MicroRNA-106a-5p Inhibited C2C12 Myogenesis via Targeting PIK3R1 and Modulating the PI3K/AKT Signaling

Li, Xiao; Zhu, Youbo; Zhang, Huifang; Ma, Guangjun; Wu, Guofang; Xiang, Aoqi; Shi, Xin’e; Yang, Gongshe; Sun, Shiduo

doi:10.3390/genes9070333

Cited by 25 publications

(23 citation statements)

References 40 publications

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“…Moreover, PIK3R1 expression is regulated by multiple miRNAs. For example, miR-198 and miR-106a-5p can target PIK3R1 to regulate cancer progression 34,35. The present study predicted and verified that PIK3R1 was a downstream target of miR-498.…”

supporting

confidence: 76%

Circ_0000105 promotes liver cancer by regulating miR‐498/PIK3R1

Sun

Huang

2020

The Journal of Gene Medicine

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Background: A growing number of studies demonstrate that circular RNA (circRNA) has a prominent role in the regulation of numerous biological behaviors of tumor cells. The present study aimed to investigate the expression, function and molecular mechanisms of circ_0000105 in liver cancer. Methods: A quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to obtain the expressions of circ_0000105 and miR-498 in liver cancer tissues and cells. The association between the expression level of circ_0000105 and the clinicopathological characteristics of liver cancer patients was analyzed. qRT-PCR and western blotting were utilized to investigate the expression of phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1) in cells. Cell counting kit-8, bromodeoxyuridine and flow cytometry assays were utilized to determine liver cancer cell proliferation and apoptosis, respectively. Bioinformatics, a luciferase reporter gene experiment and a RNA immunoprecipitation experiment were conducted to predict and confirm the targeting correlation of circ_0000105 and miR-498, as well as miR-498 and PIK3R1. Results: Circ_0000105 was highly expressed in liver cancer tissues and cell lines. Moreover, its high expression was associated with an increase in the T stage of liver cancer patients and a low degree of tumor differentiation. Circ_0000105 overexpression promoted liver cancer cell proliferation and inhibited apoptosis, whereas knocking down circ_0000105 triggered the opposite effect. miR-498 was a downstream target of circ_0000105, inhibiting liver cancer cell proliferation and promoting apoptosis. Mechanistically, circ_0000105 indirectly up-regulated the expression of PIK3R1 by adsorbing miR-498. Conclusions: Circ_0000105 plays a cancer-promoting role in liver cancer by regulating the miR-498/PIK3R1 axis.

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supporting

confidence: 76%

Circ_0000105 promotes liver cancer by regulating miR‐498/PIK3R1

Sun

Huang

2020

The Journal of Gene Medicine

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“…Furthermore, PIK3R1 level is reduced by miR-16-5p, which inhibits cell cycle and enhances cell apoptosis by modulating of the PI3K/AKT/NF-KB pathway [41]. Besides, miR-495, miR-106a-5p, miR-455 and miR-15 were directly or indirectly contribute to the regulation of PIK3R1 expression [42,43]. In the present study, we demonstrated that miR-17-5p could bind to PIK3R1 3′UTR directly.…”

Section: Discussionmentioning

confidence: 51%

Silencing of miR-17-5p suppresses cell proliferation and promotes cell apoptosis by directly targeting PIK3R1 in laryngeal squamous cell carcinoma

et al. 2020

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Background: Increasing evidence has suggested that microRNAs (miRNAs) act as key post-transcriptional regulators in tumor progression. Previous studies have confirmed that miR-17-5p functions as an oncogene in multiple cancers and contributes to tumor progression. However, the role and biological functions of miR-17-5p in the development of laryngeal squamous cell carcinoma (LSCC) still remain unknown.Methods: qRT-PCR was used to detect miRNA and mRNA expression levels in LSCC tissues and cell lines. CCK-8 assay was used to measure cell viability and flow cytometry was performed to evaluate cell apoptosis. Western blot analysis was used to detect the protein levels of BAX, BCL-2, cleaved Caspase-3, PIK3R1 and AKT. Luciferase reporter assay was used to detect the effect of miR-17-5p on PIK3R1 expression. Xenograft animal model was used to test the effect of miR-17-5p on LSCC cell in vivo. Results:In the present study, we found that miR-17-5p expression level was upregulated in LSCC tissues and cell lines. Depletion of miR-17-5p in LSCC cells significantly reduced cell proliferation and promoted cell apoptosis in vitro and in vivo. Mechanically, knockdown of miR-17-5p in LSCC cells inhibited BCL-2 expression while enhanced BAX and cleaved Caspase-3 protein expression. Moreover, depletion of miR-17-5p in LSCC cells suppressed AKT phosphorylation but did not influence PTEN expression. Importantly, miR-17-5p positively regulated PIK3R1 expression by directly binding to its 3′-untranslated region (UTR). Additionally, PIK3R1, which expression was downregulated in LSCC tissues and cell lines, was involved in LSCC cell survival by modulating the activation of AKT signal pathway. Dysregulation of miR-17-5p/PIK3R1 axis was participated in LSCC cell proliferation and apoptosis by inhibiting the activation of the PI3K/AKT signaling pathway. Conclusions:In conclusion, our study indicates that the miR-17-5p/PIK3R1 axis plays an essential role in the development of LSCC and provides a potential therapeutic target for LSCC treatment. BackgroundLaryngeal squamous cell carcinoma (LSCC) is the most common head and neck malignancy accounting for more than 95% of head and neck squamous cell carcinoma (HNSCC), with 177,422 new cases and 94,771

