&lt;p&gt;miR-491-5p functions as a tumor suppressor by targeting IGF2 in colorectal cancer&lt;/p&gt;

Lü, Lei; Cai, Ming; Peng, Meixia; Wang, Fei; Zhai, Xiaofeng

doi:10.2147/cmar.s183085

Cited by 37 publications

(35 citation statements)

References 21 publications

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“…Previously, this microRNA was found to suppress cell proliferation and invasion in non-small cell lung cancer by inhibiting IGF2BP1 [42]. Interestingly, miR-491 was recently reported to act as a tumor-suppressive microRNA by inhibiting the known IGF2BP targets IGF2 and HMGA2 [43,44].…”

Section: Post-transcriptional Regulation Of the Pors By Micrornasmentioning

confidence: 99%

RNA Binding Proteins as Drivers and Therapeutic Target Candidates in Pancreatic Ductal Adenocarcinoma

Glaß

Michl

Hüttelmaier

2020

IJMS

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Pancreatic ductal adenocarcinomas (PDAC) belong to the most frequent and most deadly malignancies in the western world. Mutations in KRAS and TP53 along with some other frequent polymorphisms occur almost universally and are likely to be responsible for tumor initiation. However, these mutations cannot explain the heterogeneity in therapeutic responses observed in PDAC patients, which limits efficiency of current therapeutic strategies. Instead, recent classifications of PDAC tumor samples are based on transcriptomics data and thus include information about epigenetic, transcriptomic, and post-transcriptomic deregulations. RNA binding proteins (RBPs) are important post-transcriptional regulators involved in every aspect of the RNA life cycle and thus considerably influence the transcriptome. In this study, we systematically investigated deregulated expression, prognostic value, and essentiality reported for RBPs in PDAC or PDAC cancer models using publicly available data. We identified 44 RBPs with suggested oncogenic potential. These include various proteins, e.g., IGF2 mRNA binding proteins (IGF2BPs), with reported tumor-promoting roles. We further characterized these RBPs and found common patterns regarding their expression, interaction, and regulation by microRNAs. These analyses suggest four prime candidate oncogenic RBPs with partially validated target potential: APOBEC1, IGF2BP1 and 3, and OASL.

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Section: Post-transcriptional Regulation Of the Pors By Micrornasmentioning

confidence: 99%

RNA Binding Proteins as Drivers and Therapeutic Target Candidates in Pancreatic Ductal Adenocarcinoma

Glaß

Michl

Hüttelmaier

2020

IJMS

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“…Overexpression or inhibition of miR-491-5p in HEK-293 cells also showed a similar trend to U87 cells, with higher overall expression level, indicating that miR-491-5p may regulate gene expression through the 3ʹUTR region of the GRIN1 gene. To the best of our knowledge, miR-491-5p mainly participates in tumor events by regulating intermediate genes; [42][43][44] the current results suggest that miR-491-5p could participate in nervous system related events by regulating the GRIN1 gene. Kim et al 18 preliminarily demonstrated that the GRIN1 gene 3ʹUTR is one of the targets of has-miR-1908-5p.…”

Section: Figurementioning

confidence: 89%

<p>Functional Analysis of the 3ʹ Untranslated Region of the Human <em>GRIN1</em> Gene in Regulating Gene Expression in vitro</p>

Liu

Jinghua

et al. 2020

NDT

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Purpose: Abnormal expression of the NR1 subunit of the N-methyl-d-aspartate (NMDA) receptor may potentially increase the susceptibility to neuropsychiatric diseases. The purpose of this study was to investigate the functional sequence of the 3ʹUTR of the human GRIN1 gene, which encodes the GluN1 receptor to determine the effect on the expression of GluN1 receptor. Methods: We transferred seven recombinant pmirGLO recombinant vectors containing the 3ʹUTR truncated fragment of the GRIN1 gene into HEK-293, SK-N-SH, and U87 cell lines and compared the relative fluorescence intensity of adjacent length fragments. The TargetScan database was used to predict miRNAs. Then, miRNA mimics/inhibitors were co-transfected into the three cell lines with the 3ʹUTR of GRIN1 (pmirGLO-GRIN1), to investigate their influence on GRIN1 gene expression. Results: Compared with the pmirGLo-Basic vector, the relative fluorescence intensity of the complete GRIN1 gene 3ʹUTR recombinant sequence −27 bp-+1284 bp (the next base of the stop codon is +1) was significantly decreased in all three cell lines. The relative fluorescence intensities were significantly different between −27 bp-+294 bp and −27 bp-+497 bp regions, and between −27 bp-+708 bp and −27 bp-+907 bp regions. According to the prediction of the TargetScan database and analysis, miR-212-5p, miR-324-3p and miR-326 may bind to +295 bp-+497 bp, while miR-491-5p may bind to +798 bp-+907 bp. After co-transfection of miRNA mimic/inhibitor or mimic/inhibitor NC with a recombinant vector in the 3ʹUTR region of GRIN1 gene, we found that has-miR-491-5p inhibited GRIN1 expression significantly in all three cell lines, while has-miR-326 inhibitor upregulated GRIN1 expression in HEK-293 and U87 cells. Conclusion: miR-491-5p may bind to the 3ʹUTR of the GRIN1 gene (+799 bp-+805 bp, the next base of the stop codon is +1) and down-regulate gene expression in HEK-293, SK-N-SH, and U87 cell lines, which implicates a potential role of miR-491-5p in central nervous system diseases.

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“…miRNAs dysregulation has been identified as a marker of caners. And also found the miRNAs expression changes in gastric cancer [11][12][13] . Recently discovered miRNA miR-491, is downregulated in several types of cancer, including breast cancer, oral squamous cell carcinoma, hepatocellular carcinoma, pancreatic, glioblastoma, ovarian cancer and hepatocellular carcinoma [13][14][15] .…”

Section: Discussionmentioning

confidence: 99%

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

Wei¹,

Zhang

et al. 2020

Preprint

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Background: 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. Methods: Functional experiments including CCK-8 assay and transwell assay were performed. Furthermore, the underlying mechanism was explored through qRT-PCR and western blot assay. In addition, the function of miR-491-5p was also identified in vivo.Results: 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(Epithelial-mesenchymal transition), cell adhesion genes and IFITM2. Conclusions: These data show that miR-491-5p function as a tumor suppressor in GC both in vitro and in vivo.

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<p>miR-491-5p functions as a tumor suppressor by targeting IGF2 in colorectal cancer</p>

Cited by 37 publications

References 21 publications

RNA Binding Proteins as Drivers and Therapeutic Target Candidates in Pancreatic Ductal Adenocarcinoma

RNA Binding Proteins as Drivers and Therapeutic Target Candidates in Pancreatic Ductal Adenocarcinoma

<p>Functional Analysis of the 3ʹ Untranslated Region of the Human <em>GRIN1</em> Gene in Regulating Gene Expression in vitro</p>

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

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