scholarly journals Dual-targeted peptide-conjugated multifunctional fluorescent probe with AIEgen for efficient nucleus-specific imaging and long-term tracing of cancer cells

2017 ◽  
Vol 8 (6) ◽  
pp. 4571-4578 ◽  
Author(s):  
Yong Cheng ◽  
Chunli Sun ◽  
Xiaowen Ou ◽  
Bifeng Liu ◽  
Xiaoding Lou ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Fluorescent Probe ◽  
Cancer Cell ◽  
Cell Behaviors ◽  
Low Toxicity

Precisely targeted transportation of a long-term tracing regent to a nucleus with low toxicity is one of the most challenging concerns in revealing cancer cell behaviors.

scholarly journals Matrix Metalloproteinase 8 (Collagenase 2) Induces the Expression of Interleukins 6 and 8 in Breast Cancer Cells

2013 ◽  
Vol 288 (23) ◽  
pp. 16282-16294 ◽  
Author(s):  
Sally Thirkettle ◽  
Julie Decock ◽  
Hugh Arnold ◽  
Caroline J. Pennington ◽  
Diane M. Jaworski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines

Matrix metalloproteinase 8 (MMP-8) is a tumor-suppressive protease that cleaves numerous substrates, including matrix proteins and chemokines. In particular, MMP-8 proteolytically activates IL-8 and, thereby, regulates neutrophil chemotaxis in vivo. We explored the effects of expression of either a WT or catalytically inactive (E198A) mutant version of MMP-8 in human breast cancer cell lines. Analysis of serum-free conditioned media from three breast cancer cell lines (MCF-7, SK-BR-3, and MDA-MB-231) expressing WT MMP-8 revealed elevated levels of IL-6 and IL-8. This increase was mirrored at the mRNA level and was dependent on MMP-8 catalytic activity. However, sustained expression of WT MMP-8 by breast cancer cells was non-permissive for long-term growth, as shown by reduced colony formation compared with cells expressing either control vector or E198A mutant MMP-8. In long-term culture of transfected MDA-MB-231 cells, expression of WT but not E198A mutant MMP-8 was lost, with IL-6 and IL-8 levels returning to base line. Rare clonal isolates of MDA-MB-231 cells expressing WT MMP-8 were generated, and these showed constitutively high levels of IL-6 and IL-8, although production of the interleukins was no longer dependent upon MMP-8 activity. These studies support a causal connection between MMP-8 activity and the IL-6/IL-8 network, with an acute response to MMP-8 involving induction of the proinflammatory mediators, which may in part serve to compensate for the deleterious effects of MMP-8 on breast cancer cell growth. This axis may be relevant to the recognized ability of MMP-8 to orchestrate the innate immune system in inflammation in vivo.

Cancer Cell Growth in the Near Infrared Region by Using Silica Coated Gold Nanorods

NANO ◽  
2020 ◽  
Vol 15 (01) ◽  
pp. 2050001 ◽  
Author(s):  
Tuntun Wang ◽  
Kwi Seok Yeom ◽  
Sitansu Sekhar Nanda ◽  
Seong Soo A. An ◽  
Dong Kee Yi
Keyword(s):  
Protein Folding ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gold Nanorods ◽  
Near Infrared ◽  
Infrared Region ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Cell Behaviors

Gold nanorods (AuNRs) have been considered as suitable materials for diverse biomedical applications in controlling cell behaviors. The nanoisland system with well-dispersed silica coated Au nanorods (Si-AuNRs) was used to demonstrate the enhanced cell growth of normal and cancer cells (MDA-MB-231 mammalian breast cancer cells) from the induced expressions of the heat shock proteins (HSPs). The over-expressions of HSP could help in protein folding in cell proliferations and growths of both the normal and cancer cells. In the current study, interesting mechanisms of cancer cell growth with Si-AuNRs than the conventional systems, such as incubator, would be presented. We believe that the growth of cancer cells in near infrared (NIR) region using Si-AuNRs induced the activities of HSPs, which could help the protein folding in cell growth and survival in comparison to the cells grown in the incubator only. The cell growth enhancing technology could be expanded in diverse applications in cell culture systems.

scholarly journals Long-Term Nitric Oxide Exposure Enhances Lung Cancer Cell Migration