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“…In siCDR1as pro les, the most enriched pathways of the downregulated mRNAs were (PI3K)-AKT signaling pathway, Focal adhesion, Rap1 signaling pathway, and MAPK signaling pathway. The downregulation of PI3K/AKT signaling pathway by miR-106a-5p was shown to inhibit myogenic differentiation of C2C12 myoblast [62]. Also, according to Jiang et al the knockdown of PI3-Kinase or its downstream target AKT prevents muscle differentiation in cell culture, while activation of PI3-Kinase and Akt induces myogenic differentiation [63,64].…”

Section: Discussionmentioning

confidence: 97%

“…Considering the knockdown of DICER1, we realized that the KEGG pathways of the downregulated mRNAs include PI3K-AKT signaling pathway [62], Focal adhesion [66], and ECM receptor interaction [66], which are also recognized to be associated with muscle development. Moreover, FoxO signaling pathway [66], MAPK signaling pathway [70], Rap1 signaling pathway [68,69], and mTOR signaling pathway [77] were also known to be associated with the upregulated miRNAs.…”

Section: Discussionmentioning

confidence: 99%

CDR1as related miRNA-mRNA networks in differentiating goat skeletal muscle satellite cells

Kyei

Liu

et al. 2020

Preprint

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Background: Myogenesis is a complex process controlled by several coding and non-coding RNAs (ncRNAs) such as circular RNAs (circRNAs) that well-known function as endogenous microRNAs (miRNAs) sponges. Over the past few years, numerous circRNAs have been known and their roles in biological processes have begun to be understood. Cerebellar Degeneration-Related protein 1 antisense (CDR1as), the most spotlighted circRNA as miR-7 sponge that has been blooming circRNAs’ research for a decade, and can potentially sponge several miRNAs in disease and muscle physiology. Nevertheless, the linear-RNAs-differed character that the acute interventions for circRNAs do not affect miRNAs levels, and has retarded the transcriptome-wide discovery of miRNAs sponged by. Therefore, the purpose of this study was to provide the transcriptomic effect of CDR1as during muscle differentiation.Methods: siCDR1as and siDICER1 were transfected into goat skeletal muscle satellite cells (SMSCs). RNA-seq technology and bioinformatics tools were used to analyze genes that are deregulated by siCDR1as and siDICER1. quantitative PCR was used to verify the expression levels of the differentially expressed mRNAs and miRNAs. Results: Here, to systematically identify miRNAs targeting CDR1as, we employed the critical enzyme DICER1 that governs the biogenesis of miRNAs. The deficiency of either DICER1 or CDR1as inhibited myogenic differentiation of SMSCs, and knockdown of DICER1 decreased the expression of CDR1as. Moreover, we screened for the targeted messenger RNAs (mRNAs) and miRNAs in SMSCs transfected with siDICER1 or siCDR1as respectively and found out that some well-known muscle-related pathways such as phosphoinositide 3-kinase (PI3K)-AKT signaling pathway, Rap1 signaling pathway, and MAPK signaling pathway were enriched in all groups. Further, regarding the miRNAs identified in siDICER1 and siCDR1as together with the sequence complementary information, we identified 11 miRNAs including miR-1, miR-206, and miR-27a-5p which are more likely to be novel targets for CDR1as. Conclusion: In summary, our study provides a perspective on the potential functions and relationship between CDR1as and DICER1 during muscle development.

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MicroRNA-106a-5p Inhibited C2C12 Myogenesis via Targeting PIK3R1 and Modulating the PI3K/AKT Signaling

Cited by 25 publications

References 40 publications

Circ_0000105 promotes liver cancer by regulating miR‐498/PIK3R1

Circ_0000105 promotes liver cancer by regulating miR‐498/PIK3R1

Silencing of miR-17-5p suppresses cell proliferation and promotes cell apoptosis by directly targeting PIK3R1 in laryngeal squamous cell carcinoma

CDR1as related miRNA-mRNA networks in differentiating goat skeletal muscle satellite cells

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