Largazole as a Novel and Selective Anti-Breast Cancer Agent

2013 ◽  
Author(s):  
Xuedong Liu
Keyword(s):  
Breast Cancer ◽  
Cancer Agent

Trichoderma longibrachiatum derived metabolite as a potential source of anti‐breast‐cancer agent

Biologia ◽  
2021 ◽  
Vol 76 (5) ◽  
pp. 1595-1601
Author(s):  
Nasim Ebrahimi ◽  
Farzane Amirmahani ◽  
Batul Sadeghi ◽  
Masoud Ghanaatian
Keyword(s):  
Breast Cancer ◽  
Trichoderma Longibrachiatum ◽  
Potential Source ◽  
Cancer Agent

scholarly journals Metformin induces Ferroptosis by inhibiting UFMylation of SLC7A11 in breast cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Jingjing Yang ◽  
Yulu Zhou ◽  
Shuduo Xie ◽  
Ji Wang ◽  
Zhaoqing Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Treatment ◽  
Morphological Changes ◽  
Tumor Model ◽  
Independent Manner ◽  
Regulated Cell Death ◽  
Anti Cancer ◽  
Cancer Agent ◽  
Approved Drugs

Abstract Background Ferroptosis is a newly defined form of regulated cell death characterized by the iron-dependent accumulation of lipid peroxidation and is involved in various pathophysiological conditions, including cancer. Targeting ferroptosis is considered to be a novel anti-cancer strategy. The identification of FDA-approved drugs as ferroptosis inducers is proposed to be a new promising approach for cancer treatment. Despite a growing body of evidence indicating the potential efficacy of the anti-diabetic metformin as an anti-cancer agent, the exact mechanism underlying this efficacy has not yet been fully elucidated. Methods The UFMylation of SLC7A11 is detected by immunoprecipitation and the expression of UFM1 and SLC7A11 in tumor tissues was detected by immunohistochemical staining. The level of ferroptosis is determined by the level of free iron, total/lipid Ros and GSH in the cells and the morphological changes of mitochondria are observed by transmission electron microscope. The mechanism in vivo was verified by in situ implantation tumor model in nude mice. Results Metformin induces ferroptosis in an AMPK-independent manner to suppress tumor growth. Mechanistically, we demonstrate that metformin increases the intracellular Fe2+ and lipid ROS levels. Specifically, metformin reduces the protein stability of SLC7A11, which is a critical ferroptosis regulator, by inhibiting its UFMylation process. Furthermore, metformin combined with sulfasalazine, the system xc− inhibitor, can work in a synergistic manner to induce ferroptosis and inhibit the proliferation of breast cancer cells. Conclusions This study is the first to demonstrate that the ability of metformin to induce ferroptosis may be a novel mechanism underlying its anti-cancer effect. In addition, we identified SLC7A11 as a new UFMylation substrate and found that targeting the UFM1/SLC7A11 pathway could be a promising cancer treatment strategy.

Centchroman—a non-steroidal anti-cancer agent for advanced breast cancer: Phase-II study

1989 ◽  
Vol 43 (5) ◽  
pp. 781-783 ◽  
Author(s):  
N. C. Misra ◽  
P. K. Nigam ◽  
Ruby Gupta ◽  
A. K. Agarwal ◽  
V. P. Kamboj
Keyword(s):  
Breast Cancer ◽  
Advanced Breast Cancer ◽  
Phase Ii ◽  
Phase Ii Study ◽  
Advanced Breast ◽  
Anti Cancer ◽  
Cancer Agent

scholarly journals New piperidine derivative DTPEP acts as dual-acting anti-breast cancer agent by targeting ERα and downregulating PI3K/Akt-PKCα leading to caspase-dependent apoptosis

2018 ◽  
Vol 51 (6) ◽  
pp. e12501 ◽  
Author(s):  
A. Arun ◽  
M.I. Ansari ◽  
P. Popli ◽  
S. Jaiswal ◽  
A.K. Mishra ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Piperidine Derivative ◽  
Cancer Agent

scholarly journals New bow-tie cationic carbosilane dendritic system with a curcumin core as an anti-breast cancer agent

2018 ◽  
Vol 42 (14) ◽  
pp. 11732-11738 ◽  
Author(s):  
Tania Lozano-Cruz ◽  
Rafael Gómez ◽  
F. Javier de la Mata ◽  
Paula Ortega
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Water Soluble ◽  
The Core ◽  
Carbosilane Dendrimer ◽  
Cancer Agent ◽  
Bow Tie

A water soluble “bow-tie” cationic carbosilane dendrimer with curcumin in the core displays antioxidant and antitumoral activities against breast cancer cells.

Breast Cancer Therapeutics Based on Fusarochromanone and EGFR Inhibitors

2021 ◽  
Author(s):  
Natalie Carroll ◽  
Alena Smith ◽  
Brian A. Salvatore ◽  
Elahe Mahdavian
Keyword(s):  
Breast Cancer ◽  
Mode Of Action ◽  
Cancer Therapeutics ◽  
Egfr Inhibitors ◽  
Cancer Therapies ◽  
Racemic Form ◽  
Combination Treatments ◽  
Anti Cancer ◽  
Cancer Agent ◽  
Cancer Activity

