scholarly journals Green-synthesized silver nanoparticles with aqueous extract of green algae Chaetomorpha ligustica and its anticancer potential

2021 ◽  
Vol 10 (1) ◽  
pp. 711-721
Author(s):  
Sabah Ahmed Al-Zahrani ◽  
Ramesa Shafi Bhat ◽  
Sarah A. Al Rashed ◽  
Amer Mahmood ◽  
Ahmed Al Fahad ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Zeta Potential ◽  
Ftir Spectroscopy ◽  
Cell Lines ◽  
Cancer Cell ◽  
Green Algae ◽  
Cancer Cell Lines ◽  
Gas Chromatography Mass Spectrometry ◽  
Dependent Manner ◽  
Vis Spectroscopy

Abstract Marine green algae are rich in various bioactive components with known anticancer activity. Some anticancer drugs present in green algae are in clinical trials nowadays. Algae-mediated silver nanoparticles (AgNPs) have been of a great interest in cancer treatment due to their unique physico-chemical properties. In this study, we evaluate the anticancer efficiency of marine alga Chaetomorpha ligustica collected from the Arabian Gulf against colon cancer cell lines HT29 and HCT116. The anticancer potential of biosynthesized AgNPs from C. ligustica extract is also reported. Fourier transform infrared (FTIR) spectroscopy and gas chromatography-mass spectrometry analyses were used to identify the phytoconstituents present in algae extract. The synthesized AgNPs were confirmed via UV-Vis spectroscopy, whereas their morphology and stability were recorded by transmission electron microscopy (TEM), zeta potential, and zetasizer. We recorded absorption peak at 420 nm; TEM images showed an average size of 8.8 nm, whereas zeta potential and zetasizer study showed aggregation of nanoparticles. FTIR spectroscopy peaks of C. ligustica AgNPs were a little different from those of the C. ligustica extract. Both extracts showed cytotoxicity against cancer cell lines in a dose-dependent manner, but nanoparticles were found to be more toxic than algae extract. HT29 was found to be more sensitive than HCT116. For the first time, species of C. ligustica have been used and reported for the synthesis of nanoparticles. C. ligustica and its biogenic nanoparticles need to be scaled up for many biomedical applications especially in cancer research.

Comparison of cytotoxicity and genotoxicity effects of silver nanoparticles on human cervix and breast cancer cell lines

2016 ◽  
Vol 36 (9) ◽  
pp. 931-948 ◽  
Author(s):  
K Juarez-Moreno ◽  
EB Gonzalez ◽  
N Girón-Vazquez ◽  
RA Chávez-Santoscoy ◽  
JD Mota-Morales ◽  
...  
Keyword(s):  
Dna Damage ◽  
Silver Nanoparticles ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gynecological Cancer ◽  
Cancer Cell Lines ◽  
Surrounding Tissue ◽  
Breast Cancer Cell Lines ◽  
Dependent Manner ◽  
Mcf7 Cells

The wide application of silver nanoparticles (AgNPs) has pointed out the need to evaluate their potential risk and toxic effects on human health. Herein, the cytotoxic effects of Argovit™ AgNPs were evaluated on eight cancer cell lines. Further cytotoxic studies were performed in gynecological cancer cell lines from cervical (HeLa) and breast (MDA-MB-231 and MCF7) cancer. In both cases, the half maximal inhibitory concentration (IC50) of AgNPs produced the formation of reactive oxygen species (ROS) after 24 h of incubation, but it was not statistically significant compared with untreated cells. However, HeLa, MDA-MB-231, and MCF7 cells treated with the maximal IC of AgNPs induced the formation of ROS either at 12 or 24 h of incubation. Genotoxicity achieved by comet assay in HeLa, MDA-MB-231, and MCF7 cells revealed that exposure to IC50 of AgNPs does not induced noticeable DNA damage in the cells. However, the IC of AgNPs provoked severe DNA damage after 12 and 24 h of exposure. We conclude that, Argovit (polyvinylpyrrolidone-coated AgNPs) induce a cytotoxic effect in a time and dose-dependent manner in all the eight cancer cell lines tested. Nevertheless, the genotoxic effect is mainly restricted by the concentration effect. The results contribute to explore new therapeutic applications of AgNPs for malignances in murine models and to study in deep the cytotoxic and genotoxic effects of AgNPs in healthy cells at the surrounding tissue of the neoplasia.

scholarly journals Analyzing Cytotoxic and Apoptogenic Properties ofScutellaria litwinowiiRoot Extract on Cancer Cell Lines

