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  • Open Access

    REVIEW

    Review on marine collagen peptides induce cancer cell apoptosis, necrosis, and autophagy by reducing oxidized free radicals

    YINGHUA LUO1,#, YU ZHANG2,#, TONG ZHANG2,#, YANNAN LI2, HUI XUE2, JINGLONG CAO2, WENSHUANG HOU2, JIAN LIU2, YUHE CUI2, TING XU2, CHENGHAO JIN2,3,*

    BIOCELL, Vol.47, No.5, pp. 965-975, 2023, DOI:10.32604/biocell.2023.027729

    Abstract Marine collagen peptides (MCPs) are natural products prepared by hydrolyzing marine collagen protein through a variety of chemical methods or enzymes. MCPs have a range of structures and biological activities and are widely present in marine species. MCPs also have a small molecular weight, are easily modified, and absorbed by the body. These properties have attracted great interest from researchers studying antioxidant, anti-tumor, and anti-aging activities. MCPs of specific molecular weights have significant anti-tumor activity and no toxic side effects. Thus, MCPs have the potential use as anti-cancer adjuvant drugs. Free radicals produced by oxidation are closely related to human… More >

  • Open Access

    ARTICLE

    Vitamin B3 inhibits apoptosis and promotes autophagy of islet β cells under high glucose stress

    YU ZHANG1,2, XI’AN ZHOU1,2, CHUNYAN ZHANG1,2, DENGNI LAI5, DONGBO LIU1,3,4, YANYANG WU1,2,3,4,*

    BIOCELL, Vol.47, No.4, pp. 859-868, 2023, DOI:10.32604/biocell.2023.026429

    Abstract Background: Hyperglycemia is a typical symptom of diabetes. High glucose induces apoptosis of islet β cells. While autophagy functions in cytoprotection and autophagic cell death. The interaction between autophagy and apoptosis is important in the modulation of the function of islet β cells. Vitamin B3 can induce autophagy and inhibit islet β apoptosis.Method: The mechanism of vitamin B3-mediated protective effect on the function of islet β cells was explored by the method of western blot, immunofluorescence and flow cytometry.Results: In the present study, high glucose stress increased the apoptosis rate, while vitamin B3 reduced the apoptosis rate. The effect of… More >

  • Open Access

    ARTICLE

    SPINK1 contributes to proliferation and clonal formation of HT29 cells through Beclin1 associated enhanced autophagy

    NA HU1,2,#, SHIQING ZHANG2,3,#, AQUAN JIN2, LIANYING GUO2, ZHENYUN QU2, JUN WANG2,*

    Oncology Research, Vol.30, No.2, pp. 89-97, 2022, DOI:10.32604/or.2022.027058

    Abstract We aimed to explore the molecular mechanism that were involved in SPINK1-induced proliferation and clonogenic survival of human colorectal carcinoma (CRC) HT29 cells. Initially, we generated HT29 cells either permanently silencing or overexpressing SPINK1 protein. The results showed that SPINK1 overexpression (OE) significantly stimulated the proliferation and clonal formation of HT29 cells at the varied time points. Secondly, we found SPINK1 OE enhanced the ratio of LC3II/LC3I and the level of autophagy-related gene 5 (ATG5), whereas SPINK1 knockdown (Kd) reversed the above outcome under normal culturing and/or fasting condition in the cells, indicating its role in autophagy enhancement. Moreover, LC3-GFP-transfected… More >

  • Open Access

    REVIEW

    Research progress of protein phosphatase 2A in cellular autophagy

    HONGMEI WU#, DI LI#, YUANYUAN HUANG, RUYUAN LIU, XIAONIAN ZHU*

    BIOCELL, Vol.47, No.3, pp. 485-491, 2023, DOI:10.32604/biocell.2023.026049

    Abstract Autophagy is an important metabolic process. It facilitates the recycling of intracellular substances by removing, degrading, and recycling damaged organelles, proteins, and lipids in lysosomal vacuoles and plays an important role in maintaining cellular homeostasis. Protein phosphatase 2A (PP2A) is a key serine/threonine phosphatase and one of the main cell cycle regulatory enzymes. As PP2A activity is essential for the cell, dysfunction or dysregulation of PP2A can affect various physiological processes, including autophagy. Here, we review the autophagy-related factors that target PP2A in different diseases, such as breast cancer, colorectal cancer, liver cancer, and Alzheimer’s disease, to maintain cell homeostasis… More >

  • Open Access

    REVIEW

    Is autophagy induction by PARP inhibitors a target for therapeutic benefit?

