Magnetic nanoparticles for the measurement of cell mechanics using force-induced remnant magnetization spectroscopy

Nanoscale ◽  
2020 ◽  
Vol 12 (27) ◽  
pp. 14573-14580
Author(s):  
Min Xu ◽  
Xueyan Feng ◽  
Feng Feng ◽  
Hantao Pei ◽  
Ruping Liu ◽  
...  
Keyword(s):  
Magnetic Nanoparticles ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Mechanics ◽  
Magnetic Nanoparticle ◽  
Adhesion Force ◽  
Force Spectroscopy ◽  
Remnant Magnetization ◽  
A Cell ◽  
Novel Method

Interactions of magnetic nanoparticles with cells were investigated from a cell mechanics perspective, and magnetic nanoparticle-based force spectroscopy was developed as a novel method to measure the adhesion force among various cancer cell lines.

scholarly journals Synthesis of Novel 2-Thioxothiazolidin-4-one and Thiazolidine-2, 4-dione Derivatives as Potential Anticancer Agents

2018 ◽  
Vol 13 (5) ◽  
pp. 1934578X1801300
Author(s):  
Alleni Suman Kumar ◽  
Rathod Aravind Kumar ◽  
Elala Pravardhan Reddy ◽  
Vavilapalli Satyanarayana ◽  
Jajula Kashanna ◽  
...  
Keyword(s):  
Anticancer Activity ◽  
Cell Lines ◽  
Cancer Cell ◽  
Anticancer Agents ◽  
Preliminary Data ◽  
Cancer Cell Lines ◽  
Structure Evolution ◽  
Model Compounds ◽  
Diverse Range ◽  
Novel Method

A variety of novel thiazolidine derivatives (2-thioxothiazolidin-4-one and thiazolidine-2, 4-dione derivatives) have been prepared by using 2,4-diphenyl-2 H-chromene-3-carbaldehyde and its derivatives as starting materials. This is the first example of the preparation of thiazolidine derivatives through this novel method. Structure evolution of the resulting thiazolidine derivatives leads to anticancer agents. Our preliminary data for some model compounds on three cancer cell lines (MCF7, A549 and B-16) suggested reasonable anticancer activity against the A549 and B-16 cell lines, with IC50 values of 20.7 and 20.4 μM, respectively. This method is operationally simple and works with a diverse range of substrates.

Multidrug Resistance Reversal Agent, NSC77037, Identified with a Cell-Based Screening Assay

2010 ◽  
Vol 15 (3) ◽  
pp. 287-296 ◽  
Author(s):  
Michiro Susa ◽  
Edwin Choy ◽  
Cao Yang ◽  
Joseph Schwab ◽  
Henry Mankin ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Cancer Patients ◽  
Cell Lines ◽  
Cancer Cell ◽  
Small Molecule ◽  
Cancer Resistance ◽  
Screening Assay ◽  
A Cell ◽  
Resistance Protein ◽  
Mdr Reversal

The development of multidrug resistance (MDR) remains a significant obstacle in treating cancer patients with chemotherapy. To identify small-molecule compounds that can reverse MDR, the authors used a cell-based screening assay with an MDR ovarian cancer cell line. Incubating MDR cells with a sublethal concentration of paclitaxel in combination with each of 2000 small-molecule compounds from the National Cancer Institute Diversity Set Library, they identified NSC77037. The cytotoxic activity of NSC77037 and the duration of its effect were evaluated in vitro using a panel of cancer cell lines expressing permeability glycoprotein (Pgp), multiple drug resistance protein 1 (MRP 1), and breast cancer resistance protein (BCRP). The mechanism of its effects was further analyzed by assessing the retention of calcein and Pgp-ATPase activity. The relative potency of MDR reversal by NSC77037 was significantly higher than that of frequently used MDR reversal agents such as verapamil and cyclosporine A. NSC77037 reversed Pgp without reversing MRP or BCRP-mediated MDR. NSC77037, at a concentration of >10 µM, moderately inhibited the proliferation of both sensitive and resistant cell lines, but the inhibitory effect of NSC77037 was not altered by coincubation with the Pgp inhibitor verapamil, suggesting that NSC77037 itself is not a substrate of Pgp. NSC77037 directly inhibited the function of Pgp in a dose-dependent manner, but it did not alter the protein expression level of Pgp. The use of NSC77037 to restore sensitivity to chemotherapy or to prevent resistance could be a potential treatment strategy for cancer patients.

scholarly journals Hypoxia and Human Genome Stability: Downregulation of BRCA2 Expression in Breast Cancer Cell Lines

