Upregulation of MicroRNA-15a Contributes to Pathogenesis of Abdominal Aortic Aneurysm (AAA) by Modulating the Expression of Cyclin-Dependent Kinase Inhibitor 2B (CDKN2B)

Gao, Peng; Si, Jiyuan; Yang, Bin; Yu, Jixiang

doi:10.12659/msm.898233

Cited by 25 publications

(8 citation statements)

References 34 publications

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“…By examining the relative expression in tumor tissues and their adjacent normal tissues, we discovered miR-15a-5p and miR-15b-5p was prominently upregulated in tumor tissues. MiR-15a-5p and miR-15b-5p have been previously reported as promoters in diseases such as abdominal aortic aneurysm, osteoarthritis chondrocytes and colorectal adenocarcinoma [24][25][26]. For further evidence, miR-15a/b-5p loss-of-function experiments were carried out and the oncogenic property of miR-15a/b-5p was confirmed.…”

Section: Discussionmentioning

confidence: 90%

FENDRR suppresses cervical cancer proliferation and invasion by targeting miR-15a/b-5p and regulating TUBA1A expression

et al. 2020

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Background: Previous literature has revealed long non-coding RNAs (lncRNAs) are crucial regulators for cell functions and gene expression. LncRNA fetal-lethal non-coding developmental regulatory RNA (FENDRR) was reported as a biological suppressor in several types of human cancers, yet relevant mechanisms and biological effects of FENDRR with regards to cervical cancer (CC) are not explored until now. Methods: In this study, quantitative real-time polymerase chain reaction (qRT-PCR) analysis detected gene expression in tissues and cells. Gain-or loss-of-function experiments revealed the biological effects of FENDRR and miR-15a/b-5p on CC cell functions. Bioinformatics tools were used to predict the relevant genes. Mechanism experiments including RNA immunoprecipitation (RIP) assay, pull down assay and luciferase reporter assay depicted the binding situation and coexistence of indicated genes. Results: FENDRR was downregulated in CC tissues and cells, which suppressed CC progression. MiR-15a-5p and miR-15b-5p shared binding sites with FENDRR and had interaction with FENDRR. Tubulin alpha1A (TUBA1A) was downregulated in CC tissues and positively modulated by FENDRR. TUBA1A was the target of miR-15a/b-5p. TUBA1A silencing rescued the effect of FENDRR overexpression on CC cell growth and migration. Conclusion: FENDRR inhibits CC progression through upregulating TUBA1A in a miR-15a/b-5p-dependent manner.

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Section: Discussionmentioning

confidence: 90%

FENDRR suppresses cervical cancer proliferation and invasion by targeting miR-15a/b-5p and regulating TUBA1A expression

et al. 2020

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“…Remarkably, miR-181b was determined highly expressed in human AAA and correlated with decreased expression of tissue inhibitor of metalloproteinase-3 and elastin, which promoted the progression of AAA [28]. In addition, miR-15a was reported a negative regulatory role in the expression of CDKN2B and thus promoting the apoptosis of VSMC, which might lead to the pathogenesis of AAA [35]. Further studies are warranted to confirm the hsa_circ_0005360/miR-181b and hsa_circ_0002168/miR-15a axis in AAA.…”

Section: Discussionmentioning

confidence: 98%

Circular RNA expression profile and its potential regulative role in human abdominal aortic aneurysm

