scholarly journals Marine Carotenoid Fucoxanthin Possesses Anti-Metastasis Activity: Molecular Evidence

Marine Drugs ◽  
2019 ◽  
Vol 17 (6) ◽  
pp. 338 ◽  
Author(s):  
Sukant Garg ◽  
Sajal Afzal ◽  
Ahmed Elwakeel ◽  
Damini Sharma ◽  
Navaneethan Radhakrishnan ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Cell Phenotype ◽  
Molecular Evidence ◽  
Mechanistic Studies ◽  
Normal Cells ◽  
Therapy Regimen ◽  
Molecular Assays ◽  
Transcriptional Suppression ◽  
P53 Status

Fucoxanthin is commonly found in marine organisms; however, to date, it has been one of the scarcely explored natural compounds. We investigated its activities in human cancer cell culture-based viability, migration, and molecular assays, and found that it possesses strong anticancer and anti-metastatic activities that work irrespective of the p53 status of cancer cells. In our experiments, fucoxanthin caused the transcriptional suppression of mortalin. Cell phenotype-driven molecular analyses on control and treated cells demonstrated that fucoxanthin caused a decrease in hallmark proteins associated with cell proliferation, survival, and the metastatic spread of cancer cells at doses that were relatively safe to the normal cells. The data suggested that the cancer therapy regimen may benefit from the recruitment of fucoxanthin; hence, it warrants further attention for basic mechanistic studies as well as drug development.

scholarly journals N-ω-chloroacetyl-l-ornithine, a new competitive inhibitor of ornithine decarboxylase, induces selective growth inhibition and cytotoxicity on human cancer cells versus normal cells

2014 ◽  
Vol 30 (3) ◽  
pp. 345-353 ◽  
Author(s):  
Miriam Marlene Medina-Enríquez ◽  
Verónica Alcántara-Farfán ◽  
Leopoldo Aguilar-Faisal ◽  
José Guadalupe Trujillo-Ferrara ◽  
Lorena Rodríguez-Páez ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Cancer Cells ◽  
Ornithine Decarboxylase ◽  
Human Cancer ◽  
Competitive Inhibitor ◽  
Selective Growth ◽  
Normal Cells ◽  
Human Cancer Cells

scholarly journals Increased levels of superoxide and H2O2 mediate the differential susceptibility of cancer cells versus normal cells to glucose deprivation

2009 ◽  
Vol 418 (1) ◽  
pp. 29-37 ◽  
Author(s):  
Nùkhet Aykin-Burns ◽  
Iman M. Ahmad ◽  
Yueming Zhu ◽  
Larry W. Oberley ◽  
Douglas R. Spitz
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Human Cancer ◽  
Differential Susceptibility ◽  
Glucose Deprivation ◽  
Human Colon ◽  
Normal Cells ◽  
Ht29 Cells ◽  
And Oxidative Stress

Cancer cells, relative to normal cells, demonstrate increased sensitivity to glucose-deprivation-induced cytotoxicity. To determine whether oxidative stress mediated by O2•− and hydroperoxides contributed to the differential susceptibility of human epithelial cancer cells to glucose deprivation, the oxidation of DHE (dihydroethidine; for O2•−) and CDCFH2 [5- (and 6-)carboxy-2′,7′-dichlorodihydrofluorescein diacetate; for hydroperoxides] was measured in human colon and breast cancer cells (HT29, HCT116, SW480 and MB231) and compared with that in normal human cells [FHC cells, 33Co cells and HMECs (human mammary epithelial cells)]. Cancer cells showed significant increases in DHE (2–20-fold) and CDCFH2 (1.8–10-fold) oxidation, relative to normal cells, that were more pronounced in the presence of the mitochondrial electron-transport-chain blocker, antimycin A. Furthermore, HCT116 and MB231 cells were more susceptible to glucose-deprivation-induced cytotoxicity and oxidative stress, relative to 33Co cells and HMECs. HT29 cells were also more susceptible to 2DG (2-deoxyglucose)-induced cytotoxicity, relative to FHC cells. Overexpression of manganese SOD (superoxide dismutase) and mitochondrially targeted catalase significantly protected HCT116 and MB231 cells from glucose-deprivation-induced cytotoxicity and oxidative stress and also protected HT29 cells from 2DG-induced cytotoxicity. These results show that cancer cells (relative to normal cells) demonstrate increased steady-state levels of ROS (reactive oxygen species; i.e. O2•− and H2O2) that contribute to differential susceptibility to glucose-deprivation-induced cytotoxicity and oxidative stress. These studies support the hypotheses that cancer cells increase glucose metabolism to compensate for excess metabolic production of ROS and that inhibition of glucose and hydroperoxide metabolism may provide a biochemical target for selectively enhancing cytotoxicity and oxidative stress in human cancer cells.

Identification of Parasporin Genes in Vietnamese Isolates of Bacillus thuringiensis

2008 ◽  
Vol 63 (1-2) ◽  
pp. 139-143 ◽  
Author(s):  
Koichi Yasutake ◽  
Akiko Uemori ◽  
Ngo D. Binh ◽  
Eiichi Mizuki ◽  
Michio Ohba
Keyword(s):  
Bacillus Thuringiensis ◽  
Cancer Cells ◽  
Human Cancer ◽  
Nucleotide Sequence Analysis ◽  
Hep G2 ◽  
Normal Cells ◽  
Proteolytic Activation ◽  
Human Cancer Cells ◽  
Genes Encoding

Four genes encoding parasporins, cytotoxins preferentially killing human cancer cells in vitro, were isolated from four Vietnamese strains of Bacillus thuringiensis. Nucleotide sequence analysis revealed that: (1) three genes fall into the two known classes, ps1Aa and ps1Ab, and (2) another one belongs to ps1Ac, a novel gene class established in this study. Upon proteolytic activation, parasporal protein of the organism with ps1Ac exhibited strong cytocidal activity against human cancer cells, HeLa and Hep G2, but not to non-cancer normal cells, UtSMC and HC.

