocellular Carcinoma

Zhū

Liu

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: The long-noncoding RNA colorectal neoplasia differentially expressed (CRNDE) gene was first found to be activated in colorectal neoplasia. Now, it also has been found to be upregulated in many other solid tumors. Whether CRNDE affects tumorigenesis remains unknown. Methods: We conducted bioinformatics, real-time polymerase chain reaction (PCR), Western blot analysis, cell proliferation assay, colony formation assay, wound healing assay, cell migration and invasion assays, RNA immunoprecipitation, and reporter vector construction and luciferase assays. Results: CRNDE was upregulated in hepatocellular carcinoma (HCC). The overexpression of CRNDE promoted HCC cellular proliferation, migration, and invasion in intro and in vivo, and acted as an oncogene in HCC progression. Furthermore, CRNDE impaired miR-136-5P expression in a RISC manner, and a reciprocal repression feedback loop was possible between CRNDE and miR-136-5P. We found that the neighboring mRNA of CRNDE was IRX5, and IRX5 increased the tumorigenicity of HCC cells. IRX5 was a potential downstream target gene of miR-136-5P. MiR-136 regulated IRX5 by interacting with its 3’UTR. In addition, miR-136-5P was involved in the CRNDE-regulated expression of IRX5. Conclusion: CRNDE acted as a tumor oncogene by exhibiting oncogenic properties of human HCC and revealed a novel CRNDE-miR-136-5P-IRX5 regulatory network in HCC. CRNDE may be considered to be a potential target for HCC therapies based on its ability to upregulate IRX5, and it deserves further investigation.

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“…The function of LINC00052 varies depending on the location of tumors. It acts as a tumor suppressor through inhibiting cell proliferation, invasion and migration in hepatocellular carcinoma (Xiong et al 2016;Yan et al 2018;Zhu et al 2017), whereas it could promote breast cancer growth (Salameh et al 2017) and gastric cell metastasis and proliferation (Shan et al 2017).…”

Section: Discussionmentioning

confidence: 99%

Peer Review #2 of "Comprehensive analysis of lncRNA-associated competing endogenous RNA network in tongue squamous cell carcinoma (v0.2)"

2019

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Background. Increasing evidence has demonstrated that long non-coding RNAs (lncRNAs) play an important role in the competitive endogenous RNA (ceRNA) networks in that they regulate protein-coding gene expression by sponging microRNAs (miRNAs). However, the understanding of the ceRNA network in tongue squamous cell carcinoma (TSCC) remains limited. Methods. Expression profile data regarding mRNAs, miRNAs and lncRNAs as well as clinical information on 122 TSCC tissues and 15 normal controls from The Cancer Genome Atlas (TCGA) database were collected. We used the edgR package to identify differentially expressed mRNAs (DEmRNAs), lncRNAs (DElncRNAs) and miRNAs (DEmiRNAs) between TSCC samples and normal samples. In order to explore the functions of DEmRNAs, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed. Subsequently, a ceRNA network was established based on the identified DElncRNAs-DEmiRNAs and DEmiRNAs-DEmRNAs interactions. The RNAs within the ceRNA network were analyzed for their correlation with overall disease survival. Finally, lncRNAs were specifically analyzed for their correlation with clinical features in the included TSCC patient samples. Results. A total of 1867 mRNAs, 828 lncRNAs and 81 miRNAs were identified as differentially expressed in TSCC tissues (|log 2 fold change| ≥ 2; adjusted P value < 0.01). The resulting ceRNA network included 16 mRNAs, 56 lncRNAs and 6 miRNAs. Six out of the 56 lncRNAs were found to be associated with the overall survival in TSCC patients (P < 0.05); 10 lncRNAs were correlated with TSCC progression (P < 0.05). Conclusion. Our study deepens the understanding of ceRNA network regulatory mechanisms in TSCC. Furthermore, we identified ten lncRNAs (PART1, LINC00261, AL163952.1, C2orf48, FAM87A, LINC00052, LINC00472, STEAP3-AS1, TSPEAR-AS1 and ERVH48-1) as novel, potential prognostic biomarkers and therapeutic targets for TSCC.

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LINC00052 regulates the expression of NTRK3 by miR-128 and miR-485-3p to strengthen HCC cells invasion and migration

Cited by 63 publications

References 29 publications

Midazolam inhibits proliferation and accelerates apoptosis of hepatocellular carcinoma cells by elevating microRNA‐124‐3p and suppressing PIM‐1

Midazolam inhibits proliferation and accelerates apoptosis of hepatocellular carcinoma cells by elevating microRNA‐124‐3p and suppressing PIM‐1

Long-Noncoding RNA Colorectal Neoplasia Differentially Expressed Gene as a Potential Target to Upregulate the Expression of IRX5 by miR-136-5P to Promote Oncogenic Properties in Hepatocellular Carcinoma

Peer Review #2 of "Comprehensive analysis of lncRNA-associated competing endogenous RNA network in tongue squamous cell carcinoma (v0.2)"

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