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Arpasinee Sanuphan ◽  
Preedakorn Chunhacha ◽  
Varisa Pongrakhananon ◽  
Pithi Chanvorachote
Keyword(s):  
Nitric Oxide ◽  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Biology ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Dependent Manner

Nitric oxide (NO) found in the vicinity of lung cancer cells may play a role in the regulation of cancer cell behaviors. To explore the possible effects of NO on cell motility, human lung cancer cells were exposed to nontoxic concentrations of NO for 0–14 days, and the migratory characteristics of the cells were determined. The present study found that long-term treatment with NO significantly enhanced cell migration in a dose- and time-dependent manner. Furthermore, we found that the increased migratory action was associated with the increased expression of caveolin-1 (Cav-1), which in turn activated the focal adhesion kinase (FAK) and ATP-dependent tyrosine kinase (Akt) pathways. Notably, the NO-treated cells exhibited an increased number of filopodia per cell, as well as an increase in the levels of cell division cycle 42 (Cdc42) protein. Together, these results indicate that extended NO exposure has a novel effect on cell migration through a Cav-1-dependent mechanism, a finding that strengthens our understanding of cancer biology.

scholarly journals Exploring cysteine regulation in cancer cell survival with a highly specific “Lock and Key” fluorescent probe for cysteine

2019 ◽  
Vol 10 (43) ◽  
pp. 10065-10071 ◽  
Author(s):  
Jing Liu ◽  
Mengxing Liu ◽  
Hongxing Zhang ◽  
Xuehong Wei ◽  
Juanjuan Wang ◽  
...  
Keyword(s):  
Cell Survival ◽  
Cancer Cells ◽  
Fluorescent Probe ◽  
Cancer Cell ◽  
Cancer Cell Survival

Using a highly specific “lock and key” fluorescent Cys probe, we confirmed that targeting Cys metabolism to deplete intracellular Cys is a more potent strategy to sensitize cancer cells to chemotherapies.

Amphiphilic fluorescent probe self-encored in plasma to detect pH fluctuations in cancer cell membranes

2021 ◽  
Author(s):  
Arup Podder ◽  
Manu M. Joseph ◽  
Shayeri Biswas ◽  
Sanjib Samanta ◽  
Kaustabh K. Maiti ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cancer Cells ◽  
Fluorescent Probe ◽  
Cancer Cell ◽  
Cell Membranes ◽  
Normal Cells ◽  
Turn On ◽  
Ph Fluctuations

Newly developed an amphiphilic “turn-on” fluorescent probe (P1CS) enables to distinguish of cancer cells from normal cells through mapping of pH fluctuations in cell-surface.

A near-infrared biothiol-specific fluorescent probe for cancer cell recognition

The Analyst ◽  
2019 ◽  
Vol 144 (16) ◽  
pp. 4750-4756 ◽  
Author(s):  
Li Liu ◽  
Rui-Jie Lv ◽  
Jong-Kai Leung ◽  
Qian Zou ◽  
Yue Wang ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Fluorescent Probe ◽  
Cancer Cell ◽  
Cancer Diagnosis ◽  
Near Infrared ◽  
Great Promise ◽  
Cell Recognition ◽  
Normal Cells

A novel near-infrared biothiol-specific fluorescent probe can discriminate cancer cells from normal cells showing great promise for cancer diagnosis.

Biofabricated tumor microenvironments for studying colorectal cancer in vitro and in vivo.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e14689-e14689
Author(s):  
Mahesh Devarasetty ◽  
Samuel Herberg ◽  
Anthony Dominijanni ◽  
Ethan Willey-Shelkey ◽  
Aleksander Skardal ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Stromal Cells ◽  
Cell Phenotype ◽  
Micro Structure ◽  
Therapeutic Development

