Cationic liposomes as efficient nanocarriers for the drug delivery of an anticancer cholesterol-based ruthenium complex

2015 ◽  
Vol 3 (15) ◽  
pp. 3011-3023 ◽  
Author(s):  
Giuseppe Vitiello ◽  
Alessandra Luchini ◽  
Gerardino D'Errico ◽  
Rita Santamaria ◽  
Antonella Capuozzo ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Cancer Cells ◽  
Inhibitory Activity ◽  
Ruthenium Complex ◽  
Human Cancer ◽  
High Growth ◽  
Human Cancer Cells ◽  
Growth Inhibitory ◽  
Growth Inhibitory Activity ◽  
Mcf 7

Cationic nanovectors loaded with Ru-based nucleolipids exert a high growth-inhibitory activity against human cancer cells (MCF-7 (A), WiDr (B), and HeLa (C)).

scholarly journals Growth inhibitory activity of biflavonoids and diterpenoids from the leaves of the Libyan Juniperus phoenicea against human cancer cells

2019 ◽  
Vol 33 (8) ◽  
pp. 2075-2082 ◽  
Author(s):  
Afaf Al Groshi ◽  
Hiba A. Jasim ◽  
Andrew R. Evans ◽  
Fyaz M.D. Ismail ◽  
Nicola M. Dempster ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Inhibitory Activity ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
Growth Inhibitory ◽  
Growth Inhibitory Activity ◽  
Juniperus Phoenicea

Glanduliferins A and B, two new glucosylated steroids from Impatiens glandulifera, with in vitro growth inhibitory activity in human cancer cells

Fitoterapia ◽  
2016 ◽  
Vol 109 ◽  
pp. 138-145 ◽  
Author(s):  
Alessio Cimmino ◽  
Véronique Mathieu ◽  
Marco Evidente ◽  
Marlène Ferderin ◽  
Laetitia Moreno Y Banuls ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Inhibitory Activity ◽  
Human Cancer ◽  
In Vitro Growth ◽  
Impatiens Glandulifera ◽  
Human Cancer Cells ◽  
Growth Inhibitory ◽  
Growth Inhibitory Activity

Obtusifoliol related steroids from Euphorbia sogdiana with cell growth inhibitory activity and apoptotic effects on breast cancer cells (MCF-7 and MDA-MB231)

Steroids ◽  
2016 ◽  
Vol 115 ◽  
pp. 90-97 ◽  
Author(s):  
Mahmoud Aghaei ◽  
Zeinab Yazdiniapour ◽  
Mustafa Ghanadian ◽  
Behzad Zolfaghari ◽  
Virginia Lanzotti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Inhibitory Activity ◽  
Breast Cancer Cells ◽  
Growth Inhibitory ◽  
Growth Inhibitory Activity ◽  
Apoptotic Effects ◽  
Mcf 7

scholarly journals Ruthenium-based PACT agents based on bisquinoline chelates: synthesis, photochemistry, and cytotoxicity

2021 ◽  
Author(s):  
Anja Busemann ◽  
Ingrid Flaspohler ◽  
Xue-Quan Zhou ◽  
Claudia Schmidt ◽  
Sina K. Goetzfried ◽  
...  
Keyword(s):  
Quantum Yield ◽  
Singlet Oxygen ◽  
Cancer Cells ◽  
Cellular Uptake ◽  
Ruthenium Complex ◽  
Human Cancer ◽  
Light Irradiation ◽  
Quantum Yields ◽  
Light Activation ◽  
Human Cancer Cells

AbstractThe known ruthenium complex [Ru(tpy)(bpy)(Hmte)](PF6)2 ([1](PF6)2, where tpy = 2,2’:6’,2″-terpyridine, bpy = 2,2’-bipyridine, Hmte = 2-(methylthio)ethanol) is photosubstitutionally active but non-toxic to cancer cells even upon light irradiation. In this work, the two analogs complexes [Ru(tpy)(NN)(Hmte)](PF6)2, where NN = 3,3'-biisoquinoline (i-biq, [2](PF6)2) and di(isoquinolin-3-yl)amine (i-Hdiqa, [3](PF6)2), were synthesized and their photochemistry and phototoxicity evaluated to assess their suitability as photoactivated chemotherapy (PACT) agents. The increase of the aromatic surface of [2](PF6)2 and [3](PF6)2, compared to [1](PF6)2, leads to higher lipophilicity and higher cellular uptake for the former complexes. Such improved uptake is directly correlated to the cytotoxicity of these compounds in the dark: while [2](PF6)2 and [3](PF6)2 showed low EC50 values in human cancer cells, [1](PF6)2 is not cytotoxic due to poor cellular uptake. While stable in the dark, all complexes substituted the protecting thioether ligand upon light irradiation (520 nm), with the highest photosubstitution quantum yield found for [3](PF6)2 (Φ[3] = 0.070). Compounds [2](PF6)2 and [3](PF6)2 were found both more cytotoxic after light activation than in the dark, with a photo index of 4. Considering the very low singlet oxygen quantum yields of these compounds, and the lack of cytotoxicity of the photoreleased Hmte thioether ligand, it can be concluded that the toxicity observed after light activation is due to the photoreleased aqua complexes [Ru(tpy)(NN)(OH2)]2+, and thus that [2](PF6)2 and [3](PF6)2 are promising PACT candidates. Graphic abstract

Indole-3-carbinol inhibits the proliferation of colorectal carcinoma LoVo cells through activation of the apoptotic signaling pathway