Zhou

Shi

Cai

et al. 2020

BMC Cardiovasc Disord

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Background: This study aimed to identify the differentially expressed circular RNAs (circRNAs) between human abdominal aortic aneurysm (AAA) and the control group. Methods: High-throughput sequencing was applied to determine the circRNA expression profiles of 4 paired aortic samples. Real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was carried out to testify 6 randomly selected dysregulated circRNAs. Kyoto Encyclopedia of Genes and Genomes and Gene ontology (GO) analysis were conducted for functional annotation of the parental genes. Additionally, interaction networks between circRNA and 5 putative microRNA (miRNA) partners were constructed.Results: Finally, 411 differentially expressed circRNAs were discovered, including 266 downregulated and 145 upregulated circRNAs. Compared with the control group, the expression level of hsa (Homo sapiens) _circ_0005360 (LDLR) and hsa_circ_0002168 (TMEM189) were proved significantly lower in the AAA group by qRT-PCR. Regarding upregulated circRNAs, the most enriched GO molecular function, biological process and cellular component terms were poly(A) RNA binding, negative regulation of transcription from RNA polymerase II promoter and nucleoplasm, respectively. Moreover, circRNA/miRNA interaction networks showed that hsa_circ_0005360/miR-181b and hsa_circ_ 0002168/miR-15a axis might have a regulative role in human AAA. Conclusions: This study revealed new circRNAs potentially related to the pathogenesis of AAA. Further experimental studies are warranted to clarify the potential molecular mechanisms.

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“…**p<0.01 modulating the target gene chemokine ligand 10 (CXCL10) [34]. On the contrary, the abundance of miR-15a-5p was clarified as one of the pathogenic factors of the abdominal aortic aneurysm by interfering cyclin dependent kinase inhibitor 2B [35]. However, the molecular mechanism of miR-15a-5p in BC cell regulation requires further exploration.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of SNHG12 accelerates cell proliferation, migration, invasion and restrain cell apoptosis in breast cancer by enhancing regulating SALL4 expression via sponging miR-15a-5p

Yuan¹,

Li²,

Hu³

et al. 2020

neo

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Breast cancer (BC) is malignant cancer that threatens the health of millions of females worldwide. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 12 (SNHG12) has been identified as an oncogene in multiple cancers. However, the regulatory role of SNHG12 in BC cell progression is still obscured. The levels of SNHG12, miR-15a-5p, and Sal-like 4 (SALL4) in BC tumor tissues and cells were measured by qRT-PCR. Cell viability, apoptosis, migration, and invasion were examined by CCK8, flow cytometry, and transwell assay, respectively. The interaction between miR-15a-5p and SNHG12 or SALL4 was evaluated by dual-luciferase reporter assay. Protein expression of SALL4 was analyzed by western blot. Xenograft mice were established by subcutaneously injecting BC cells stably transfected with sh-SNHG12 and sh-NC. SNHG12 and SALL4 expressions were upregulated whereas miR-15a-5p was downregulated in BC tumors compared with normal tissues. Besides, miR-15a-5p was correlated with SNHG12 and SALL4 inversely as calculated by Pearson's correlation coefficient. More importantly, SNHG12 knockdown attenuated BC tumor growth in vitro and in vivo. Subsequently, dual-luciferase reporter assay confirmed the interaction between miR-15a-5p and SNHG12 or SALL4. The rescue experiments revealed that miR-15a-5p inhibitor restored SNHG12 silencing induced inhibition on BC cell proliferation, migration, invasion, and promotion of apoptosis. Additionally, SNHG12 was found to accelerate BC cell progression by absorbing miR-15a-5p to enhance SALL4 expression. SNHG12 promotes cell proliferation, migration, and invasion but suppresses apoptosis in BC by upregulating SALL4 expression via sponging miR-15a-5p, representing potential targets for the development of novel diagnosis and treatment methods.

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Upregulation of MicroRNA-15a Contributes to Pathogenesis of Abdominal Aortic Aneurysm (AAA) by Modulating the Expression of Cyclin-Dependent Kinase Inhibitor 2B (CDKN2B)

Cited by 25 publications

References 34 publications

FENDRR suppresses cervical cancer proliferation and invasion by targeting miR-15a/b-5p and regulating TUBA1A expression

FENDRR suppresses cervical cancer proliferation and invasion by targeting miR-15a/b-5p and regulating TUBA1A expression

Circular RNA expression profile and its potential regulative role in human abdominal aortic aneurysm

Upregulation of SNHG12 accelerates cell proliferation, migration, invasion and restrain cell apoptosis in breast cancer by enhancing regulating SALL4 expression via sponging miR-15a-5p

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