LINNA TAN^1,2, YUYONG TAN^1,2, DELIANG LIU^1,2,*

BIOCELL, Vol.44, No.4, pp. 535-543, 2020, DOI:10.32604/biocell.2020.09171 - 24 December 2020

Abstract ULK1 (unc-51 like autophagy activating kinase 1), a mammalian serine/threonine kinase, is a key component of autophagy initiation complex and helps to induce all types of autophagy. Canonical autophagy is a process in which, through the interactions of a series of autophagy-related proteins, damaged organelles or misfolded proteins are engulfed by autophagosomes and then merged with lysosomes to be degraded. Thus, canonical autophagy is an important constituent part of the cellular “quality control.” Besides, accumulating evidence indicates that ULK1 exerts autophagy-independent effects in a cell-specific manner. For example, ULK1 facilitates neurite elongation through the regulation More >

MASOUMEH OGHABI^1,2, AVA SAFAROGHLI-AZAR^1,2, ATIEH POURBAGHERI-SIGAROODI^1,2, MOHAMMAD SAYYADI³, MOHSEN HAMIDPOUR¹, MOHAMMAD HOSSEIN MOHAMMADI¹, DAVOOD BASHASH^1,*

BIOCELL, Vol.44, No.2, pp. 183-192, 2020, DOI:10.32604/biocell.2020.08880 - 27 May 2020

Abstract Pathogenesis of chronic myeloid leukemia (CML) has mostly been studied with regard to the oncogenic role of BCR/ABL fusion; however, recent disclosures have declared that the challenges with the treatment of CML patients would not be resolved until the role of other aberrancies is ignored. Given the involvement of cyclin-dependent kinases (CDKs) in the pathogenesis of CML, the present study aimed to investigate the effects of a multi-CDK inhibitor AT7519 on BCR/ABL-harboring CML-derived K562 cells. Our results showed that AT7519 effectively reduced the survival of K562 and induced its anti-proliferative effect through the induction of… More >

Sara Youssry¹, Maher A. Kamel²

European Cytokine Network, Vol.30, No.4, pp. 135-143, 2019, DOI:10.1684/ecn.2019.0437

Abstract Background and aims: Chronic hepatic inflammation is an important pathogenic mediator of nonalcoholic fatty liver disease (NAFLD) that contributes to disease severity. It is commonly suggested that autophagy dysfunction may be an underlying cause of nonalcoholic fatty liver disease. However, the exact role of autophagy in lipid metabolism remains controversial. There has been a growing interest in the role of folate supplementation for the treatment and/or prevention of NAFLD. We aimed in this study to investigate the effects of different doses of folate supplementation on several immune markers and autophagy trying to explore the complex… More >

Hyun-Jung Moon,1 So-Young Park,1 Su-Hoon Lee, Chi-Dug Kang, Sun-Hee Kim

Oncology Research, Vol.27, No.7, pp. 835-847, 2019, DOI:10.3727/096504019X15517850319579

Abstract Recently, novel therapeutic strategies have been designed with the aim of killing cancer stem-like cells (CSCs), and considerable interest has been generated in the development of specific therapies that target stemnessrelated marker of CSCs. In this study, nonsteroidal anti-inflammatory drugs (NSAIDs) significantly potentiated Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG)-mediated cytotoxicity through apoptotic and autophagic cell death induction, but COX-2-inhibitory function was not required for NSAIDinduced autophagy in CD44-overexpressing human chronic myeloid leukemia K562 (CD44^highK562) cells. Importantly, we found that treatment with NSAIDs resulted in a dose-dependent increase in LC3-II level and decrease in p62 level and simultaneous reduction… More >

Qing Wei¹, Rui Zhu¹, Junying Zhu, Rongping Zhao, Min Li

Oncology Research, Vol.27, No.7, pp. 827-834, 2019, DOI:10.3727/096504018X15462920753012

Abstract Emerging evidence suggests that 17β-estradiol (E2) and estrogen receptor (ER) signaling are protective against hepatocellular carcinoma (HCC). In our previous study, we showed that E2 suppressed the carcinogenesis and progression of HCC by targeting NLRP3 inflammasome activation, whereas the molecular mechanism by which the NLRP3 inflammasome initiated cancer cell death was not elucidated. The present study aimed to investigate the effect of NLRP3 inflammasome activation on cell death pathways and autophagy of HCC cells. First, we observed an increasing mortality in E2-treated HCC cells, and then apoptotic and pyroptotic cell death were both detected. The… More >