Abstract Background: Fusarochromanone (FC101) is a small molecule with potent anti-cancer activity. It was originally derived from the fungal plant pathogen, Fusarium equiseti, and it has also been synthesized in non-racemic form in our lab. Numerous studies reveal the promising biological activity of FC101, including potent anti-angiogenic and anti-cancer activity. While FC101 is potent as a single drug treatment across many cancer cell lines, current cancer therapies often incorporate a combination of drugs in order to increase efficacy and decrease the development of drug resistance. In this study, we leverage drug combinations and cellular phenotypic screens to address important questions about FC101’s mode of action and its potential synergies as an anti-cancer therapeutic agent in triple negative breast cancer (TNBC).Method: We hypothesized that FC101’s activity against TNBC is similar to the known mTOR inhibitor, everolimus, because FC101 reduces the phosphorylation of two key mTOR substrates, S6K and S6. Since everolimus synergistically enhances the anti-cancer activities of known EGFR inhibitors (erlotinib or lapatinib) in TNBC, we performed analogous studies with FC101. Phenotypic cellular assays helped assess whether FC101 (in both single and combination treatments) acts similarly to everolimus.Results: FC101 outperformed all other single treatments in both cell proliferation and viability assays. Unlike everolimus, however, FC101 brought about a sustained decrease in cell viability in drug washout studies. None of the other drugs were able to maintain comparable effects upon removal of the treatment agents. Although we observed slightly additive effects when the TNBC cells were treated with FC101 and either EGFR inhibitor, those effects were not truly synergistic in the manner displayed with everolimus. Conclusion: Our results rule out direct inhibition of mTOR by FC101 and suggest that FC101 acts through a different mechanism than everolimus. This lays the foundation for the refinement of our hypothesis in order to better understand FC101’s mode of action as a novel anti-cancer agent.

scholarly journals Development of a Cationic Amphiphilic Helical Peptidomimetic (B18L) As A Novel Anti-Cancer Drug Lead

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2448 ◽  
Author(s):  
Yuan Lyu ◽  
Steven Kopcho ◽  
Folnetti A. Alvarez ◽  
Bryson C. Okeoma ◽  
Chioma M. Okeoma
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Cancer Drug ◽  
Cancer Cell Death ◽  
Drug Lead ◽  
Anti Cancer ◽  
Cancer Agent ◽  
Caspase Substrate ◽  
Dynamics Simulations

BST-2 is a novel driver of cancer progression whose expression confers oncogenic properties to breast cancer cells. As such, targeting BST-2 in tumors may be an effective therapeutic approach against breast cancer. Here, we sought to develop potent cytotoxic anti-cancer agent using the second-generation BST-2-based anti-adhesion peptide, B18, as backbone. To this end, we designed a series of five B18-derived peptidomimetics. Among these, B18L, a cationic amphiphilic α-helical peptidomimetic, was selected as the drug lead because it displayed superior anti-cancer activity against both drug-resistant and drug-sensitive cancer cells, with minimal toxicity on normal cells. Probing mechanism of action using molecular dynamics simulations, biochemical and membrane biophysics studies, we observed that B18L binds BST-2 and possesses membranolytic characteristics. Furthermore, molecular biology studies show that B18L dysregulates cancer signaling pathways resulting in decreased Src and Erk1/2 phosphorylation, increased expression of pro-apoptotic Bcl2 proteins, caspase 3 cleavage products, as well as processing of the caspase substrate, poly (ADP-ribose) polymerase-1 (PARP-1), to the characteristic apoptotic fragment. These data indicate that through the coordinated regulation of membrane, mitochondrial and signaling events, B18L executes cancer cell death and thus has the potential to be developed into a potent and selective anti-cancer compound.

Design, Synthesis and Molecular Docking Studies of 4-{3-[2-(2-Morpholin-4-yl-ethoxy)phenyl]-5-phenyl-pyrazol-1-yl}-benzenesulfonamide as Anti-Breast Cancer Agent

2020 ◽  
Vol 5 (4) ◽  
pp. 301-306
Author(s):  
Praveen Kumar ◽  
Jai Prakash Kumar ◽  
Juhi Barnwal ◽  
Ritu Singh
Keyword(s):  
Breast Cancer ◽  
Molecular Docking ◽  
Anticancer Activity ◽  
Mtt Assay ◽  
Cancer Cell Line ◽  
Docking Studies ◽  
Mcf7 Cells ◽  
Standard Drug ◽  
Molecular Docking Studies ◽  
Cancer Agent

Novel 4-{3-[2-(2-morpholin-4-yl-ethoxy)phenyl]-5-phenyl-pyrazol- 1-yl}benzenesulfonamide (7) was synthesized and evaluated for its anti-breast cancer activity. It was prepared by cyclocondensation reaction of morpholine-substituted β-diketone, 1-[2-(2-morpholin-4-yl-ethoxy)- phenyl]-3-phenyl-propane-1,3-dione (3) with 4-hydrazinobenzenesulfonamide hydrochloride (6). Chemical structure of titled compound (7) was confirmed by FTIR, 1H & 13C NMR and HRMS spectroscoic analyses. The anticancer activity of titled compound 7 was evaluated against MCF-7 breast cancer cell line by MTT assay. Molecular docking was performed to predict its plausible binding with the estrogen receptor α(ERα) using Molecular Operating Environment 2019.0101 software. The MTT assay results showed that titled compound 7 exhibited better anticancer activity against MCF7 cells (IC50: 4.25 μM) than standard drug, 4-hydroxytamoxifen (IC50: 8.22 μM). Results of molecular docking studies were found in good agreement with the results of anticancer evaluation, as the binding score of titled compound 7 (-16.9872 kcal/mol) was lower as compared to 4-hydroxytamoxifen (-15.1112 kcal/mol). The new cationic interaction of titled compound 7 with Trp383 and hydrogen bonding interaction with Phe404 in active site of ERα made its anticancer activity better than 4-hydroxytamoxifen. Thus, 4-{3-[2-(2-morpholin-4-yl-ethoxy)phenyl]-5-phenyl-pyrazol- 1-yl}benzenesulfonamide (7) was emerged as a potent anti-breast cancer agent.

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