• HONG WANG

      Articles written in Journal of Biosciences

    • Long non-coding RNA HOTAIR regulates proliferation and invasion via activating Notch signalling pathway in retinoblastoma

      CHANGXIA DONG SHAOYI LIU YONGBIN LV CHUNPING ZHANG HEYING GAO LIXIA TAN HONG WANG

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      Retinoblastoma is the most frequently occurring tumour in the eyes in early childhood. Novel targets that areimportant for the diagnosis or treatment of retinoblastoma could be valuable in increasing the survival rate of patientsaffected by this disease. Long non-coding RNAs (lncRNAs) are a recently discovered type of RNAs with no proteincodingfunction; yet it has become increasingly clear that lncRNAs are responsible for important gene regulatoryfunctions in various diseases. In this study, the expression of lncRNA HOTAIR was measured by qRT-PCR, andHOTAIR expression was found to be significantly upregulated in human retinoblastomas tissues as compared with thatin paracancerous tissues. Knockdown of HOTAIR restricted the proliferation and invasion of the more invasiveretinoblastoma Y79 cells, and led to G0/G1 arrest, possibly through inhibiting phospho-RB1, RB1 and CCNE.Furthermore, we found that the Notch signalling pathway was activated abnormally in retinoblastoma cell lines, whileknockdown of HOTAIR attenuated the endogenous Notch signalling pathway in vitro and in vivo. In addition,knockdown of HOTAIR could inhibit the tumour progression in a xenograft model of retinoblastoma. In summary,our findings indicate that HOTAIR may play important roles in retinoblastoma progression via Notch pathway.HOTAIR has the potential to enhance the development of novel targeted diagnostic and therapeutic approaches forretinoblastoma.

    • Deubiquitylation and stabilization of Acf7 by ubiquitin carboxylterminal hydrolase 14 (USP14) is critical for NSCLC migration

      GUOBEI YAN NA LIU JUNHUA WANG JUN TIAN HONGBIN LIU SUPING LI WENCHAO LIU XIAOLIANG LI KAI LI HONG WANG

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      The ubiquitin–proteasome system is an essential regulator of Acf7, which serves as a key effector for themaintenance of the EMT program and migration. However, the precise mechanism for the deubiquitination ofAcf7 is still not fully understood. Using a proteomic approach, we identified ubiquitin-specific peptidase 14(USP14) as an Acf7-associated deubiquitinase. Our findings show that there was an interaction between USP14and Acf7. The expression of USP14 and Acf7 were elevated in lung cancer tissues compared to adjacentnormal cells. Employing the overexpression of USP14 and the USP14 knockdown assay indicated that USP14can greatly increase the steady-state levels of Acf7 by inhibiting the degradation of Acf7 through the ubiquitin–proteasome pathway. Here we identified USP14 as a deubiquitinating enzyme that regulated Acf7 ubiquitinationand protein levels. Moreover, knockdown of USP14 inhibited cell migration, however, overexpressionof wild-type USP14 but not USP14 mutants promoted cell migration. Together, these results suggest thatUSP14 plays an important role in the NSCLC migration through modulating Acf7 stability.

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