scholarly journals Temperature-controlled MPa-pressure ultrasonic cell manipulation in a microfluidic chip

Lab on a Chip ◽  
2015 ◽  
Vol 15 (16) ◽  
pp. 3341-3349 ◽  
Author(s):  
Mathias Ohlin ◽  
Ida Iranmanesh ◽  
Athanasia E. Christakou ◽  
Martin Wiklund
Keyword(s):  
Lung Cancer ◽  
High Pressure ◽  
Cancer Cells ◽  
Microfluidic Chip ◽  
Acoustic Streaming ◽  
Cell Manipulation ◽  
Wave Trapping ◽  
Ultrasonic Standing Wave ◽  
Temperature Controlled

We study the effect of 1 MPa-pressure ultrasonic-standing-wave trapping of cells during one hour in a fully temperature- and acoustic streaming-controlled microfluidic chip, and conclude that the viability of lung cancer cells are not affected by this high-pressure, long-term acoustophoresis treatment.

scholarly journals Negative Regulation of PTEN by MicroRNA-221 and Its Association with Drug Resistance and Cellular Senescence in Lung Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Ning Wang ◽  
Chen Zhu ◽  
Ye Xu ◽  
Wenliang Qian ◽  
Min Zheng
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Cell Lines ◽  
Term Treatment ◽  
Lung Cancer Cells ◽  
Akt Pathway ◽  
Long Term Treatment ◽  
Important Regulator

Objective.Chemotherapy is the routine method for treating many cancers, but long-term treatment may result in developing resistance to the drugs. The aim of this study was to identify whether noncoding RNAs play a role in drug resistance and how they affect drug resistance.Materials and Methods.The expression levels of miR-221 in different lung cancer cell lines H226, H1299, and A549 were measured. H1299 and A549 cell lines were transfected to overexpress and downexpress miR-221, and cell viability and cell senescence were determined. The PTEN/Akt pathway was then examined by real-time polymerase chain reaction and Western blot analysis.Results. MiR-221 together with proteins MDR1 and ABCG2 was upregulated in Cisplatin-resistant A549 lung cancer cells. Anti-miR-221 inhibits proliferation and induces senescence in lung cancer cells. PTEN/Akt pathway axis was identified as a target of drug resistance induced by miR-221.Conclusion. Our results revealed that miR-221 is an important regulator for chemotherapy sensitivity and showed miR-221 as a potential target for drug sensitization.

scholarly journals New Paradigms to Assess Consequences of Long-Term, Low-Dose Curcumin Exposure in Lung Cancer Cells

Molecules ◽  
2020 ◽  
Vol 25 (2) ◽  
pp. 366 ◽  
Author(s):  
Gintare Smagurauskaite ◽  
Jagdish Mahale ◽  
Karen Brown ◽  
Anne L. Thomas ◽  
Lynne M. Howells
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Low Dose ◽  
Resistant Cell ◽  
Treatment Withdrawal ◽  
Curcumin Treatment ◽  
Chemotherapy Drugs ◽  
Long Term Treatment

Curcumin has been investigated extensively for cancer prevention, but it has been proposed that long-term treatments may promote clonal evolution and gain of cellular resistance, potentially rendering cancer cells less sensitive to future therapeutic interventions. Here, we used long-term, low-dose treatments to determine the potential for adverse effects in non-small cell lung cancer (NSCLC) cells. IC50s for curcumin, cisplatin, and pemetrexed in A549, PC9, and PC9ER NSCLC cells were evaluated using growth curves. IC50s were subsequently re-assessed following long-term, low-dose curcumin treatment and a three-month treatment withdrawal period, with a concurrent assessment of oncology-related protein expression. Doublet cisplatin/pemetrexed-resistant cell lines were created and the IC50 for curcumin was determined. Organotypic NSCLC-fibroblast co-culture models were used to assess the effects of curcumin on invasive capacity. Following long-term treatment/treatment withdrawal, there was no significant change in IC50s for the chemotherapy drugs, with chemotherapy-resistant cell lines exhibiting similar sensitivity to curcumin as their non-resistant counterparts. Curcumin (0.25–0.5 µM) was able to inhibit the invasion of both native and chemo-resistant NSCLC cells in the organotypic co-culture model. In summary, long-term curcumin treatment in models of NSCLC neither resulted in the acquisition of pro-carcinogenic phenotypes nor caused resistance to chemotherapy agents.

