Classical Cancer Biology: Misconceptions and Limitations

2017 ◽  
Author(s):  
Abicumaran Uthamacumaran
Keyword(s):  
Cancer Cells ◽  
Cancer Biology ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Transformed Cells ◽  
Epigenetic Landscape ◽  
Normal Cells ◽  
Cancer Models ◽  
Stem Cell Division ◽  
Insight Into

Cancer is the co-evolution of cancer cells and their turbulent microenvironment, characterized by dynamical hyper-chaotic gene expression profiles. However, cancers should not be viewed as the result of random mutations and malfunctioning information processing systems. Rather, it is the selective advantages conferred by adaptive evolution of cellular biosystems. Although on a systemic scale, cancer is defined as a disease, on a cellular basis they outperform healthy (non-transformed cells) in terms of survival and reproductive success. Their enhanced longevity pathways, metastatic invasion, extended telomeres, dynamical morphogenesis, regenerative stem cell division and environment-specific metabolic cascades indicate they are adaptive evolutionary cell states that have surpassed the boundaries normal cells are confined to. Therefore, the paper presents a brief summary of currently existing classical cancer models in the field of mathematical biology and the misconceptions of cancer epimetabolomes to further advance cancer research beyond its current limits. Through an insight into the mathematical behaviors of cancer cells, a quantum adaptive epigenetic landscape is proposed to explain the selective evolutionary dominance of cancer cells.

scholarly journals Gene Expression and Transcriptome Profiling of Changes in a Cancer Cell Line Post-Exposure to Cadmium Telluride Quantum Dots: Possible Implications in Oncogenesis

Dose-Response ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 155932582110198
Author(s):  
Mohammed S. Aldughaim ◽  
Mashael R. Al-Anazi ◽  
Marie Fe F. Bohol ◽  
Dilek Colak ◽  
Hani Alothaid ◽  
...  
Keyword(s):  
Gene Expression ◽  
Quantum Dots ◽  
Cancer Cells ◽  
Cadmium Telluride ◽  
Cancer Progression ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Dependent Manner ◽  
Cdte Qds ◽  
Cadmium Telluride Quantum Dots

Cadmium telluride quantum dots (CdTe-QDs) are acquiring great interest in terms of their applications in biomedical sciences. Despite earlier sporadic studies on possible oncogenic roles and anticancer properties of CdTe-QDs, there is limited information regarding the oncogenic potential of CdTe-QDs in cancer progression. Here, we investigated the oncogenic effects of CdTe-QDs on the gene expression profiles of Chang cancer cells. Chang cancer cells were treated with 2 different doses of CdTe-QDs (10 and 25 μg/ml) at different time intervals (6, 12, and 24 h). Functional annotations helped identify the gene expression profile in terms of its biological process, canonical pathways, and gene interaction networks activated. It was found that the gene expression profiles varied in a time and dose-dependent manner. Validation of transcriptional changes of several genes through quantitative PCR showed that several genes upregulated by CdTe-QD exposure were somewhat linked with oncogenesis. CdTe-QD-triggered functional pathways that appear to associate with gene expression, cell proliferation, migration, adhesion, cell-cycle progression, signal transduction, and metabolism. Overall, CdTe-QD exposure led to changes in the gene expression profiles of the Chang cancer cells, highlighting that this nanoparticle can further drive oncogenesis and cancer progression, a finding that indicates the merit of immediate in vivo investigation.

scholarly journals 1100: Gene Expression Profiles of Doxazosin-Treated LNCaP Prostate Cancer Cells

2004 ◽  
Vol 171 (4S) ◽  
pp. 290-290
Author(s):  
José M. Arencibia ◽  
Mónica Del Río ◽  
Ana Bonnin ◽  
Mónica López-Barahona
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Cancer Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Prostate Cancer Cells

Gene expression profiles of folate deficient colon cancer cells

2003 ◽  
Vol 124 (4) ◽  
pp. A239
Author(s):  
Petar Novakovic ◽  
Kyoung-Jin Sohn ◽  
Young-In J. Kim
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Colon Cancer Cells

scholarly journals Mechanical Stretch Kills Transformed Cancer Cells

2018 ◽  
Author(s):  
Ajay Tijore ◽  
Mingxi Yao ◽  
Yu-Hsiu Wang ◽  
Yasaman Nematbakhsh ◽  
Anushya Hariharan ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Calcium Influx ◽  
Mechanical Stretch ◽  
Cyclic Stretch ◽  
Transformed Cells ◽  
Normal Cells ◽  
Calcium Dependent ◽  
Cyclic Stretching ◽  
Protease Activation ◽  
Different Tissues