2021 ◽  
pp. 096032712110214
Author(s):  
JY Lee ◽  
HM Lim ◽  
CM Lee ◽  
S-H Park ◽  
MJ Nam
Keyword(s):  
Colorectal Carcinoma ◽  
Cancer Cells ◽  
Inhibitory Activity ◽  
Annexin V ◽  
Fluorescein Isothiocyanate ◽  
Cell Counting ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Growth Inhibitory ◽  
Growth Inhibitory Activity ◽  
Lovo Cells

Indole-3-carbinol (I3C) is a phytochemical that exhibits growth-inhibitory activity against various cancer cells. However, there are limited studies on the effects of I3C on colon cancer cells. In this study, the growth-inhibitory activity of I3C against the human colorectal carcinoma cell line (LoVo) was examined. The results of the 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide, colony formation, and cell counting assays revealed that I3C suppressed the proliferation of LoVo cells. Microscopy and wound-healing analyses revealed that I3C affected the morphology and inhibited the migration of LoVo cells, respectively. I3C induced apoptosis and DNA fragmentation as evidenced by the results of fluorescein isothiocyanate-conjugated annexin V staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling assay, respectively. Additionally, I3C arrested the cell cycle at the G0/G1 phase and enhanced the reactive oxygen species levels. Western blotting analysis revealed that treatment with I3C resulted in the activation of apoptotic proteins, such as poly(ADP-ribose) polymerase, caspase-3, caspase-7, caspase-9, Bax, Bim, and p53 in LoVo cells. These results indicate that I3C induces apoptosis in LoVo cells by upregulating p53, leading to the activation of Bax and caspases. Taken together, I3C exerts cytotoxic effects on LoVo cells by activating apoptosis.

scholarly journals Inhibition of NADPH Oxidases Activity by Diphenyleneiodonium Chloride as a Mechanism of Senescence Induction in Human Cancer Cells

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1248
Author(s):  
Katarzyna Piszczatowska ◽  
Dorota Przybylska ◽  
Ewa Sikora ◽  
Grażyna Mosieniak
Keyword(s):  
Cancer Cells ◽  
Therapeutic Potential ◽  
Human Cancer ◽  
Cell Metabolism ◽  
Human Colon ◽  
Nadph Oxidases ◽  
Human Colon Cancer ◽  
Inhibition Of Proliferation ◽  
Human Cancer Cells ◽  
Mcf 7

NADPH oxidases (NOX) are commonly expressed ROS-producing enzymes that participate in the regulation of many signaling pathways, which influence cell metabolism, survival, and proliferation. Due to their high expression in several different types of cancer it was postulated that NOX promote tumor progression, growth, and survival. Thus, the inhibition of NOX activity was considered to have therapeutic potential. One of the possible outcomes of anticancer therapy, which has recently gained much interest, is cancer cell senescence. The induction of senescence leads to prolonged inhibition of proliferation and contributes to tumor growth restriction. The aim of our studies was to investigate the influence of low, non-toxic doses of diphenyleneiodonium chloride (DPI), a potent inhibitor of flavoenzymes including NADPH oxidases, on p53-proficient and p53-deficient HCT116 human colon cancer cells and MCF-7 breast cancer cells. We demonstrated that the temporal treatment of HCT116 and MCF-7 cancer cells (both p53 wild-type) with DPI caused induction of senescence, that was correlated with decreased level of ROS and upregulation of p53/p21 proteins. On the contrary, in the case of p53−/− HCT116 cells, apoptosis was shown to be the prevailing effect of DPI treatment. Thus, our studies provided a proof that inhibiting ROS production, and by this means influencing ROS sensitive pathways, remains an alternative strategy to facilitate so called therapy-induced senescence in cancers.

scholarly journals Maytenus disticha Extract and an Isolated β-Dihydroagarofuran Induce Mitochondrial Depolarization and Apoptosis in Human Cancer Cells by Increasing Mitochondrial Reactive Oxygen Species

Biomolecules ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 377
Author(s):  
Iván González-Chavarría ◽  
Felix Duprat ◽  
Francisco J. Roa ◽  
Nery Jara ◽  
Jorge R. Toledo ◽  
...  
Keyword(s):  
Cytotoxic Activity ◽  
Cancer Cells ◽  
Human Cancer ◽  
Ros Generation ◽  
Active Components ◽  
Total Extract ◽  
Human Cancer Cells ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Membrane Depolarization ◽  
Mcf 7

Maytenus disticha (Hook F.), belonging to the Celastraceae family, is an evergreen shrub, native of the central southern mountains of Chile. Previous studies demonstrated that the total extract of M. disticha (MD) has an acetylcholinesterase inhibitory activity along with growth regulatory and insecticidal activities. β-Dihydroagarofurans sesquiterpenes are the most active components in the plant. However, its activity in cancer has not been analyzed yet. Here, we demonstrate that MD has a cytotoxic activity on breast (MCF-7), lung (PC9), and prostate (C4-2B) human cancer cells with an IC50 (µg/mL) of 40, 4.7, and 5 µg/mL, respectively, an increasing Bax/Bcl2 ratio, and inducing a mitochondrial membrane depolarization. The β-dihydroagarofuran-type sesquiterpene (MD-6), dihydromyricetin (MD-9), and dihydromyricetin-3-O-β-glucoside (MD-10) were isolated as the major compounds from MD extracts. From these compounds, only MD-6 showed cytotoxic activity on MCF-7, PC9, and C4-2B with an IC50 of 31.02, 17.58, and 42.19 µM, respectively. Furthermore, the MD-6 increases cell ROS generation, and MD and MD-6 induce a mitochondrial superoxide generation and apoptosis on MCF-7, PC9, and C4-2B, which suggests that the cytotoxic effect of MD is mediated in part by the β-dihydroagarofuran-type that induces apoptosis by a mitochondrial dysfunction.

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