Mutational landscape induced by chronic exposure to environmental PM and PM in A549 lung epithelial cell.

Exposure to particulate matter (PM) has been linked to an increased risk of multiple diseases, primarily lung cancer, through various molecular mechanisms. However, the mutagenic potential of PM remains unclear. This study aimed to provide a comprehensive description of genetic mutations and mutagenic signatures resulting from chronic exposure to PM or PM.

Sampling, composition, and biological effects of Mexico City airborne particulate matter from multiple periods.

Air pollution is a worldwide environmental problem with an impact on human health. Particulate matter of ten micrometers or less aerodynamic diameter (PM) as well as its fine fraction (PM) is related to multiple pulmonary diseases. The impact of air pollution in Mexico City, and importantly, particulate matter has been studied and considered as a risk factor for two decades ago.

Airborne particulate matter (PM) induces cell invasion through Aryl Hydrocarbon Receptor and Activator Protein 1 (AP-1) pathway deregulation in A549 lung epithelial cells.

Background: Particulate matter with an aerodynamic size ≤ 10 μm (PM) is a risk factor for lung cancer development, mainly because some components are highly toxic. Polycyclic aromatic hydrocarbons (PAHs) are present in PM, such as benzo[a]pyrene (BaP), which is a well-known genotoxic and carcinogenic compound to humans, capable of activating AP-1 transcription factor family genes through the Aryl Hydrocarbon Receptor (AhR). Because effects of BaP include metalloprotease 9 (MMP-9) activation, cell invasion, and other pathways related to carcinogenesis, we aimed to demonstrate that PM (10 µg/cm) exposure induces the activation of AP-1 family members as well as cell invasion in lung epithelial cells, through AhR pathway.

Nucleotide Excision Repair Pathway Activity Is Inhibited by Airborne Particulate Matter (PM) through XPA Deregulation in Lung Epithelial Cells.

Airborne particulate matter with a diameter size of ≤10 µm (PM) is a carcinogen that contains polycyclic aromatic hydrocarbons (PAH), which form PAH-DNA adducts. However, the way in which these adducts are managed by DNA repair pathways in cells exposed to PM has been partially described. We evaluated the effect of PM on nucleotide excision repair (NER) activity and on the levels of different proteins of this pathway that eliminate bulky DNA adducts.

Particulate matter (PM) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells.

Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability.

Particulate Matter (PM) Promotes Cell Invasion through Epithelial-Mesenchymal Transition (EMT) by TGF-β Activation in A549 Lung Cells.

Air pollution presents a major environmental problem, inducing harmful effects on human health. Particulate matter of 10 μm or less in diameter (PM) is considered an important risk factor in lung carcinogenesis. Epithelial-mesenchymal transition (EMT) is a regulatory program capable of inducing invasion and metastasis in cancer.

Long non-coding RNA NORAD upregulation induced by airborne particulate matter (PM) exposure leads to aneuploidy in A549 lung cells.

Air pollution is a worldwide problem that affects human health predominantly in the largest cities. Particulate matter of 10 μm or less in diameter (PM) is considered a risk factor for multiple diseases, including lung cancer. The long non-coding RNA NORAD and the components of the spindle assembly checkpoint (SAC) ensure proper chromosomal segregation.

Irreversible disruption of the cytoskeleton as induced by non-cytotoxic exposure to titanium dioxide nanoparticles in lung epithelial cells.

Exposure to TiO NPs induces several cellular alterations after NPs uptake including disruption of cytoskeleton that is crucial for lung physiology but is not considered as a footprint of cell damage. We aimed to investigate cytoskeleton disturbances and the impact on cell migration induced by an acute TiO NPs exposure (24 h) and the recovery capability after 6 days of NPs-free treatment, which allowed investigating if cytoskeleton damage was reversible. Exposure to TiO NPs (10 μg/cm) for 24 h induced a decrease 20.

Erratum: A combination of inhibitors of glycolysis, glutaminolysis and fatty acid synthesis decrease the expression of chemokines in human colon cancer cells.

[This corrects the article DOI: 10.3892/ol.2019.

