Increasing evidence indicates that circular RNAs (circRNAs) play a crucial role in regulating microRNAs (miRs) and mRNAs during breast cancer (BC) progression. Based on the in silico analysis of circRNA/miR/mRNA in BC, we aim to define an important role of circRNA_000554 in BC in relation to miR‐182 and zinc finger protein 36 (ZFP36). Low expression of circRNA_000554 and ZFP36, and high miR‐182 expression were determined in the clinical BC tissues. CircRNA_000554 acted as a sponge of miR‐182, and miR‐182 directly targeted ZFP36. After that, in order to evaluate the effects of circRNA_000554, miR‐182, and ZFP36 on cellular process, we evaluated in vitro epithelial‐mesenchymal transition (EMT) and in vivo tumor growth after delivering a series of overexpression plasmids, mimic, inhibitor, or shRNAs into BC cells. Increasing circRNA_000554 suppressed EMT, cell invasion and migration during BC by depleting miR‐182 and increasing ZFP36. The inhibitory effect of circRNA_000554 on tumor growth was validated in vivo. Taken together, the present study confirms that circRNA_000554 functioned as an inhibitor of EMT in BC and suggests a molecular mechanism that circRNA_000554 bound to miR‐182 to upregulate ZFP36 in this process.
We investigated the effects of lncRNA AK139328 and PI3K/Akt signaling during rat hindlimb ischemia-reperfusion (I/R) injury. Rat vascular endothelial cells (VECs) subjected to oxygen-glucose deprivation showed high lncRNA AK139328 expression and decreased PI3K/Akt signaling, whereas lncRNA AK139328 knockdown increased PI3K/Akt signaling in VECs. Correspondingly, gastrocnemius muscles from rats subjected to hindlimb I/R showed high levels of lncRNA AK139328 and low PI3K/Akt/eNOS signaling. I/R also increased serum levels of TNF-α, VCAM-1 and malondialdehyde, serum creatine kinase activity and the number of circulating endothelial cells (CECs). Gastrocnemius tissue from rats subjected to I/R exhibited inflammation, apoptosis and trauma with loosely attached, swollen VECs associated with inflammatory immune cells. LncRNA AK139328 knockdown increased PI3K/ Akt/eNOS signaling in gastrocnemius muscles subjected to I/R, and decreased serum levels of TNF-α, VCAM-1 and malondialdehyde, serum creatine kinase activity and numbers of CECs. LncRNA AK139328 knockdown also decreased inflammation, apoptosis and trauma in gastrocnemius muscles, which showed tightly attached VECs that were not associated with inflammatory immune cells. Inhibition of PI3K/ Akt signaling by wortmannin or LY294002 reversed the effects of lncRNA AK139328 knockdown. In conclusion, I/R induces expression of lncRNA AK139328, which suppresses PI3K/Akt signaling required to prevent I/R-related pathology in VECs.
Optogenetic systems and tetracycline‐induced expression systems have been used in biological research. In gene circuits, light and tetracycline are often used to control the activation or inhibition of gene expression. In our study, we used a blue light induction system and tetracycline induction system to construct an “OR” logic gate, which can specifically induce the expression of p53 protein or E‐cadherin in the case of blue light or tetracycline, thus inhibiting the growth of cutaneous squamous cell carcinoma cells. Cutaneous squamous cell carcinoma is a kind of skin surface tumour. The activation of two tumour suppressor genes has a synergistic inhibitory effect on cutaneous squamous cell carcinoma, and blue light and tetracycline also provide a flexible means for gene regulation.
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