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Daniele Fanale ◽  
Viviana Bazan ◽  
Stefano Caruso ◽  
Marta Castiglia ◽  
Giuseppe Bronte ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Homologous Recombination ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Genetic Instability ◽  
Excision Repair ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
A Cell

Previously, it has been reported that hypoxia causes increased mutagenesis and alteration in DNA repair mechanisms. In 2005, an interesting study showed that hypoxia-induced decreases in BRCA1 expression and the consequent suppression of homologous recombination may lead to genetic instability. However, nothing is yet known about the involvement of BRCA2 in hypoxic conditions in breast cancer. Initially, a cell proliferation assay allowed us to hypothesize that hypoxia could negatively regulate the breast cancer cell growth in short term in vitro studies. Subsequently, we analyzed gene expression in breast cancer cell lines exposed to hypoxic condition by microarray analysis. Interestingly, genes involved in DNA damage repair pathways such as mismatch repair, nucleotide excision repair, nonhomologous end-joining and homologous recombination repair were downregulated. In particular, we focused on the BRCA2 downregulation which was confirmed at mRNA and protein level. In addition, breast cancer cells were treated with dimethyloxalylglycine (DMOG), a cell-permeable inhibitor of both proline and asparaginyl hydroxylases able to induce HIF-1αstabilization in normoxia, providing results comparable to those previously described. These findings may provide new insights into the mechanisms underlying genetic instability mediated by hypoxia and BRCA involvement in sporadic breast cancers.

scholarly journals Digital Karyotyping for Rapid Authentication of Cell Lines

2019 ◽  
Author(s):  
Ahmed Ibrahim Samir Khalil ◽  
Anupam Chattopadhyay ◽  
Amartya Sanyal
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
De Novo ◽  
Simulated Data ◽  
Read Depth ◽  
Cancer Cell Lines ◽  
Scientific Data ◽  
Cell Line Authentication ◽  
A Cell

Abstract Background The widespread concern about genetic drift and cross-contamination of cell lines calls for a pressing need for their authentication. The current genetic techniques for authentication are time-consuming and require specific documentary standard and laboratory protocols. Given the fact that whole-genome sequencing (WGS) data are readily available, read depth (RD)-based computational analyses has allowed the estimation of genetic profiles of cell lines. Results We propose WGS-derived aneuploidy profiling as a prototype of digital karyotyping for authentication of cancer cell lines. Here, we describe a Python-based software AStra for de novo estimation of the genome-wide aneuploidy profile, the copy number of every genomic loci, from raw WGS reads. We demonstrated that aneuploidy profile offers a unique signature that can distinguish the clonal variants (strains) of a cell line. We evaluated our approach using simulated data and variety of cancer cell lines. We further showed that cell lines exhibit distinct aneuploidy patterns which corroborate well with the experimental observations. Conclusions AStra is a simple, user-friendly, and free tool that provides the elementary information about the chromosomal aneuploidy for cell line authentication. AStra provides an analytical and visualization platform for rapid and easy comparison between different cell lines/strains. We recommend AStra for rapid first-pass quality assessment of scientific data that employ cancer cell lines. AStra is an open source software and is available at https://github.com/AISKhalil/AStra.

scholarly journals Smart Modification on Magnetic Nanoparticles Dramatically Enhances Their Therapeutic Properties

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 4095
Author(s):  
Nuria Lafuente-Gómez ◽  
Paula Milán-Rois ◽  
David García-Soriano ◽  
Yurena Luengo ◽  
Marco Cordani ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Magnetic Nanoparticles ◽  
Cell Lines ◽  
Cancer Cell ◽  
Plasma Proteins ◽  
Cancer Cell Lines ◽  
Synergistic Activity ◽  
Multiple Parameters ◽  
The Stability ◽  
Smart Drug

Magnetic nanoparticles (MNP) are employed as nanocarriers and in magnetic hyperthermia (MH) for the treatment of cancers. Herein, a smart drug delivery system composed of MNP functionalized with the cytotoxic drug gemcitabine (MNP-GEM) has been thoroughly evaluated. The linker employed is based on a disulfide bond and allows the controlled release of GEM under a highly reducing environment, which is frequently present in the cytoplasm of tumor cells. The stability, MH, and the interaction with plasma proteins of the nanoparticles are evaluated, highlighting their great potential for biological applications. Their cytotoxicity is assessed in three pancreatic cancer cell lines with different sensitivity to GEM, including the generation of reactive oxygen species (ROS), the effects on the cell cycle, and the mechanisms of cell death involved. Remarkably, the proposed nanocarrier is better internalized than unmodified nanoparticles, and it is particularly effective in PANC-1 cells, resistant to GEM, but not in non-tumoral keratinocytes. Additionally, its combination with MH produces a synergistic cytotoxic effect in all cancer cell lines tested. In conclusion, MNP-GEM presents a promising potential for treating pancreatic cancer, due to multiple parameters, such as reduced binding to plasma proteins, increased internalization, and synergistic activity when combined with MH.