Airborne Particulate Matter (PM) Inhibits Apoptosis through PI3K/AKT/FoxO3a Pathway in Lung Epithelial Cells: The Role of a Second Oxidant Stimulus.

Outdoor particulate matter (PM) exposure is carcinogenic to humans. The cellular mechanism by which PM is associated specifically with lung cancer includes oxidative stress and damage to proteins, lipids, and DNA in the absence of apoptosis, suggesting that PM induces cellular survival. We aimed to evaluate the PI3K/AKT/FoxO3a pathway as a mechanism of cell survival in lung epithelial A549 cells exposed to PM that were subsequently challenged with hydrogen peroxide (HO).

A combination of inhibitors of glycolysis, glutaminolysis and fatty acid synthesis decrease the expression of chemokines in human colon cancer cells.

Lonidamine, 6-Diazo-5-oxo-L-norleucine (DON) and orlistat are well known inhibitors of glycolysis, glutaminolysis and of fatty acid synthesis, respectively. Although their antitumor effects have been explored in detail, the potential inhibition of the malignant metabolic phenotype and its influence on the expression of chemokines and growth factors involved in colon cancer, have not been previously reported to the best of our knowledge. In the present study, dose-response curves with orlistat, lonidamine or DON were generated from cell viability assays conducted in SW480 colon cancer cells.

Airborne particulate matter induces mitotic slippage and chromosomal missegregation through disruption of the spindle assembly checkpoint (SAC).

Particulate matter (PM) is a risk factor for lung cancer development and chromosomal missegregation and cell cycle disruptions are key cellular events that trigger tumorigenesis. We aimed to study the effect of PM (PM with an aerodynamic diameter ≤10 μm) on mitotic arrest and chromosomal segregation, evaluating the spindle assembly checkpoint (SAC) protein dynamics in the human lung A549 adenocarcinoma cell line. For this purpose, synchronized cells were exposed to PM for 24 h to obtain the frequency of micronucleated (MN) and trinucleated (TN) cells.

Cytotoxic Activity and Structure-Activity Relationship of Triazole-Containing Bis(Aryl Ether) Macrocycles.

Cancer continues to be a worldwide health problem. Certain macrocyclic molecules have become attractive therapeutic alternatives for this disease because of their efficacy and, frequently, their novel mechanisms of action. Herein, we report the synthesis of a series of 20-, 21-, and 22-membered macrocycles containing triazole and bis(aryl ether) moieties.

Orlistat as a FASN inhibitor and multitargeted agent for cancer therapy.

Introduction: Cancer cells have increased glycolysis and glutaminolysis. Their third feature is increased de novo lipogenesis. As such, fatty acid (FA) synthesis enzymes are over-expressed in cancer and their depletion causes antitumor effects.

Atmospheric particulate matter (PM10) exposure-induced cell cycle arrest and apoptosis evasion through STAT3 activation via PKCζ and Src kinases in lung cells.

Atmospheric particulate matter with aerodynamic diameter ≤10 μm (PM10) is a risk factor for the development of lung cancer, but cellular pathways are not completely understood. STAT3 is a p21(Waf1/Cip1) transcription factor and is associated with proliferation and cell survival and is upregulated in lung cancer. PM10 exposure induces p21(Waf1/Cip1) expression, which could be related to STAT3 activation.

Particulate matter (PM₁₀) induces metalloprotease activity and invasion in airway epithelial cells.

Airborne particulate matter with an aerodynamic diameter ≤ 10 μm (PM10) is a risk factor for the development of lung diseases and cancer. The aim of this work was to identify alterations in airway epithelial (A549) cells induced by PM10 that could explain how subtoxic exposure (10 μg/cm(2)) promotes a more aggressive in vitro phenotype. Our results showed that cells exposed to PM10 from an industrial zone (IZ) and an urban commercial zone (CZ) induced an increase in protease activity and invasiveness; however, the cell mechanism is different, as only PM10 from CZ up-regulated the activity of metalloproteases MMP-2 and MMP-9 and disrupted E-cadherin/β-catenin expression after 48 h of exposure.

