scholarly journals Investigations into Idiosyncratic Drug-Induced Hepatotoxicity and Chronic Proliferation of Cancer Cells using a Label-Free Method

2018 ◽  
Vol 114 (3) ◽  
pp. 336a
Author(s):  
Corina T. Bot ◽  
Sonja Stölzle-Feix ◽  
Krisztina Juhasz ◽  
Elena Dragicevic ◽  
Leo Doerr ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Label Free ◽  
Drug Induced

scholarly journals Investigating the effects of Pentoxifylline on human breast cancer cells using Raman spectroscopy

2015 ◽  
Vol 08 (02) ◽  
pp. 1550004 ◽  
Author(s):  
Peeyush N. Goel ◽  
S. P. Singh ◽  
C. Murali Krishna ◽  
R. P. Gude
Keyword(s):  
Breast Cancer ◽  
Raman Spectroscopy ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Label Free ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Drug Induced ◽  
Linear Discriminant

Breast cancer is one of the leading causes of cancer-related deaths in a global scenario. In the present study, biochemical changes exerted upon Pentoxifylline (PTX) treatment had been appraised in human breast cancer cells using Raman spectroscopy. There are no clinically approved methods to monitor such therapeutic responses available. The spectral profiling is suggestive of changes in DNA, protein and lipid contents showing a linear relationship with drug dosage. Further, multivariate analysis using principal-component based linear-discriminant-analysis (PC-LDA) was employed for classifying the control and the PTX treated groups. These findings support the feasibility of Raman spectroscopy as an alternate/adjunct label-free, objective method for monitoring drug-induced modifications against breast cancer cells.

scholarly journals Albendazole Exhibits Anti-Neoplastic Actions against Gastric Cancer Cells by Affecting STAT3 and STAT5 Activation by Pleiotropic Mechanism(s)

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 362
Author(s):  
Min Hee Yang ◽  
In Jin Ha ◽  
Jae-Young Um ◽  
Kwang Seok Ahn
Keyword(s):  
Gastric Cancer ◽  
Reactive Oxygen Species ◽  
Transcription Factors ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Oxygen Species ◽  
Gastric Cancer Cells ◽  
Drug Induced ◽  
Cellular Apoptosis ◽  
Interfering Rna

Albendazole (ABZ) has been reported to display anti-tumoral actions against various maliganncies, but possible impact of ABZ on gastric cancer has not been deciphered. As aberrant phosphorylation of STAT3 and STAT5 proteins can regulate the growth and progression of gastric cancer, we postulated that ABZ may interrupt the activation of these oncogenic transcription factors. We found that ABZ exposure abrogated STAT3/5 activation, inhibited phosphorylation of Janus-activated kinases 1/2 and Src and enhanced the levels of SHP-1 protein. Silencing of SHP-1 gene by small interfering RNA (siRNA) reversed the ABZ-promoted attenuation of STAT3 as well as STAT5 activation and cellular apoptosis. In addition, these effects were noted to be driven by an augmented levels of reactive oxygen species caused by drug-induced GSH/GSSG imbalance. Thus, the data indicates that ABZ can modulate the activation of STAT3 and STAT5 by pleiotropic mechanisms in gastric cancer cells.

scholarly journals A Novel Nanobody Precisely Visualizes Phosphorylated Histone H2AX in Living Cancer Cells under Drug-Induced Replication Stress

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3317
Author(s):  
Eric Moeglin ◽  
Dominique Desplancq ◽  
Audrey Stoessel ◽  
Christian Massute ◽  
Jeremy Ranniger ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Mammalian Cells ◽  
Chromatin Modification ◽  
Replication Stress ◽  
Living Cells ◽  
Single Step ◽  
Dna Double Strand Breaks ◽  
Drug Induced ◽  
Histone H2ax ◽  
C Terminus

Histone H2AX phosphorylated at serine 139 (γ-H2AX) is a hallmark of DNA damage, signaling the presence of DNA double-strand breaks and global replication stress in mammalian cells. While γ-H2AX can be visualized with antibodies in fixed cells, its detection in living cells was so far not possible. Here, we used immune libraries and phage display to isolate nanobodies that specifically bind to γ-H2AX. We solved the crystal structure of the most soluble nanobody in complex with the phosphopeptide corresponding to the C-terminus of γ-H2AX and show the atomic constituents behind its specificity. We engineered a bivalent version of this nanobody and show that bivalency is essential to quantitatively visualize γ-H2AX in fixed drug-treated cells. After labelling with a chemical fluorophore, we were able to detect γ-H2AX in a single-step assay with the same sensitivity as with validated antibodies. Moreover, we produced fluorescent nanobody-dTomato fusion proteins and applied a transduction strategy to visualize with precision γ-H2AX foci present in intact living cells following drug treatment. Together, this novel tool allows performing fast screenings of genotoxic drugs and enables to study the dynamics of this particular chromatin modification in individual cancer cells under a variety of conditions.

