Kuiming Zhang

Capicua (Cic), a transcriptional repressor frequently mutated in brain cancer oligodendroglioma, is highly expressed in adult neurons. However, its function in the dendritic growth of neurons in the hippocampus remains poorly understood. Here, we confirmed that Cic was expressed in hippocampal neurons during the main period of dendritogenesis, suggesting that Cic has a function in dendrite growth. Loss-of-function and gain-of function assays indicated that Cic plays a central role in the inhibition of dendritic morphogenesis and dendritic spinesin vitro. Further studies showed that overexpression of Cic reduced the expression of Ets in HT22 cells, whilein vitroknockdown of Cic in hippocampal neurons significantly elevated the expression of Ets. These results suggest that Cic may negatively control dendrite growth through Ets, which was confirmed by ShRNA knockdown of either Etv4 or Etv5 abolishing the phenotype of Cic knockdown in cultured neurons. Taken together, our results suggest that Cic inhibits dendritic morphogenesis and the growth of dendritic spines through Ets.

Gliomas are the most commonly occurring primary malignant brain tumors in the central nervous system of adults. They are rarely curable and the prognosis for high grade gliomas is generally poor. Recently, long non‐coding RNA (lncRNA) human ovarian cancer‐specific transcript 2 (HOST2) has been reported to be expressed at high levels in human ovarian cancer, involving tumorigenesis. However, little is still known about whether and how HOST2 regulates glioma development and progression. Therefore, this study aims to investigate the role of HOST2 in human glioma cells. Reverse transcription quantitative real‐time polymerase chain reaction (RT‐qPCR) was used to determine the expression of lncRNA HOST2, let‐7b, and PBX3 in human glioma cells. Cultured human glioma cells were treated with siRNA (si)‐lncRNA HOST2, let‐7b mimic, si‐lncRNA HOST2 + let‐7b inhibitor, and si‐PBX3. Parameters including cell viability, colony formation, cell migration, and cell invasion were detected by cell counting kit‐8 assay, colony formation assay, scratch test, and Transwell assay respectively to determine the effects of down‐regulated HOST2 on glioma cells. Tumor formation in nude mice was evaluated by subcutaneous tumor formation experiment. Results showed that HOST2 and PBX3 were highly expressed in glioma tissue whereas let‐7b was expressed at much lower levels. In response to treatment with si‐lncRNA HOST2, si‐PBX3, and let‐7b mimic, glioma cell lines exhibited decreased cell viability, suppressed cell migration, invasion, and reduced colony formation of glioma cells. This was accompanied by an attenuated tumor formation with smaller volume and weight in nude mice, suggesting that down‐regulated HOST2 could inhibit the tumorigenicity of glioma cells. Lastly, we found that lncRNA HOST2 was highly expressed in glioma tissues and its down‐regulation could inhibit the growth and invasion of glioma cells. © 2018 IUBMB Life, 71(1):93–104, 2019