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 Long-term persistent infection of HPV 16 E6 up-regulate SP1 and hTERT by inhibiting LKB1 in lung cancer cells

PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0182775 ◽  
Author(s):  
Jing-Hua Yang ◽  
Xiao-Yan Li ◽  
Xin Wang ◽  
Wei-Jian Hou ◽  
Xue-Shan Qiu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Persistent Infection ◽  
Lung Cancer Cells ◽  
Hpv 16

scholarly journals Exposure of Breast and Lung Cancer Cells to a Novel Estrone Analog Prior to Radiation Enhances Bcl-2-Mediated Cell Death

2018 ◽  
Vol 19 (10) ◽  
pp. 2887 ◽  
Author(s):  
Elsie Nolte ◽  
Anna Joubert ◽  
Roy Lakier ◽  
Ado van Rensburg ◽  
Anne Mercier
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Low Dose ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Term Survival ◽  
Dna Damage And Repair ◽  
Mcf 7

Following exposure of cells to gamma-radiation, a cascade of intracellular consequences may be observed in a semitemporal manner. This includes deoxyribonucleic acid (DNA) damage and reactive oxygen species (ROS) accumulation initially, with consequent signaling for DNA repair and facilitative regulation of the cell cycle. Failure to rectify the damage or ROS levels leads to induction of senescence or apoptosis. 2-Ethyl-3-O-sulfamoyl-estra-1,3,5(10),15-tetraen-17-ol (ESE-15-ol), a 2-methoxyestradiole analog designed in silico for superior pharmacokinetics, was investigated for its potential to enhance apoptotic signaling and decrease the long-term survival of cells exposed to radiation. Sequential early intracellular effects within radiation-treated MCF-7 breast- and A549 lung cancer cells pre-exposed to low-dose ESE-15-ol were investigated using various flow cytometric protocols, spectrophotometry, and microscopy. Long-term cellular survival and proliferation was examined using clonogenic studies, which demonstrated a significant decrease in the presensitized cells. Combination-treated cells exhibited increased superoxide formation, and decreased Bcl-2 expression and -phosphorylation. Induction of apoptosis and elevation of the sub-G1 phase was evident in the pre-exposed MCF-7 cells, although only minimally in the A549 cells at 48-h. These results indicate that low-dose ESE-15-ol may increase tumor response to radiation. Future studies will investigate the effect of ESE-15-ol pre-exposure on radiation-induced DNA damage and repair mechanisms.

scholarly journals AKR1B10 (Aldo-keto reductase family 1 B10) promotes brain metastasis of lung cancer cells in a multi-organ microfluidic chip model

2019 ◽  
Vol 91 ◽  
pp. 195-208 ◽  
Author(s):  
Wenwen Liu ◽  
Jing Song ◽  
Xiaohui Du ◽  
Yang Zhou ◽  
Yang Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Brain Metastasis ◽  
Cancer Cells ◽  
Microfluidic Chip ◽  
Lung Cancer Cells

scholarly journals Ultrasonic Based Tissue Modelling and Engineering

Micromachines ◽  
2018 ◽  
Vol 9 (11) ◽  
pp. 594 ◽  
Author(s):  
Karl Olofsson ◽  
Björn Hammarström ◽  
Martin Wiklund
Keyword(s):  
Explant Culture ◽  
Cell Manipulation ◽  
Label Free ◽  
Particle Manipulation ◽  
Tissue Organization ◽  
Ultrasonic Standing Wave ◽  
Tissue Modelling

Systems and devices for in vitro tissue modelling and engineering are valuable tools, which combine the strength between the controlled laboratory environment and the complex tissue organization and environment in vivo. Device-based tissue engineering is also a possible avenue for future explant culture in regenerative medicine. The most fundamental requirements on platforms intended for tissue modelling and engineering are their ability to shape and maintain cell aggregates over long-term culture. An emerging technology for tissue shaping and culture is ultrasonic standing wave (USW) particle manipulation, which offers label-free and gentle positioning and aggregation of cells. The pressure nodes defined by the USW, where cells are trapped in most cases, are stable over time and can be both static and dynamic depending on actuation schemes. In this review article, we highlight the potential of USW cell manipulation as a tool for tissue modelling and engineering.

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