LAN ZHOU^1,#, QI ZHANG^2,#, BO TIAN^1,*, FENG YANG^1,*

BIOCELL, Vol.48, No.7, pp. 1081-1093, 2024, DOI:10.32604/biocell.2024.049878 - 03 July 2024

Abstract Background: Glioblastoma, a notably malignant tumor within the central nervous system, is distinguished by its aggressive behavior. Silvestrol, a robust inhibitor of the RNA helicase eukaryotic initiation factor 4A (eIF4A), has shown significant potential as an anticancer compound. Yet, the impact of silvestrol on glioblastoma, especially its molecular mechanisms, has not been fully elucidated. Methods: This investigation employed a variety of in vitro assays, such as cell counting kit-8 (CCK-8), clonogenic, 5-ethynyl-2′-deoxyuridine (EDU), wound healing, and flow cytometry, to evaluate cell cycle progression, apoptosis, cell viability, and migration. Western blot analysis was also performed to study… More >

Hui Li^*1, Huicheng Chen^†1, Haibin Wang^‡, Yilong Dong^†, Min Yin^†, Liang Zhang^§, Jia Wei^*

Oncology Research, Vol.26, No.4, pp. 557-563, 2018, DOI:10.3727/096504017X15000784459799

Abstract Hepatocellular carcinoma (HCC) is a disease with poor prognosis rates and ineffective therapeutic options. Previous studies have reported the involvement of mitogen-inducible gene 6 (MIG-6) as a negative regulator in tumor formation. MicroRNAs (miRNAs) play crucial roles in the development of different types of cancer. However, the underlying mechanisms of miRNAs in HCC are poorly understood. This study was aimed to investigate the role of miR-374a in HCC and its role in the regulation of expression of MIG-6. The results showed that MIG-6 overexpression significantly inhibited cell viability of HepG2 cells after 4 days posttransfection. More >

Xiaoyan Wang^*, Yongguang Xu^*, Xinlei Chen^*, Jianmin Xiao^†

Oncology Research, Vol.26, No.3, pp. 495-502, 2018, DOI:10.3727/096504017X14982578608217

Abstract This study aimed to investigate the effect of dexmedetomidine (DEX) on osteosarcoma (OS) cell line MG63 and to explore the possible relationship between DEX and miR-520-3p in OS. The results showed that DEX could upregulate miR-520-3p, which directly targeted AKT1. Additionally, miR-520-3p also inhibited MG63 cell proliferation and migration, promoted apoptosis, and suppressed protein expressions of AKT, p-AKT, p-mTOR, and p-ERK1/2. DEX can inhibit OS cell proliferation and migration and promote apoptosis by upregulating the expression level of miR-520a-3p. DEX may serve as a potential therapeutic agent in OS treatment, and miR-520a-3p may be a More >

P. Muddasani¹, H-J. Im¹

Molecular & Cellular Biomechanics, Vol.3, No.4, pp. 159-161, 2006, DOI:10.32604/mcb.2006.003.159

Abstract This article has no abstract. More >