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Zahra Tayarani-Najaran ◽  
Seyed Ahmad Emami ◽  
Javad Asili ◽  
Alireza Mirzaei ◽  
Seyed Hadi Mousavi
Keyword(s):  
Flow Cytometry ◽  
Cell Lines ◽  
Cancer Cell ◽  
Methylene Chloride ◽  
Apoptotic Cell ◽  
Malignant Cell ◽  
Cancer Cell Lines ◽  
Dependent Manner ◽  
Antitumor Effects ◽  
Mcf 7

TheScutellariaspecies (Lamiaceae) is used as a source of flavonoids to treat a variety of diseases in traditional medicine. In spite of many reports about the cytotoxic and antitumor effects of some species of this genus, anticancer researches on one of the Iranian speciesS. litwinowiihave not yet been conducted.The cytotoxic properties of total methanol extract ofS. litwinowiiand its fractions were investigated on different cancer cell lines including AGS, HeLa, MCF-7, PC12 and NIH 3T3. Meanwhile, the role of apoptosis in this toxicity was explored. The cells were cultured in DMEM medium and incubated with different concentrations of herb plant extracts. Cell viability was quantitated by MTT assay. Apoptotic cells were determined using propidium iodide staining of DNA fragmentation by flow cytometry (sub-G1 peak).Scutellaria litwinowiiinhibited the growth of malignant cells in a dose-dependent manner. Among solvent fractions ofS. litwinowii, the methylene chloride fraction was found to be more toxic compared to other fractions. The IC50values of this fraction against AGS, HeLa, MCF-7 and PC12 cell lines after 24 h were determined, 121.2 ± 3.1, 40.9 ± 2.5, 115.9 ± 3.5 and 64.5 ± 3.4μg/ml, respectively.Scutellaria litwinowiiinduced a sub-G1 peak in the flow cytometry histogram of treated cells compared to control cells indicating that apoptotic cell death is involved inS. litwinowiitoxicity.Scutellaria litwinowiiexerts cytotoxic and proapototic effects in a variety of malignant cell lines and could be considered as a potential chemotherapeutic agent in cancer treatment.

scholarly journals Design, Synthesis and Biological Evaluation of a New Series of 1-Aryl-3-{4-[(pyridin-2-ylmethyl)thio]phenyl}urea Derivatives as Antiproliferative Agents

Molecules ◽  
2019 ◽  
Vol 24 (11) ◽  
pp. 2108 ◽  
Author(s):  
Chuanming Zhang ◽  
Xiaoyu Tan ◽  
Jian Feng ◽  
Ning Ding ◽  
Yongpeng Li ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
A549 Cells ◽  
Cancer Cell Lines ◽  
Biological Evaluation ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Urea Derivatives ◽  
Antiproliferative Agents

To discover new antiproliferative agents with high efficacy and selectivity, a new series of 1-aryl-3-{4-[(pyridin-2-ylmethyl)thio]phenyl}urea derivatives (7a–7t) were designed, synthesized and evaluated for their antiproliferative activity against A549, HCT-116 and PC-3 cancer cell lines in vitro. Most of the target compounds demonstrated significant antiproliferative effects on all the selective cancer cell lines. Among them, the target compound, 1-[4-chloro-3-(trifluoromethyl)phenyl]-3-{4-{{[3-methyl-4-(2,2,2-trifluoroethoxy)pyridin-2-yl]methyl}thio}phenyl}urea (7i) was identified to be the most active one against three cell lines, which was more potent than the positive control with an IC50 value of 1.53 ± 0.46, 1.11 ± 0.34 and 1.98 ± 1.27 μM, respectively. Further cellular mechanism studies confirmed that compound 7i could induce the apoptosis of A549 cells in a concentration-dependent manner and elucidated compound 7i arrests cell cycle at G1 phase by flow cytometry analysis. Herein, the studies suggested that the 1-aryl-3-{4-[(pyridin-2-ylmethyl)thio]phenyl}urea skeleton might be regarded as new chemotypes for designing effective antiproliferative agents.

scholarly journals Synthesis and Biological Evaluation of New Antitubulin Agents Containing 2-(3′,4′,5′-trimethoxyanilino)-3,6-disubstituted-4,5,6,7-tetrahydrothieno[2,3-c]pyridine Scaffold

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1690
Author(s):  
Romeo Romagnoli ◽  
Filippo Prencipe ◽  
Paola Oliva ◽  
Barbara Cacciari ◽  
Jan Balzarini ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Lines ◽  
Cancer Cell ◽  
Mononuclear Cells ◽  
Cancer Cell Lines ◽  
Biological Evaluation ◽  
Pyridine Derivative ◽  
Tubulin Polymerization ◽  
Dependent Manner