    AHMED M. ELSHAZLY1,2, TUONG VI V. NGUYEN1, DAVID A. GEWIRTZ1,*

    Oncology Research, Vol.30, No.1, pp. 1-12, 2022, DOI:10.32604/or.2022.026459

    Abstract PARP inhibitors have proven to be effective in conjunction with conventional therapeutics in the treatment of various solid as well as hematologic malignancies, particularly when the tumors are deficient in DNA repair pathways. However, as the case with other chemotherapeutic agents, their effectiveness is often compromised by the development of resistance. PARP inhibitors have consistently been reported to promote autophagy, a process that maintains cellular homeostasis and acts as an energy source by the degradation and reutilization of damaged subcellular organelles and proteins. Autophagy can exhibit different functional properties, the most prominent being cytoprotective. In addition, both cytotoxic and non-protective… More >

  • Open Access

    REVIEW

    The role of 5′-adenosine monophosphate-activated protein kinase (AMPK) in skeletal muscle atrophy

    KAI DANG, HAFIZ MUHAMMAD UMER FAROOQ, YUAN GAO, XIAONI DENG, AIRONG QIAN*

    BIOCELL, Vol.47, No.2, pp. 269-281, 2023, DOI:10.32604/biocell.2023.023766

    Abstract As a key coordinator of metabolism, AMP-activated protein kinase (AMPK) is vitally involved in skeletal muscle maintenance. AMPK exerts its cellular effects through its function as a serine/threonine protein kinase by regulating many downstream targets and plays important roles in the development and growth of skeletal muscle. AMPK is activated by phosphorylation and exerts its function as a kinase in many processes, including synthesis and degradation of proteins, mitochondrial biogenesis, glucose uptake, and fatty acid and cholesterol metabolism. Skeletal muscle atrophy is a result of various diseases or disorders and is characterized by a decrease in muscle mass. The pathogenesis… More >

  • Open Access

    ARTICLE

    Nonsteroidal Anti-inflammatory Drugs Sensitize CD44-Overexpressing Cancer Cells to Hsp90 Inhibitor Through Autophagy Activation

    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 (CD44highK562) 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 in multiple stemness-related markers… More >

  • Open Access

    ARTICLE

    E2-Induced Activation of the NLRP3 Inflammasome Triggers Pyroptosis and Inhibits Autophagy in HCC Cells

    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 mortality of HCC cells was… More >

  • Open Access

    ARTICLE

    GSK-3b Promotes Cell Migration and Inhibits Autophagy by Mediating the AMPK Pathway in Breast Cancer

    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, which was correlated with worse… More >

  • Open Access

    ERRATUM

    Inhibition of Beclin-1-Mediated Autophagy by MicroRNA-17-5p Enhanced the Radiosensitivity of Glioma Cells

    Weichen Hou*, Lei Song, Yang Zhao*, Qun Liu*, Shuyan Zhang

    Oncology Research, Vol.28, No.7-8, pp. 815-818, 2020, DOI:10.3727/096504021X16240202939988

    Abstract The role of miRNAs in the radiosensitivity of glioma cells and the underlying mechanism is still far from clear. In the present study, we detected six downregulated and seven upregulated miRNAs in the serum after radiotherapy compared with paired serum samples before radiotherapy via miRNA panel PCR. Among these, miR-17-5p was highly reduced (fold change = −4.21). Further, we validated the levels of miR-17-5p in all serum samples with qRT-PCR. In addition, statistical analysis suggested that a reduced miR-17-5P level was positively associated with advanced clinical stage of glioma, incidence of relapse, and tumor differentiation. Moreover, we provided evidence that… More >

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