Magnetic nanoparticles: mechanistic studies on the cancer cell interaction

2016 ◽  
Vol 5 (5) ◽  
Author(s):  
Joe Antony Jacob ◽  
Jumah Masoud Mohammad Salmani ◽  
Baoan Chen
Keyword(s):  
Cell Death ◽  
Magnetic Nanoparticles ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Cell Interaction ◽  
Mechanistic Studies ◽  
Normal Cells ◽  
Different Types ◽  
Induction Of Apoptosis ◽  
Plausible Reason

AbstractMagnetic nanoparticles are renowned for their anticancer activity. Recent studies have elucidated that magnetic nanoparticles induce cytotoxicity by induction of apoptosis in cancer cells. The magnetic nanoparticles can also be biosynthesized, and this presents an added advantage along with the concept of limited toxicity to normal cells. This review focuses on the mechanistic studies performed on the anticancer activity of different types of magnetic nanoparticles. Apoptosis was shown to be the most plausible reason behind the cell death mediated by various types of magnetic nanoparticles.

scholarly journals Translatome-based classification reveals a dual metabolic dependency of a new tumor subtype of pancreatic cancer

2020 ◽  
Author(s):  
Sauyeun Shin ◽  
Remy Nicolle ◽  
Christine Jean ◽  
Remi Samain ◽  
Mira Ayadi ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Cancer Cells ◽  
Human Cancer ◽  
Functional Characterization ◽  
Mrna Translation ◽  
Ductal Adenocarcinoma ◽  
Synthesis Rate ◽  
Protein Synthesis Rate ◽  
Cell Phenotype ◽  
Tumor Subtype

ABSTRACTMolecular profiling of Pancreatic Ductal Adenocarcinoma (PDA), based on transcriptomic analyses, identifies two main prognostic subtypes (basal-like and classical), but does not allow personalized first-line treatment. To date, tumors have not been profiled based on protein synthesis rates, yet the step of mRNA translation is highly deregulated in both PDA cancer cells and their microenvironment. Using a collection of twenty-seven pancreatic Patient-Derived Xenografts (PDX), we performed genome-wide analysis of translated mRNA (translatome). Unsupervised bioinformatics analysis revealed a new tumor subtype harboring a low protein synthesis rate, but associated with a robust translation of mRNAs encoding effectors of the integrated stress response (ISR), including the transcription factor ATF4. Functional characterization of the “ISR-activated” human cancer cells revealed a high resistance to drugs, low autophagic capacities, and importantly, metabolic impairments in the serine synthesis and transsulfuration pathways. Overall, our study highlights the strength of translatomic profiling on PDA, which here revealed an unforeseen drug-resistant cancer cell phenotype, whose auxotrophy to both serine and cysteine may be amenable to targeted therapy.

scholarly journals Gene Expression Profile of the A549 Human Non-Small Cell Lung Carcinoma Cell Line following Treatment with the Seeds ofDescurainia sophia, a Potential Anticancer Drug

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Bu-Yeo Kim ◽  
Jun Lee ◽  
Sung Joon Park ◽  
Ok-Sun Bang ◽  
No Soo Kim
Keyword(s):  
Gene Expression ◽  
Cancer Cells ◽  
Human Cancer ◽  
Small Cell Lung Carcinoma ◽  
Ethanol Extract ◽  
Inhibitory Effect ◽  
Human Lung Cancer ◽  
Molecular Evidence ◽  
Cell Lung Carcinoma ◽  
Dose Dependent

Descurainia sophiahas been traditionally used in Korean medicine for treatment of diverse diseases and their symptoms, such as cough, asthma, and edema. Our previous results showed that ethanol extract of the seeds ofD. sophia(EEDS) has a potent cytotoxic effect on human cancer cells. In this study, we reveal the molecular events that are induced by EEDS treatment in A549 human lung cancer cells. The dose-dependent effect of EEDS on gene expression was measured via a microarray analysis. Gene ontology and pathway analyses were performed to identify functional involvement of genes regulated by EEDS. From gene expression analyses, two major dose-dependent patterns were observed after EEDS treatment. One pattern consisted of 1,680 downregulated genes primarily involved in metabolic processes (FDR < 0.01). The second pattern consisted of 1,673 upregulated genes primarily involved in signaling processes (FDR < 0.01). Pathway activity analyses revealed that the metabolism-related pathways and signaling-related pathways were regulated by the EEDS in dose-dependent and reciprocal manners. In conclusion, the identified biphasic regulatory mechanism involving activation of signaling pathways may provide molecular evidence to explain the inhibitory effect of EEDS on A549 cell growth.

Acrolein induces ribotoxic stress in human cancer cells regardless of p53 status

2018 ◽  
Vol 52 ◽  
pp. 265-271 ◽  
Author(s):  
Chun-Hao Huang ◽  
Yen-Ting Chen ◽  
Jing-Heng Lin ◽  
Hsiang-Tsui Wang
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
P53 Status
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