Exploring the potential of mucin 13 (MUC13) as a biomarker for carcinomas and other diseases

2018 ◽  
Vol 56 (11) ◽  
pp. 1945-1953 ◽  
Author(s):  
Panagiota S. Filippou ◽  
Annie H. Ren ◽  
Dimitrios Korbakis ◽  
Lampros Dimitrakopoulos ◽  
Antoninus Soosaipillai ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Surface Glycoprotein ◽  
Serum Samples ◽  
Cell Surface Glycoprotein ◽  
Ovarian Cancer Cell Lines ◽  
Human Sera ◽  
A Cell ◽  
Inflammatory Bowel

Abstract Background: Mucin 13 (MUC13) is a cell surface glycoprotein aberrantly expressed in a variety of epithelial carcinomas. Thus far, the role of MUC13 in various diseases remains elusive. To the best of our knowledge, this is the first study to examine the potential of MUC13 as a serum biomarker in a variety of carcinomas and other conditions. Methods: We developed a recombinant MUC13 protein, mouse monoclonal antibodies and enzyme immunoassay (ELISA) for MUC13. We used this assay to measure MUC13 levels in the supernatants of cancer cell lines and a large cohort of serum samples from healthy and diseased individuals. Results: MUC13 is secreted from cancer cell lines, with highest levels found in ovarian cancer cell lines. MUC13 levels in human sera were significantly increased in patients with renal failure and 20%–30% of patients with ovarian, liver, lung and other cancers. MUC13 was also elevated in 70% of patients with active cutaneous melanoma, but not uveal melanoma. Furthermore, we identified significant MUC13 elevations in the serum of patients with vasculitis (ANCA-positive) autoantibodies, but not in those with inflammatory bowel disease. Conclusions: Serum MUC13 is frequently elevated not only in a variety of malignant cases but also in some benign pathologies, thus appearing to be a non-specific disease biomarker. Nonetheless, serum MUC13 is clearly highly elevated in some carcinoma patients, and its relationship with tumor progression in this context warrant further research. Future studies that examine the correlation between serum MUC13 levels to stage of cancer could elucidate prognostic potential.

scholarly journals Quantifying Substrate Rigidity Effects on Cancer Cell Mechanics using Single Cell Force Spectroscopy

2020 ◽  
Vol 118 (3) ◽  
pp. 604a
Author(s):  
Tsung-Cheng Lin ◽  
Jingqiang Li ◽  
Sithara S. Wijeratne ◽  
Xin He ◽  
Xuewen Feng ◽  
...  
Keyword(s):  
Single Cell ◽  
Cancer Cell ◽  
Cell Mechanics ◽  
Force Spectroscopy ◽  
Substrate Rigidity ◽  
Cell Force

scholarly journals Silencing LRH-1 in colon cancer cell lines impairs proliferation and alters gene expression programs

2015 ◽  
Vol 112 (8) ◽  
pp. 2467-2472 ◽  
Author(s):  
James R. Bayrer ◽  
Sridevi Mukkamala ◽  
Elena P. Sablin ◽  
Paul Webb ◽  
Robert J. Fletterick
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
A Cell

Colorectal cancers (CRCs) account for nearly 10% of all cancer deaths in industrialized countries. Recent evidence points to a central role for the nuclear receptor liver receptor homolog-1 (LRH-1) in intestinal tumorigenesis. Interaction of LRH-1 with the Wnt/β-catenin pathway, highly active in a critical subpopulation of CRC cells, underscores the importance of elucidating LRH-1’s role in this disease. Reduction of LRH-1 diminishes tumor burden in murine models of CRC; however, it is not known whether LRH-1 is required for tumorigenesis, for proliferation, or for both. In this work, we address this question through shRNA-mediated silencing of LRH-1 in established CRC cell lines. LRH-1 mRNA knockdown results in significantly impaired proliferation in a cell line highly expressing the receptor and more modest impairment in a cell line with moderate LRH-1 expression. Cell-cycle analysis shows prolongation of G0/G1 with LRH-1 silencing, consistent with LRH-1 cell-cycle influences in other tissues. Cluster analysis of microarray gene expression demonstrates significant genome wide alterations with major effects in cell-cycle regulation, signal transduction, bile acid and cholesterol metabolism, and control of apoptosis. This study demonstrates a critical proproliferative role for LRH-1 in established colon cancer cell lines. LRH-1 exerts its effects via multiple signaling networks. Our results suggest that selected CRC patients could benefit from LRH-1 inhibitors.

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