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Clear cell renal cell carcinoma (ccRCC) is the most common subtype of RCC. Compelling evidence has highlighted the crucial role of long non-coding RNA (lncRNA) in ccRCC. Our current study aims to explore the regulatory mechanism of LINC01094 in the development of ccRCC. Dual-luciferase reporter experiment verified the targeting relationship among miR-184, LINC01094, and SLC2A3. Furthermore, the interaction between LINC01094 and miR-184 was confirmed by RNA immunoprecipitation (RIP) and RNA pull-down. Biological behaviors of ccRCC cells were investigated through cell counting kit-8 (CCK8), scratch test, Transwell, and flow cytometry. The effect of SLC2A3 on the tumorigenicity of nude mice was evaluated in vivo. In ccRCC cells and clinical tissues, LINC01094 and SLC2A3 were highly expressed while miR-184 was lowly expressed. Besides, miR-184 was verified to be a direct target of LINC01094. Silencing LINC01094, up-regulating miR-184, or reducing SLC2A3 inhibited the growth, migration, and invasion of ccRCC cells. Tumor growth was suppressed by silenced LINC01215 via reducing the expression of SLC2A3 via miR-184. Taken together, silencing LINC01094 inhibited SLC2A3 expression by up-regulating miR-184, thereby inhibiting the development of ccRCC.

Clear cell renal cell carcinoma (ccRCC) is the most common subtype of RCC. Compelling evidence has highlighted the crucial role of long non-coding RNA (lncRNA) in ccRCC. Our current study aims to explore the regulatory mechanism of LINC01094 in the development of ccRCC. Dual-luciferase reporter experiment verified the targeting relationship among miR-184, LINC01094, and SLC2A3. Furthermore, the interaction between LINC01094 and miR-184 was confirmed by RNA immunoprecipitation (RIP) and RNA pull-down. Biological behaviors of ccRCC cells were investigated through cell counting kit-8 (CCK8), scratch test, Transwell, and flow cytometry. The effect of SLC2A3 on the tumorigenicity of nude mice was evaluated in vivo. In ccRCC cells and clinical tissues, LINC01094 and SLC2A3 were highly expressed while miR-184 was lowly expressed. Besides, miR-184 was verified to be a direct target of LINC01094. Silencing LINC01094, up-regulating miR-184, or reducing SLC2A3 inhibited the growth, migration, and invasion of ccRCC cells. Tumor growth was suppressed by silenced LINC01215 via reducing the expression of SLC2A3 via miR-184. Taken together, silencing LINC01094 inhibited SLC2A3 expression by up-regulating miR-184, thereby inhibiting the development of ccRCC. [ABSTRACT FROM AUTHOR]

Stroke is considered an underlying etiology of the development of seizures. Stroke leads to glucose and oxygen deficiency in neurons, resulting in brain dysfunction and injury. Mild hypothermia is a therapeutic strategy to inhibit stroke‑induced seizures, which may be associated with the regulation of energy metabolism of the brain. Mammalian target of rapamycin (mTOR) signaling and solute carrier family 2, facilitated glucose transporter member (GLUT)‑1 are critical for energy metabolism. Furthermore, mTOR overactivation and GLUT‑1 deficiency are associated with genetically acquired seizures. It has been hypothesized that mTOR and GLUT‑1 may additionally be involved in seizures elicited by stroke. The present study established global cerebral ischemia (GCI) models of rats. Convulsive seizure behaviors frequently occurred during the first and the second days following GCI, which were accompanied with seizure discharge reflected in the EEG monitor. Expression of phosphor (p)‑mTOR and GLUT‑1 were upregulated in the cerebral cortex and hippocampus, as evidenced by immunohistochemistry and western blot analyses. Mild hypothermia and/or rapamycin (mTOR inhibitor) treatments reduced the number of epileptic attacks, seizure severity scores and seizure discharges, thereby alleviating seizures induced by GCI. Mild hypothermia and/or rapamycin treatments reduced phosphorylation levels of mTOR and the downstream effecter p70S6 in neurons, and the amount of GLUT‑1 in the cytomembrane of neurons. The present study revealed that mTOR is involved in stroke‑induced seizures and the anti‑seizure effect of mild hypothermia. The role of GLUT‑1 in stroke‑elicited seizures appears to be different from the role in seizures induced by other reasons. Further studies are necessary in order to elucidate the exact function of GLUT‑1 in stroke‑elicited seizures. [ABSTRACT FROM AUTHOR]