scholarly journals MicroRNA‑524‑5p regulates the proliferation and invasion of HTR‑8/SVneo trophoblasts by targeting NUMB in the Notch signaling pathway

2021 ◽  
Vol 23 (6) ◽  
Author(s):  
Linmei Zheng ◽  
Jie Song ◽  
Rong Tang ◽  
Xiaoju Chen ◽  
Li Wang ◽  
...  
Author(s):  
Yanan Li ◽  
Guosheng Han ◽  
Weijie Min ◽  
Mengmeng Li ◽  
Maomao Wang ◽  
...  

IntroductionGlioblastoma is the most malignant astrocytoma, and its therapeutic effect is not ideal. Notch signaling pathway plays an important role in tumor proliferation and invasion. Whether small molecule drug AT13148 can affect glioblastoma by regulating Notch signaling pathway is the focus of this study.Material and methodsIn vitro, glioblastoma U87 cell line transfected with sh-ITGB1 (U87sh-ITGB1), U87 cell line transfected with oe-ITGB1 (U87oe-ITGB1) and control group were treated with a small molecular drug AT13148. RT-qPCR, western-blot and clone formation ability assays were used to detect the mRNA and protein expression of the ITGB1 and the key gene NOTCH1, as well as the proliferation of cancer cells. Therapeutic effects of AT13148 were examined in vivo using a nude mice model of U87 cells. After treatment with AT13148, volume of tumors were calculated, and RT-qPCR and western-blot were used to evaluate the mRNA and protein expression of the ITGB1 and NOTCH1.ResultsAT13148 inhibits the activity of U87 cells. Lentiviral transfection of sh-ITGB1 and oe-ITGB1 can interfere with the expression of ITGB1 in U87 cells. AT13148 could down-regulate both the expression of ITGB1 and NOTCH1. Moreover, AT13148 affects the cloning ability of U87 cells. AT13148 can also inhibit the proliferation of U87 cells. Furthermore, AT13148 inhibited the proliferation and invasion of transplanted tumors in vivo.ConclusionsThis study indicated that AT13148 could affect the expression of ITGB1 and NOTCH1, which also could be a potential potential anti-glioblastoma small molecule drug candidate in clinic medicine.


2013 ◽  
Vol 13 (9) ◽  
pp. 957-962 ◽  
Author(s):  
Yumei Li ◽  
Jia Ma ◽  
Xiujuan Qian ◽  
Qiong Wu ◽  
Jun Xia ◽  
...  

Author(s):  
Imran Khan ◽  
Sadaf Mahfooz ◽  
Mohd Saeed ◽  
Irfan Ahmad ◽  
Irfan A. Ansari

Background: Recently Notch signaling pathway has gained attention as a potential therapeutic target for chemotherapeutic intervention. However, the efficacy of previously known Notch inhibitors in colon cancer is still unclear. The purpose of this study was to investigate the effect of andrographolide on aberrantly activated Notch signaling in SW-480 cells in vitro. Methods: The cytostatic potential of andrographolide on SW-480 cells was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay, morphology assessment and colony formation assay. The apoptotic activity was evaluated by FITC Annexin V assay, 4′,6-diamidino-2-phenylindole (DAPI), Hoechst, Rhodamine 123 and Mito Tracker CMXRos staining. Scratch assay for migratory potential assessment. 7’-Dichlorodihydrofluorescein Diacetate (DCFH-DA) staining was used to evaluate the Reactive Oxygen Species (ROS) generation. Relative mRNA expression of Bax, Bcl2, NOTCH 1 and JAGGED 1 was estimated by Real-Time Quantitative Reverse Transcription PCR (qRT-PCR). Cell cycle phase distribution was evaluated Annexin V-FITC/PI staining. Results: MTT assay demonstrated dose and time dependent cytoxicity of andrographolide on SW-480 cells. It also inhibited the migratory and colony forming potential of SW-480 cells. Furthermore, andrographolide also showed disruption of mitochondrial membrane potential and induced apoptosis through nuclear condensation. Flow cytometric evaluation showed andrographolide enhanced early and late apoptotic cells and induced upregulation of proapoptotic (Bax and Bad) and downregulation of antiapoptotic Bcl2 in treated SW-480 cells. Andrographolide augmented intracellular ROS generation and induced G0/G1 phase cell cycle arrest in colon cancer SW480 cells. Furthermore, andrographolide repressed the Notch signaling by decreasing the expression of NOTCH 1 and JAGGED 1. Conclusion: Our findings suggested that andrographolide constraint the growth of SW-480 cells through the inhibition of Notch signaling pathway.


2021 ◽  
Vol 70 (3) ◽  
pp. 261-274
Author(s):  
Ricardo Cardoso Castro ◽  
Relber Aguiar Gonçales ◽  
Fabiana Albani Zambuzi ◽  
Fabiani Gai Frantz

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