Circular RNA CircCDYL Regulates Proliferation and Apoptosis in Non-Small Cell Lung Cancer Cells by Sponging miR-185-5p and Upregulating TNRC6A

Abstract

A series of research reveal that circular RNA (circRNA) plays a vital role in regulating the development of tumor cells. In this research, we would explore the role and mechanism of circCDYL in non-small cell lung cancer (NSCLC). Methods: RT-PCR was performed to detect the expression of circCDYL in NSCLC tissues, plasma, and cell lines. The tumor cell proliferation ability was evaluated by clone formation assay, and cell cycle determination. Flow cytometry was used to detect apoptosis in NSCLC cell lines. Western blot and RT-PCR were used to assess the expression of proteins and genes. Luciferase assay was performed to confirm the relationship of circRNA-miRNA-mRNA.Results: The decreased level of circCDYL was observed in NSCLC patients' tissues and plasma, which was also downregulated in NSCLC cell lines. Forced expression of circCDYL inhibited cell viability, proliferation and induced apoptosis in A549 cells. Luciferase assay verified that circCDYL could bind with miR-185-5p and confirmed that TNRC6A was a downstream target of miR-185-5p. Overexpression of miR-185-5p or silencing of TNRC6A could inhibit the anti-tumor effect of circCDYL in A549 cells via regulating the ERK1/2 signal. Conclusion: Here, we revealed that circCDYL inhibited proliferation and induced apoptosis in NSCLC cell lines via regulating ERK1/2 signal, and the mechanism of this progression may target miR-185-5p/TNRC6A, which provided a theoretical basis for clinical therapy.

Circ_ZNF512-Mediated miR-181d-5p Inhibition Limits Cardiomyocyte Autophagy and Promotes Myocardial Ischemia/Reperfusion Injury through an EGR1/mTORC1/TFEB-Based Mechanism

“…Mechanistically, circ_ZNF512 competitively bound to miR-181d-5p and caused upregulation of the miR-181d-5p target EGR1 expression. Interaction of circRNA-miRNA-mRNA has been largely reported, where circRNAs competitively bind to miRNAs and attenuate their binding ability to the target mRNA expression. , The present study also revealed that circ_ZNF512 silencing attenuates its binding to miR-181d-5p and reduces EGR1 expression, thus promoting cardiomyocyte autophagy and attenuating myocardial injury. Silencing of circRNAs has demonstrated cardioprotective effects on the myocardial I/R injury; for instance, circNCX1 knockdown in murine cardiomyocytes and heart tissues can attenuate the apoptosis and I/R injury by acting as an endogenous miR-133a-3p sponge .…”

Cardioprotective Effect of circ_SMG6 Knockdown against Myocardial Ischemia/Reperfusion Injury Correlates with miR-138-5p-Mediated EGR1/TLR4/TRIF Inactivation

“…Furthermore, circ_SMG6 competitively bound to miR-138-5p and caused upregulation of EGR1 expression. Indeed, interaction of circRNA-miRNA-mRNA has been largely reported where circRNAs competitively bind to miRNAs and attenuate their binding ability to the target mRNA expression [ 25 , 26 ]. The present study also revealed that circ_SMG6 enhanced cardiomyocyte apoptosis and myocardial I/R injury by attenuating miR-138-5p-mediated EGR1 inhibition.…”

Biogenesis, Functions, and Role of CircRNAs in Lung Cancer

“…Continued). TNM, the high stage of tumor node metastasis; LNM, lymph node metastasis; OS, overall survival; MDR, multidrug resistance; EMT, epithelial-mesenchymal transition.CircCDYL was decreased in NSCLC patients' tissues and plasma, also downregulated in NSCLC cell lines 58. However, the overexpression of circCDYL can inhibit proliferation and induce apoptosis in NSCLC cells.…”

“…CircCDYL was decreased in NSCLC patients’ tissues and plasma, also downregulated in NSCLC cell lines. 58 However, the overexpression of circCDYL can inhibit proliferation and induce apoptosis in NSCLC cells. The downregulated circCDYL binds to miR-185-5p, and miR-185-5p was upregulated in NSCLC.…”