Background:Long non-coding RNAs are important regulators in cancer biology and function either as tumor suppressors or as oncogenes.Their dysregulation has been closely associated with tumorigenesis.LINC00265 is upreg...Background:Long non-coding RNAs are important regulators in cancer biology and function either as tumor suppressors or as oncogenes.Their dysregulation has been closely associated with tumorigenesis.LINC00265 is upregulated in lung adenocarcinoma and is a prognostic biomarker of this cancer.However,the mechanism underlying its function in cancer progression remains poorly understood.Methods:Here,the regulatory role of LINC00265 in lung adenocarcinoma was examined using lung cancer cell lines,clinical samples,and xenografts.Results:We found that high levels of LINC00265 expression were associated with shorter overall survival rate of patients,whereas knockdown of LINC00265 inhibited proliferation of cancer cell lines and tumor growth in xenografts.Western blot andflow cytometry analyses indicated that silencing of LINC00265 induced autophagy and apoptosis.Moreover,we showed that LINC00265 interacted with and stabilized the transcriptional co-repressor Switch-independent 3a(SIN3A),which is a scaffold protein functioning either as a tumor repressor or as an oncogene in a context-dependent manner.Silencing of SIN3A also reduced proliferation of lung cancer cells,which was correlated with the induction of autophagy.These observations raise the possibility that LINC00265 functions to promote the oncogenic activity of SIN3A in lung adenocarcinoma.Conclusions:Ourfindings thus identify SIN3A as a LINC00265-associated protein and should help to understand the mechanism underlying LINC00265-mediated oncogenesis.展开更多
在室内导航定位中,射频识别(Radio Frequency Identification,RFID)技术具有信号穿透性强、成本低廉等诸多优点,能够有效代替GPS完成室内组合导航。针对室内惯性导航误差发散和滤波中噪声参数不确定的问题,提出了基于自适应卡尔曼滤波(A...在室内导航定位中,射频识别(Radio Frequency Identification,RFID)技术具有信号穿透性强、成本低廉等诸多优点,能够有效代替GPS完成室内组合导航。针对室内惯性导航误差发散和滤波中噪声参数不确定的问题,提出了基于自适应卡尔曼滤波(Adaptive Kalman Filtering,AKF)的RFID/SINS组合导航系统,通过RFID定位系统抑制惯性导航误差发散,并应用AKF将噪声参数与量测输出参数关联实现实时更新。对AKF和标准卡尔曼滤波(Kalman Filtering,KF)下的RFID/SINS组合导航系统进行了仿真和实验。结果表明,在AKF下组合导航系统平均定位误差降低了10%,位置稳定性提升了7.4%,定位误差保持在0.07 m左右。基于AKF的RFID/SINS组合导航系统能够满足室内高精度定位导航的需求。展开更多
基金supported in part by the National Natural Science Foundation of China(NSFC)(82073388 to SWM)the Natural Outstanding Youth Fund of Guangdong Province(2022B1515020090 to SWM)+1 种基金Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases(2022B1212030003 to SWM)the Affiliated Hospital of Guangdong Medical University Clinical Research Program(LCYJ2020B005 to SWM).
文摘Background:Long non-coding RNAs are important regulators in cancer biology and function either as tumor suppressors or as oncogenes.Their dysregulation has been closely associated with tumorigenesis.LINC00265 is upregulated in lung adenocarcinoma and is a prognostic biomarker of this cancer.However,the mechanism underlying its function in cancer progression remains poorly understood.Methods:Here,the regulatory role of LINC00265 in lung adenocarcinoma was examined using lung cancer cell lines,clinical samples,and xenografts.Results:We found that high levels of LINC00265 expression were associated with shorter overall survival rate of patients,whereas knockdown of LINC00265 inhibited proliferation of cancer cell lines and tumor growth in xenografts.Western blot andflow cytometry analyses indicated that silencing of LINC00265 induced autophagy and apoptosis.Moreover,we showed that LINC00265 interacted with and stabilized the transcriptional co-repressor Switch-independent 3a(SIN3A),which is a scaffold protein functioning either as a tumor repressor or as an oncogene in a context-dependent manner.Silencing of SIN3A also reduced proliferation of lung cancer cells,which was correlated with the induction of autophagy.These observations raise the possibility that LINC00265 functions to promote the oncogenic activity of SIN3A in lung adenocarcinoma.Conclusions:Ourfindings thus identify SIN3A as a LINC00265-associated protein and should help to understand the mechanism underlying LINC00265-mediated oncogenesis.