Lu Guo^*, Duankai Chen^†, Xing Yin^‡, Qingfeng Shu^†

Oncology Research, Vol.27, No.4, pp. 487-494, 2019, DOI:10.3727/096504018X15323394008784

Abstract GSK-3 is a versatile protein kinase participating in many reactions. Currently, there is insufficient understanding of its influence on breast cancer (BC). In order to explore its influence on migration and invasion in BC, we investigated its expression in BC cell lines using qRT-PCR and Western blot (WB). Immunohistochemistry (IHC) was used to examine the potential of GSK-3 to predict clinical outcome in BC patients. GSK-3 knockdown was achieved using an shRNA plasmid vector in T47D cells. Our research explored the biological reactions and downstream pathways involved. We found excessive GSK-3 expression in BC tissues,… More >

Heya QIAN^1,§, Yan YAN^2,§, Zhengjie SHEN¹, Lixian XU¹, Yun ZUO¹, Tao ZHU^3,*, Yanan CHEN^1,*

BIOCELL, Vol.43, No.4, pp. 321-326, 2019, DOI:10.32604/biocell.2019.07992

Abstract The present study aims to explore the effects of p53 and its target gene Rap2B on the autophagy of U2OS cells. U2OS cells were treated with siRNA against p53, Rap2B, and PLCε. Relative expressions of p53, Rap2B, and PLCε were determined using quantitative polymerase chain reaction (qPCR) and Western blotting, respectively. Levels of IP3 in the cells were determined using Enzyme-linked Immunosorbent Assay (ELISA). Levels of Ca²⁺ were detected using Flow cytometry. Fluorescence microscopy was used to observe the autophagy of cells. Knockdown of p53 significantly decreased the expressions of Rap2B protein. Additionally, knockdown of p53 More >

Xiumei Guan¹, Hong Li¹, Xin Li¹, Xiaoyun Zhang¹, Xiaodong Cui¹, Hong Yan¹, Yuzhen Wang², Shunmei Liu², Min Cheng^3,*

Molecular & Cellular Biomechanics, Vol.16, Suppl.1, pp. 91-91, 2019, DOI:10.32604/mcb.2019.05755

Abstract Aims: Endothelial progenitor cells (EPCs) play an important role in postnatal angiogenesis and neovascularization. Previous studies have revealed shear stress could accelerate EPC proliferation, differentiation, migration and so on, which contribute to postnatal angiogenesis and neovascularization. Moreover, some studies indicate that autophagy actively participates angiogenesis by affecting EPC migration and differentiation. Here, we try to elucidate the possible roles of autophagy of EPC differentiation induced by shear stress. Methods and Results: EPCs were exposed to shear stress (12 dyne/cm²). And then the expression of autophagy markers, such as LC3Ⅱ/Ⅰ, P62andATG5, were analyzed using Western blot. The results… More >

Ji SHI; Peixin SUN, Ye ZHANG, Bing YAO, Haozhe PIAO

BIOCELL, Vol.43, No.3, pp. 119-128, 2019, DOI:10.32604/biocell.2019.07577

Abstract Glioma is the most common primary malignant brain tumor with a poor survival rate. In recent years, no significant progress has been made in the treatment of gliomas in contrast to the development of improved diagnosis via molecular typing. Newcastle disease virus (NDV), a negative-stranded RNA virus that exhibits oncolytic activity, has been investigated for its capacity to elicit antitumor activity in many types of cancers, including glioma. Therefore, application of oncolytic viruses, such as NDV, as a new treatment strategy to specifically target aberrant signaling in glioblastomas has brought new hope. For many years, More >

Peizhen Yang^*, Dezhong Sun^*, Fei Jiang^†

Oncology Research, Vol.26, No.6, pp. 941-948, 2018, DOI:10.3727/096504018X15149775533331

Abstract Ailanthone (AIL) is a quassinoid isolated from the traditional Chinese medicinal herb Ailanthus altissima. The antitumor activities of AIL have been reported in several cancers. The purpose of the present study was to explore the effect of AIL on vestibular schwannomas (VSs). Various concentrations of AIL (0–1 µM) were used to treat human primary VS cells, and then cell viability, proliferation, apoptosis, and autophagy were assessed. Expression of miR-21 in VS cells was altered by miRNA transfection. The functional actions of AIL on miR-21 dysregulated cells were also assessed. AIL significantly reduced the viability of VS… More >