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941.
Jia Chunhua Yu Xiaojing Zhang Min Liu Zhiguang Zou Peng Ma Jun Xu Yachun 《Journal of Plant Growth Regulation》2020,39(2):631-640
Journal of Plant Growth Regulation - The growth and development of cold-season plants are susceptible to high temperature. Melatonin is a plant growth regulator with potential to improve plant... 相似文献
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Shan Pan Jun Leng Xinzhou Deng Honggang Ruan Lu Zhou Muhammad Jamal Ruijing Xiao Jie Xiong Qian Yin Yingjie Wu Meng Wang Wen Yuan Liang Shao Qiuping Zhang 《Journal of cellular biochemistry》2020,121(1):574-586
The NAD-dependent deacetylase Sirtuin 1 (SIRT1) plays a vital role in leukemogenesis. Nicotinamide (NAM) is the principal NAD+ precursor and a noncompetitive inhibitor of SIRT1. In our study, we showed that NAM enhanced the sensitivity of chronic myeloid leukemia (CML) to doxorubicin (DOX) via SIRT1. We found that SIRT1 high expression in CML patients was associated with disease progression and drug resistance. Exogenous NAM efficiently repressed the deacetylation activity of SIRT1 and induced the apoptosis of DOX-resistant K562 cells (K562R) in a dose-dependent manner. Notably, the combination of NAM and DOX significantly inhibited tumor cell proliferation and induced cell apoptosis. The knockdown of SIRT1 in K562R cells enhanced NAM+DOX-induced apoptosis. SIRT1 rescue in K562R reduced the NAM+DOX-induced apoptosis. Mechanistically, the combinatory treatment significantly increased the cleavage of caspase-3 and PARP in K562R in vitro and in vivo. These results suggest the potential role of NAM in increasing the sensitivity of CML to DOX via the inhibition of SIRT1. 相似文献
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Neurochemical Research - Parkinson’s disease (PD) is a prevalent age-related neurodegenerative disease which is modulated by various molecules, including long non-coding RNAs (lncRNAs).... 相似文献
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Lifeng Wang Yanbo Zhong Baohua Yang Yunheng Zhu Xiuxiang Zhu Ziyin Xia Jun Xu Ling Xu 《Journal of cellular biochemistry》2020,121(3):2500-2509
Accepted as a malignant tumor worldwide, cervical cancer (CC) has attracted much attention for its high incidence and mortality rates. Previous studies have elucidated the critical regulatory function that long noncoding RNAs (lncRNAs) exert on the tumorigenesis and progression of diverse tumors. Although multiple investigations have depicted that LINC00958 has a great impact on the complex biological process of many cancers, knowledge concerning the regulatory role of LINC00958 in CC remains limited and needs to be further explored. In our study, LINC00958 expression was evidently overexpressed in CC tissues and cells. Besides this, LINC00958 negatively regulated miR-625-5p expression and was verified to bind with miR-625-5p in CC. Subsequently, it was testified by a series of experiments that LINC00958 promotes CC cell proliferation and metastasis by sponging miR-625-5p. Furthermore, the leucine-rich repeat containing the eight family member E (LRRC8E) could bind with miR-625-5p, and its expression was negatively modulated by miR-625-5p, whereas positively regulated by LINC00958 in CC. Final rescue assays verified the effects of LINC0095/LRRC8E interaction and miR-625-5p/LRRC8E interaction on CC cell proliferation and metastasis. Collectively, LINC00958 facilitates CC cell proliferation and metastasis via the miR-625-5p/LRRC8E axis. 相似文献
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