Two novel series of compounds based on the 4,5,6,7-tetrahydrothieno[2,3-c]pyridine and 4,5,6,7-tetrahydrobenzo[b]thiophene molecular skeleton, characterized by the presence of a 3′,4′,5′-trimethoxyanilino moiety and a cyano or an alkoxycarbonyl group at its 2- or 3-position, respectively, were designed, synthesized, and evaluated for antiproliferative activity on a panel of cancer cell lines and for selected highly active compounds, inhibition of tubulin polymerization, and cell cycle effects. We have identified the 2-(3′,4′,5′-trimethoxyanilino)-3-cyano-6-methoxycarbonyl-4,5,6,7-tetrahydrothieno[2,3-c]pyridine derivative 3a and its 6-ethoxycarbonyl homologue 3b as new antiproliferative agents that inhibit cancer cell growth with IC50 values ranging from 1.1 to 4.7 μM against a panel of three cancer cell lines. Their interaction with tubulin at micromolar levels leads to the accumulation of cells in the G2/M phase of the cell cycle and to an apoptotic cell death. The cell apoptosis study found that compounds 3a and 3b were very effective in the induction of apoptosis in a dose-dependent manner. These two derivatives did not induce cell death in normal human peripheral blood mononuclear cells, suggesting that they may be selective against cancer cells. Molecular docking studies confirmed that the inhibitory activity of these molecules on tubulin polymerization derived from binding to the colchicine site.

scholarly journals Synthesis and In Vitro Photocytotoxicity of 9-/13-Lipophilic Substituted Berberine Derivatives as Potential Anticancer Agents

Molecules ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 677 ◽  
Author(s):  
Hong-Jhih Lin ◽  
Jinn-Hsuan Ho ◽  
Li-Chen Tsai ◽  
Fang-Yu Yang ◽  
Ling-Ling Yang ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Hepg2 Cells ◽  
Human Cancer ◽  
Cancer Cell Lines ◽  
Dependent Manner ◽  
Human Cancer Cell ◽  
Human Cancer Cell Lines ◽  
Berberine Derivatives

The objective of this study was to synthesize the 9-/13-position substituted berberine derivatives and evaluate their cytotoxic and photocytotoxic effects against three human cancer cell lines. Among all the synthesized compounds, 9-O-dodecyl- (5e), 13-dodecyl- (6e), and 13-O-dodecyl-berberine (7e) exhibited stronger growth inhibition against three human cancer cell lines, (HepG2, HT-29 and BFTC905), in comparison with structurally related berberine (1). These three compounds also showed the photocytotoxicity in human cancer cells in a concentration-dependent and light dose-dependent manner. Through flow cytometry analysis, we found out a lipophilic group at the 9-/13-position of berberine may have facilitated its penetration into test cells and hence enhanced its photocytotoxicity on the human liver cancer cell HepG2. Further, in cell cycle analysis, 5e, 6e, and 7e induced HepG2 cells to arrest at the S phase and caused apoptosis upon irradiation. In addition, photodynamic treatment of berberine derivatives 5e, 6e, and 7e again showed a significant photocytotoxic effects on HepG2 cells, induced remarkable cell apoptosis, greatly increased intracellular ROS level, and the loss of mitochondrial membrane potential. These results over and again confirmed that berberine derivatives 5e, 6e, and 7e greatly enhanced photocytotoxicity. Taken together, the test data led us to conclude that berberine derivatives with a dodecyl group at the 9-/13-position could be great candidates for the anti-liver cancer medicines developments.

scholarly journals Degalactotigonin, a Steroidal Glycoside from Solanum nigrum, Induces Apoptosis and Cell Cycle Arrest via Inhibiting the EGFR Signaling Pathways in Pancreatic Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Hoang Le Tuan Anh ◽  
Phuong Thao Tran ◽  
Do Thi Thao ◽  
Duong Thu Trang ◽  
Nguyen Hai Dang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Solanum Nigrum ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cycle Arrest

Degalactotigonin (1) and three other steroidal compounds solasodine (2), O-acetyl solasodine (3), and soladulcoside A (4) were isolated from the methanolic extract of Solanum nigrum, and their chemical structures were elucidated by spectroscopic analyses. The isolated compounds were evaluated for cytotoxic activity against human pancreatic cancer cell lines (PANC1 and MIA-PaCa2) and lung cancer cell lines (A549, NCI-H1975, and NCI-H1299). Only degalactotigonin (1) showed potent cytotoxicity against these cancer cell lines. Compound 1 induced apoptosis in PANC1 and A549 cells. Further study on its mechanism of action in PANC1 cells demonstrated that 1 significantly inhibited EGF-induced proliferation and migration in a concentration-dependent manner. Treatment of PANC1 cells with degalactotigonin induced cell cycle arrest at G0/G1 phase. Compound 1 induced downregulation of cyclin D1 and upregulation of p21 in a time- and concentration-dependent manner and inhibited EGF-induced phosphorylation of EGFR, as well as activation of EGFR downstream signaling molecules such as Akt and ERK.