AbstractTransformed cancer cells differ from normal cells in several important features like anchorage independence, Warburg effect and mechanosensing. Consequently, transformed cancer cells develop an anaplastic morphology and respond aberrantly to external mechanical forces. Consistent with altered mechano-responsiveness, here we show that transformed cancer cells from many different tissues have reduced growth and become apoptotic upon cyclic stretch as do normal cells after the transformation. When matrix rigidity sensing is restored in transformed cancer cells, they survive and grow faster on soft surface upon cyclic stretch like normal cells but undergo anoikis without stretch by activation of death associated protein kinase1 (DAPK1). In contrast, stretch-dependent apoptosis (mechanoptosis) of transformed cells is driven by stretch-mediated calcium influx and calcium-dependent calpain 2 protease activation on both collagen and fibronectin matrices. Further, mechanosensitive calcium channel, Piezo1 is needed for mechanoptosis. Thus, cyclic stretching of transformed cells from different tissues activates apoptosis, whereas similar stretching of normal cells stimulates growth.

scholarly journals Single-cell intracellular epitope and transcript detection revealing signal transduction dynamics

2020 ◽  
Author(s):  
Francesca Rivello ◽  
Erik van Buijtenen ◽  
Kinga Matuła ◽  
Jessie A.G.L. van Buggenum ◽  
Paul Vink ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Single Cell ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Protein Levels ◽  
Inhibitory Drug ◽  
Insight Into ◽  
Transcript Detection

AbstractCurrent high-throughput single-cell multi-omics methods cannot concurrently map changes in (phospho)protein levels and the associated gene expression profiles. We present QuRIE-seq (Quantification of RNA and Intracellular Epitopes by sequencing) and use multi-factor omics analysis (MOFA+) to map signal transduction over multiple timescales. We demonstrate that QuRIE-seq can trace the activation of the B-cell receptor pathway at the minute and hour time-scale and provide insight into the mechanism of action of an inhibitory drug, Ibrutinib.

scholarly journals ”BIK/NBK Gene Expression as a Possible Marker of Circulating Breast Cancer Cells in Blood“

2011 ◽  
Vol 4 (1) ◽  
pp. 8-14
Author(s):  
E. Lopez-Munoz ◽  
N. Garcia-Hernandez ◽  
R. I. Penaloza-Espinosa ◽  
M. E. Gomez-Del Toro ◽  
G. Zarco-Espinosa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Therapeutic Target ◽  
Breast Cancer Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Breast Cancer Tissue ◽  
Cancer Tissue ◽  
Mrna Gene

The detection of circulating breast cancer cells in blood could be of special interest as an indicator of diagnosis and prognosis, and for the selection of treatment. In a previous report, our research group determined gene expression profiles in samples of breast cancer tissue, identifying over-expression of the BIK/NBK mRNA gene in 90% of the analyzed samples. In this paper, we analyze the BIK/NBK gene expression as a possible biomarker of circulating breast cancer cells in blood. We demonstrate that the BIK/NBK gene expression is not a significant biomarker in the detection of circulating breast cancer cells in the blood of women with breast cancer. Several studies have evaluated the regulation of apoptosis by estrogens in breast cancer cells, demonstrating the importance of BIK/NBK protein, in estrogen-regulated breast cancer cell apoptosis, which suggests that the regulation of its expression may be an important therapeutic target or strategy in the management of cancer, and, although we did not find statistically significant differences among the patient groups to demonstrate that BIK/NBK gene expression is a biomarker of circulating breast cancer cells in blood, we consider it necessary to continue the study of this gene in breast cancer tissue and its role in the development and progression of breast cancer, its prognostic value, and its potential use as therapeutic target.

scholarly journals Transcriptome profiling reveals Silibinin dose-dependent response network in non-small lung cancer cells

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10373
Author(s):  
Jagan Mohan Kaipa ◽  
Vytaute Starkuviene ◽  
Holger Erfle ◽  
Roland Eils ◽  
Evgeny Gladilin
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Transcriptome Profiling ◽  
Small Cell Lung ◽  
Silybum Marianum ◽  
Systematic Analysis ◽  
Response Network ◽  
Dose Dependent

Silibinin (SIL), a natural flavonolignan from the milk thistle (Silybum marianum), is known to exhibit remarkable hepatoprotective, antineoplastic and EMT inhibiting effects in different cancer cells by targeting multiple molecular targets and pathways. However, the predominant majority of previous studies investigated effects of this phytocompound in a one particular cell line. Here, we carry out a systematic analysis of dose-dependent viability response to SIL in five non-small cell lung cancer (NSCLC) lines that gradually differ with respect to their intrinsic EMT stage. By correlating gene expression profiles of NSCLC cell lines with the pattern of their SIL IC50 response, a group of cell cycle, survival and stress responsive genes, including some prominent targets of STAT3 (BIRC5, FOXM1, BRCA1), was identified. The relevancy of these computationally selected genes to SIL viability response of NSCLC cells was confirmed by the transient knockdown test. In contrast to other EMT-inhibiting compounds, no correlation between the SIL IC50 and the intrinsic EMT stage of NSCLC cells was observed. Our experimental results show that SIL viability response of differently constituted NSCLC cells is linked to a subnetwork of tightly interconnected genes whose transcriptomic pattern can be used as a benchmark for assessment of individual SIL sensitivity instead of the conventional EMT signature. Insights gained in this study pave the way for optimization of customized adjuvant therapy of malignancies using Silibinin.

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