e14689 Background: Microenvironmental mechanics have a tremendous effect on the progression, phenotype, and therapeutic response of cancer cells positioning it as a high-potential target for novel therapeutic development. Laboratory modeling of the microenvironment and its multitude of effects is imperative for developing new avenues of anti-cancer therapy that can target non-traditional vectors such as the extracellular matrix (ECM) and stromal cells. Researchers have developed in vitro models of the tumor microenvironment (TME) to meet this need. While in vitro modeling is an important step in therapeutic development, there are few studies that validate in vitro generated results to gold-standard in vivo models, and further, to patient-derived data. Previously, we have developed a model of the colorectal tumor microenvironment and found a connection between collagen ultrastructure and cancer cell phenotype. Using this characterized organoid model, we implant bioengineered TMEs into mice to track long-term growth and progression of cancer and compare our results to clinical biopsies. Methods: Tumor organoids are produced by combining stromal cells and type I collagen. Cancer cell spheroids are embedded into the organoid for long term observation. Organoids are either observed in vitro or implanted subcutaneously into mice for in vivo tracking. Results: Organoids retain structure and viability during long term culture in vitro and in vivo, and embedded cancer cells respond significantly differently depending on the architecture of the surrounding TME. Cancer cells assume a mesenchymal, invasive, and proliferative phenotype in unorganized TMEs, and revert to an epithelial phenotype in an ordered TME. In addition, analysis of biopsied tissue, across tumor grade, demonstrates a correlation between cancer cell phenotype and microenvironmental architecture. Conclusions: In all this is the first study to establish a connection between TME micro-structure and cancer cell phenotype consistently across three distinct research modalities. These results have the potential to pave the way for utilizing bioengineered microenvironmental models as therapeutic development platforms and for targeting TME micro-structure to control colorectal cancer cell progression.

scholarly journals Redox Control of the Dormant Cancer Cell Life Cycle

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2707
Author(s):  
Bowen Li ◽  
Yichun Huang ◽  
Hui Ming ◽  
Edouard C. Nice ◽  
Rongrong Xuan ◽  
...  
Keyword(s):  
Life Cycle ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Molecular Mechanisms ◽  
Tumor Therapy ◽  
Redox Signaling ◽  
Redox Control ◽  
Cell Life ◽  
Metastatic Relapse

Following efficient tumor therapy, some cancer cells may survive through a dormancy process, contributing to tumor recurrence and worse outcomes. Dormancy is considered a process where most cancer cells in a tumor cell population are quiescent with no, or only slow, proliferation. Recent advances indicate that redox mechanisms control the dormant cancer cell life cycle, including dormancy entrance, long-term dormancy, and metastatic relapse. This regulatory network is orchestrated mainly through redox modification on key regulators or global change of reactive oxygen species (ROS) levels in dormant cancer cells. Encouragingly, several strategies targeting redox signaling, including sleeping, awaking, or killing dormant cancer cells are currently under early clinical evaluation. However, the molecular mechanisms underlying redox control of the dormant cancer cell cycle are poorly understood and need further exploration. In this review, we discuss the underlying molecular basis of redox signaling in the cell life cycle of dormant cancer and the potential redox-based targeting strategies for eliminating dormant cancer cells.

Upregulation of cellular triacylglycerol – free fatty acid cycling by oleate is associated with long-term serum-free survival of human breast cancer cells

2007 ◽  
Vol 85 (3) ◽  
pp. 301-310 ◽  
Author(s):  
Ewa Przybytkowski ◽  
Érik Joly ◽  
Christopher J. Nolan ◽  
Serge Hardy ◽  
Ann-Michele Francoeur ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Free Survival ◽  
Serum Free

We previously showed that exogenous oleate protects human breast cancer cells against palmitate-induced apoptosis in part by increasing esterification of this free fatty acid (FFA) into triacylglycerol (TG). Here, we studied the mechanism whereby oleate protects these cells against apoptosis induced by serum withdrawal. The metabolism of FFA, TG, and glucose, in parallel with long-term cell survival in the absence of serum, was investigated in a panel of human breast cancer cell lines and in nontransformed MCF-10A cells after treatment with exogenous oleate. Short-term (3–24 h) exposure of MDA-MB-231 human breast cancer cells to exogenous oleate resulted in a dose-dependent long-term (10 day) serum-free survival that correlated with the accumulation of TG in lipid droplets and with upregulation of lipolysis. Both effects persisted for several days after oleate removal. Rapid TG lipolysis and FFA re-esterification, supported by high rates of glycolysis that provide the glycerol backbone for TG synthesis, are consistent with the presence of very active TG–FFA cycling in human breast cancer cells. Only the cancer cell lines capable of accumulating TG showed long-term serum-free survival after oleate treatment. The results suggest that upregulation of TG–FFA cycling induced by oleate may be involved in maintenance of human breast cancer cell survival.

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