scholarly journals Glutamine promotes ovarian cancer cell proliferation through the mTOR/S6 pathway

2015 ◽  
Vol 22 (4) ◽  
pp. 577-591 ◽  
Author(s):  
Lingqin Yuan ◽  
Xiugui Sheng ◽  
Adam K Willson ◽  
Dario R Roque ◽  
Jessica E Stine ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Stress Proteins ◽  
Ovarian Cancer Cell ◽  
Cancer Cell Lines ◽  
Glutamine Metabolism ◽  
Dependent Manner ◽  
Ovarian Cancer Cell Lines

Glutamine is one of the main nutrients used by tumor cells for biosynthesis. Therefore, targeted inhibition of glutamine metabolism may have anti-tumorigenic implications. In the present study, we aimed to evaluate the effects of glutamine on ovarian cancer cell growth. Three ovarian cancer cell lines, HEY, SKOV3, and IGROV-1, were assayed for glutamine dependence by analyzing cytotoxicity, cell cycle progression, apoptosis, cell stress, and glucose/glutamine metabolism. Our results revealed that administration of glutamine increased cell proliferation in all three ovarian cancer cell lines in a dose dependent manner. Depletion of glutamine induced reactive oxygen species and expression of endoplasmic reticulum stress proteins. In addition, glutamine increased the activity of glutaminase (GLS) and glutamate dehydrogenase (GDH) by modulating the mTOR/S6 and MAPK pathways. Inhibition of mTOR activity by rapamycin or blocking S6 expression by siRNA inhibited GDH and GLS activity, leading to a decrease in glutamine-induced cell proliferation. These studies suggest that targeting glutamine metabolism may be a promising therapeutic strategy in the treatment of ovarian cancer.

High-Throughput RNA Interference Screening Identifies Synthetic Lethality Between Oncogenic KRAS Dependency and Suppression of STK33

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3806-3806
Author(s):  
Claudia Scholl ◽  
Stefan Frohling ◽  
Ian F. Dunn ◽  
David A. Barbie ◽  
Anna C. Schinzel ◽  
...  
Keyword(s):  
Rna Interference ◽  
Protein Kinase ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
High Throughput ◽  
Synthetic Lethality ◽  
Human Cancer ◽  
Cancer Cell Lines ◽  
Dependent Manner

Abstract Activating RAS mutations are among the most common pathogenetic events in a broad spectrum of hematologic malignancies and epithelial tumors. However, oncogenic RAS has thus far not proven to be a tractable target for therapeutic intervention. An alternative to direct targeting of known oncogenes is to perform “synthetic lethality” screens to identify genes that are selectively required for cell viability in the context of specific cancer-causing mutations. Using this approach, we have discovered a synthetic lethal interaction between mutant KRAS, the most frequently mutated oncogene in human cancer, and inactivation of the gene encoding the STK33 serine/threonine protein kinase. To identify genes that are essential for cell viability in the context of mutant KRAS, we performed high-throughput loss-of-function RNA interference (RNAi) screens in eight human cancer cell lines (mutant KRAS, n=4; wildtype KRAS, n=4), representing seven different tumor types (acute myeloid leukemia, multiple myeloma, colon cancer, breast cancer, ovarian cancer, prostate cancer, glioblastoma), as well as normal human fibroblasts and mammary epithelial cells. We screened each cell line with a subset of the short hairpin RNA (shRNA) library developed by the RNAi Consortium (http://www.broad.mit.edu/genome_bio/trc/rnai.html) that consists of 5,024 individual shRNA constructs targeting 1,011 human genes, including the majority of known and putative protein kinase and phosphatase genes and a selection of known cancer-related genes. In these cell lines, suppression of STK33 preferentially inhibited the viability and proliferation of cells that were dependent on mutant KRAS. The differential requirement for STK33 based on oncogenic KRAS dependency was confirmed in 16 additional cell lines using in vitro transformation assays and human tumor xenograft models. Biochemical analyses support the hypothesis that STK33 promotes cell growth and survival in a kinase activity-dependent manner by regulating the activity of S6K1 as well as BAD-induced apoptosis selectively in mutant KRAS-dependent cells. Notably, molecular genetic characterization of cancer cell lines and analysis of patient-derived genomic data sets indicate that STK33 is not frequently mutated or overexpressed in human tumors. These observations identify STK33 as a potential target for the treatment of mutant KRAS-driven cancers that may have a broad therapeutic index in normal versus malignant cells, and illustrate the potential of RNAi for discovering critical functional dependencies created by oncogenic mutations that cannot be identified using other genomic technologies.

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