scholarly journals In Vitro Spectroscopy-Based Profiling of Urothelial Carcinoma: A Fourier Transform Infrared and Raman Imaging Study

Cancers ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 123
Author(s):  
Monika Kujdowicz ◽  
Wojciech Placha ◽  
Brygida Mech ◽  
Karolina Chrabaszcz ◽  
Krzysztof Okoń ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Fourier Transform ◽  
Cancer Cells ◽  
Cell Line ◽  
Cell Lines ◽  
Malignant Neoplasm ◽  
Fourier Transform Infrared ◽  
Diagnostic Tools ◽  
Label Free ◽  
Bladder Cancer Cells

Markers of bladder cancer cells remain elusive, which is a major cause of the low recognition of this malignant neoplasm and its recurrence. This implies an urgent need for additional diagnostic tools which are based on the identification of the chemism of bladder cancer. In this study, we employed label-free techniques of molecular imaging—Fourier Transform Infrared and Raman spectroscopic imaging—to investigate bladder cancer cell lines of various invasiveness (T24a, T24p, HT-1376, and J82). The urothelial HCV-29 cell line was the healthy control. Specific biomolecules discriminated spatial distribution of the nucleus and cytoplasm and indicated the presence of lipid bodies and graininess in some cell lines. The most prominent discriminators are the total content of lipids and sugar moieties as well as the presence of glycogen and other carbohydrates, un/saturated lipids, cytochromes, and a level of S-S bridges in proteins. The combination of the obtained hyperspectral database and chemometric methods showed a clear differentiation of each cell line at the level of the nuclei and cytoplasm and pointed out spectral signals which differentiated bladder cancer cells. Registered spectral markers correlated with biochemical composition changes can be associated with pathogenesis and potentially used for the diagnosis of bladder cancer and response to experimental therapies.

Abstract 188: Deep learning enables label-free profiling of the tumor microenvironment and enrichment of rare cancer cells

2021 ◽  
Author(s):  
Mahyar Salek ◽  
Hou-pu Chou ◽  
Prashast Khandelwal ◽  
Krishna P. Pant ◽  
Thomas J. Musci ◽  
...  
Keyword(s):  
Deep Learning ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Rare Cancer ◽  
Label Free

scholarly journals Dynamic Proteomics Reveals High Plasticity of Cellular Proteome: Growth-Related and Drug-Induced Changes in Cancer Cells are Comparable

PROTEOMICS ◽  
2018 ◽  
Vol 18 (24) ◽  
pp. 1800118 ◽  
Author(s):  
Pierre Sabatier ◽  
Amir Ata Saei ◽  
Shiyu Wang ◽  
Roman A. Zubarev
Keyword(s):  
Cancer Cells ◽  
High Plasticity ◽  
Drug Induced ◽  
Induced Changes

scholarly journals Widespread multi-targeted therapy resistance via drug-induced secretome fucosylation

2021 ◽  
Author(s):  
Mark Borris D. Aldonza ◽  
Junghwa Cha ◽  
Insung Yong ◽  
Jayoung Ku ◽  
Dabin Lee ◽  
...  
Keyword(s):  
Targeted Therapies ◽  
Large Scale ◽  
Kinase Inhibitors ◽  
Tumor Regression ◽  
Therapy Resistance ◽  
Critical Component ◽  
Label Free ◽  
Drug Induced ◽  
Pan Cancer ◽  
Core Fucosylation

AbstractCancer secretome is a reservoir for aberrant glycosylation. How therapies alter this post-translational cancer hallmark and the consequences thereof remain elusive. Here we show that an elevated secretome fucosylation is a pan-cancer signature of both response and resistance to multiple targeted therapies. Large-scale pharmacogenomics revealed that fucosylation genes display widespread association with resistance to these therapies. In both cancer cell cultures and patients, targeted kinase inhibitors distinctively induced core fucosylation of secreted proteins less than 60 kDa. Label-free proteomics of N-glycoproteomes revealed that fucosylation of the antioxidant PON1 is a critical component of the therapy-induced secretome. Core fucosylation in the Golgi impacts PON1 stability and folding prior to secretion, promoting a more degradation-resistant PON1. Non-specific and PON1-specific secretome de-N-glycosylation both limited the expansion of resistant clones in a tumor regression model. Our findings demonstrate that core fucosylation is a common modification indirectly induced by targeted therapies that paradoxically promotes resistance.

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