Induction of c-Jun by air particulate matter (PM₁₀) of Mexico city: Participation of polycyclic aromatic hydrocarbons.

The carcinogenic potential of urban particulate matter (PM) has been partly attributed to polycyclic aromatic hydrocarbons (PAHs) content, which activates the aryl hydrocarbon receptor (AhR). Here we report the effect of PM with an aerodynamic size of 10 μm (PM10) on the induction of AhR pathway in A549 cells, evaluating its downstream targets CYP1B1, IL-6, IL-8 and c-Jun. Significant increases in CYP1B1 protein and enzyme activity; IL-6 and IL-8 secretion and c-Jun protein were found in response to PM10.

Cell cycle synchronization reveals greater G2/M-phase accumulation of lung epithelial cells exposed to titanium dioxide nanoparticles.

Titanium dioxide has been classified in the 2B group as a possible human carcinogen by the International Agency for Research on Cancer, and amid concerns of its exposure, cell cycle alterations are an important one. However, several studies show inconclusive effects, mainly because it is difficult to compare cell cycle effects caused by TiO2 nanoparticle (NP) exposure between different shapes and sizes of NP, cell culture types, and time of exposure. In addition, cell cycle is frequently analyzed without cell cycle synchronization, which may also mask some effects.

Cytoplasmic p21(CIP1/WAF1), ERK1/2 activation, and cytoskeletal remodeling are associated with the senescence-like phenotype after airborne particulate matter (PM(10)) exposure in lung cells.

The exposure to particulate matter with a mean aerodynamic diameter ≤10 μm (PM10) from urban zones is considered to be a risk factor in the development of cancer. The aim of this work was to determine if PM10 exposure induces factors related to the acquisition of a neoplastic phenotype, such as cytoskeletal remodeling, changes in the subcellular localization of p21(CIP1/WAF1), an increase in β-galactosidase activity and changes in cell cycle. To test our hypothesis, PM10 from an industrial zone (IZ) and a commercial zone (CZ) were collected, and human adenocarcinoma lung cell cultures (A549) were exposed to a sublethal PM10 concentration (10 μg/cm(2)) for 24 h and 48 h.

Particulate matter promotes in vitro receptor-recognizable low-density lipoprotein oxidation and dysfunction of lipid receptors.

Particulate matter may promote cardiovascular disease, possibly as a consequence of its oxidative potential. Studies using susceptible animals indicate that particulate matter aggravates atherosclerosis by increasing lipid/macrophage content in plaques. Macrophage lipid uptake requires oxidized low-density lipoprotein and scavenger receptors; same receptors are involved in particulate matter uptake.

The alpha-mangostin prevention on cisplatin-induced apoptotic death in LLC-PK1 cells is associated to an inhibition of ROS production and p53 induction.

Cisplatin (CDDP) is a widely useful chemotherapeutic agent for the treatment of tumors including lung, ovary and testis. Acute renal injury, however, is the main side effect observed after CDDP treatment. This side effect is related to the apoptotic death in proximal tubular cells in the kidney and p53 protein has a central role in this process.

PM(10) impairs the antioxidant defense system and exacerbates oxidative stress driven cell death.

The aim of this study was to investigate the effect of airborne particulate matter with a mean aerodynamic diameter of < or =10microm (PM(10)) on oxidative stress markers and antioxidant enzymatic activity and its relevance in the face of acute oxidative challenge in a human lung epithelial cell line (A549). PM(10)-induced reactive oxygen species (ROS) generation and oxidative damage with no changes in cellular viability. In addition, PM(10) decreased glutathione (GSH) levels (54.

DNA damage response of A549 cells treated with particulate matter (PM10) of urban air pollutants.

We describe the events triggered by a sub-lethal concentration of airborne particulate matter (PM(10)) in A549 cells, which include the formation DNA double-strand breaks, gammaH2A.X generation, and 53BP1 recruitment. To protect the genome, cells activated ATM/ATR/Chk1/Chk2/p53 pathway but, after 48 h, cells turned into a senescence-like state.