Chemical Biology & Drug Design
·
2023
·Vol. 102
·期 1
·101-114
·
IF 3
Meiya Mao,Xiaojiao Zheng,Yuehua Sheng,Jinghan Chai,Huiqing Ding
Evodiamine (EVO) has been demonstrated to promote apoptosis of ovarian cancer cells, and upregulate miR-152-3p level in colorectal cancer. Here, we explore part of the network mechanism of EVO and miR-152-3p in ovarian cancer. The bioinformatics website, dual luciferase reporter assay, and quantitative real-time polymerase chain reaction were applied to analyze the network among EVO, lncRNA, miR-152-3p, and mRNA. The effect and mechanism of EVO on ovarian cancer cells were determined using cell counting kit-8, flow cytometry, TUNEL, Western blot, and rescue experiments. As a result, EVO dose-dependently attenuated cell viability, induced G2/M phase arrest and apoptosis, promoted miR-152-3p level (4.5- or 2-fold changes), and inhibited expressions of NEAT1 (0.225- or 0.367-fold changes), CDK8 (0.625- or 0.571-fold changes), and CDK19 (0.25- or 0.147-fold changes) in OVCAR-3 and SKOV-3 cells. In addition, EVO decreased Bcl-2 expression, but increased the expressions of Bax and c-caspase-3. NEAT1 targeted miR-152-3p which bound to CDK19. The impacts of EVO on cell viability, cycle, apoptosis, and apoptosis-related proteins were partially reversed by miR-152-3p inhibitor, NEAT1 overexpression, or CDK19 overexpression. Furthermore, miR-152-3p mimic offset the effects of NEAT1 or CDK19 overexpression. The role of NEAT1 overexpression in the biological phenotype of ovarian cancer cells was counteracted by shCDK19. In conclusion, EVO attenuates ovarian cancer cell progression via the NEAT1-miR-152-3p-CDK19 axis.
研究领域:
肿瘤学
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分子生物学
·
药理学
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产品关联
DOI
PubMed
高影响因子
HUMAN GENE THERAPY
·
2020
·
IF 4.51
Kaihua Zhai,Boyu Liu,Lin Gao
Long-noncoding RNA taurine upregulated gene 1 (TUG1) participates in nervous system diseases, but its function in Parkinson's disease (PD) remains unclear. This study explored the function and mechanism of TUG1 in PD. A PD model was constructed using SH-SY5Y cells induced by 1-methyl-4-phenylpyridinium (MPP+) in vitro and mice treated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in vivo. The expressions of TUG1, miR-152-3p, phosphatase and tensin homologue (PTEN), tyrosine hydroxylase (TH), and Bcl-2, and cleaved caspase-3 expressions were determined by quantitative reverse transcription-PCR and Western blotting. The viability, apoptosis, reactive oxygen species, and release of inflammatory factors from SH-SY5Y cells and substantia nigra tissues were detected by commercial kits. The interaction between TUG1 and miR-152-3p was analyzed by dual-luciferase reporter assay. Hematoxylin/eosin and immunohistochemical staining was performed for assessing the pathological damage and proportion of TH-positive cells. In PD cell model and mice model, TUG1 expression was upregulated and that of miR-152-3p was downregulated. Further research showed that TUG1 sponged and regulated miR-152-3p expression. Silencing of TUG1 not only protected SH-SY5Y cells against cell apoptosis, oxidative stress, and neuroinflammation in vitro, pathological damage and neuroinflammation in vivo, but also suppressed the expressions of PTEN and cleaved caspase-3, and increased the expressions of TH and Bcl-2 in MPP+-treated SH-SY5Y cells. However, the protective role of siTUG1 in SH-SY5Y cells was significantly inhibited by the miR-152-3p inhibitor. Thus, knocking down TUG1 might have a protective effect on PD through the miR-152-3p/PTEN pathway.
研究领域:
神经科学
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分子生物学
·
病理学
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DOI
PubMed
高影响因子
NEW JOURNAL OF CHEMISTRY
·
2025
·
IF 2.5
Jingwen Zhu,Xia Zong,Taijing Xu,Ying Chen,Xinjue Dai,Xiaowei Cao,Changhua Lu
Early detection of biomarkers has a crucial role in preventing blindness caused by diabetic retinopathy (DR). In this work, we developed a rapid, highly sensitive method for the simultaneous detection of DR-related biomarkers (miR-21 and miR-152) based on an Au nano-hexagon (AuNHs) integrated microarray chip combined with a competitive recognition strategy. The nucleic acid aptamer-modified AuNHs array served as capture substrate, while Au nano-trisoctahedrons (AuNTs) with complementary strands of nucleic acid aptamers mounted on their surface and Raman signaling molecules served as SERS probes (AuNTs@4-MBA@H1 and AuNTs@DTNB@H2). SERS probes carrying Raman signaling molecules (4-MBA and DTNB) were displaced by the target miRNAs in the experiments because they had a higher binding affinity to nucleic acid aptamers than their structural analogs (H1 and H2). This approach led to a notable decrease in the Raman signal. The competitive recognition strategy was straightforward and useful, and required only a one-step dropwise reaction to detect both miRNAs simultaneously and effectively. The microarray chip designed accordingly had the advantages of sensitive, rapid and high-throughput detection, and the detection time was only 8 min. The limits of detection (LOD) for miR-21 and miR-152 were as low as 2.76 × 10−14 M and 1.94 × 10−14 M, respectively. The utility of the method in complex systems was verified by detecting miRNAs in the serum of DR rats, and the accuracy of the method was verified against the detection results of a RT-qPCR method. This method provides a new idea and manner for the detection of miRNAs in serum, which is crucial for the early diagnosis of DR.
研究领域:
生物医学工程
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分子诊断学
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纳米技术
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DOI
高影响因子
EXPERIMENTAL NEUROLOGY
·
2026
·
IF 4.8
Junli Xiao,Ming Wang,Haiyan Zuo,WeiChen Yan
Objective Intracerebral hemorrhage (ICH) is a fatal cerebrovascular disease. This study explored the intrinsic relationship between ICH and lncRNA CRNDE. Methods Injecting the lentiviral interference vector (sh-CRNDE) into the ICH mice (induced by collagenase). Subsequently, the neurological deficits were evaluated through Garcia scoring, the corner turn test, and the water maze test. The levels of CRNDE and inflammatory factors in the brain tissue were detected by RT-qPCR and ELISA, respectively. In vitro experiments, microglia and neuronal cells were respectively cultured with hemoglobin and Hemin. Subsequently, the level of M1 polarization markers was detected by RT-qPCR. In neuronal cells, the proliferation activity was evaluated by CCK-8. The apoptosis level was comprehensively assessed based on the results of flow cytometry and the level of LDH. Finally, the effects of inhibiting the CRNDE/miR-152-3p axis on ROCK1 and the phenotype of ICH were re-verified in animal models and cell models. Results In ICH mice, inhibition of CRNDE prevented the neurological deficits and neuroinflammation. Blocking CRNDE also significantly alleviated the M1 polarization of microglia and the apoptosis of neuronal cells. CRNDE sponges miR-152-3p through the ceRNA mechanism and regulates ROCK1. Inhibition of miR-152-3p or overexpression of ROCK1 weakens the inhibitory effect of sh-CRNDE on neurological deficits, M1 polarization, and the apoptosis of neurons. Moreover, in cell models, inhibition of ROCK1 showed the same protective effect as CRNDE downregulation. Conclusion In ICH, CRNDE upregulates ROCK1 by adsorbing miR-152-3p. This regulatory axis exacerbates neuroinflammation and neurofunctional disorders.
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PubMed
高影响因子
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