Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effects of cigarette smoke extract derived from heated tobacco products on the proliferation of lung cancer stem cells.

ABSTRACT: Epidemiological studies have suggested that cigarette smoking can increase a person's risk of developing several types of cancer, including lung cancer. Lung cancer originates from cancer stem cells (CSCs), which constitute a minor cell population in tumors, and contribute to drug resistance and recurrence. Heated tobacco products (HTPs) produce aerosols that contain nicotine and toxic chemicals. Current evidence, however, is insufficient to accurately determine if HTPs are less harmful than burned cigarettes. This study has investigated the effects of cigarette smoke extract (CSE) from HTPs on lung CSCs in lung cancer cell lines. We found that CSEs induced the proliferation of lung CSCs and increased the expression levels of stem cell markers. In addition, CSE induced epithelial-mesenchymal transition (EMT) expression and cytokine production. These results suggest that HTPs can induce lung CSCs in vitro.

SUBMITTER: Hirata N

PROVIDER: S-EPMC9742876 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Effects of cigarette smoke extract derived from heated tobacco products on the proliferation of lung cancer stem cells.

Hirata Naoya N Horinouchi Takahiro T Kanda Yasunari Y

Toxicology reports 20220607

Epidemiological studies have suggested that cigarette smoking can increase a person's risk of developing several types of cancer, including lung cancer. Lung cancer originates from cancer stem cells (CSCs), which constitute a minor cell population in tumors, and contribute to drug resistance and recurrence. Heated tobacco products (HTPs) produce aerosols that contain nicotine and toxic chemicals. Current evidence, however, is insufficient to accurately determine if HTPs are less harmful than bur ...[more]

PMID: 36518441

Similar Datasets

Cigarette smoke extract and heated tobacco products promote ferritin cleavage and iron accumulation in human corneal epithelial cells.

Project description:The cornea is directly exposed to cigarette smoke, and smoking is a risk factor for several corneal diseases including dry eye syndrome. Currently, heated tobacco products (HTPs) are widely used as substitutes for cigarette smoking around the world. In the present study, we investigated the molecular mechanism(s) leading to cellular injury induced by cigarette smoke extract (CSE) or HTPs. Exposure to CSE perturbed the formation of tight junctions, leading to an increase in cell volume, a decrease in transepithelial electrical resistance (TER) in the human corneal epithelial cell-transformed (HCE-T) cell line. Moreover, CSE exposure induced both lipid peroxidation and ferrous [Fe(II)] ion accumulation in autolysosomal compartments. Interestingly, a cleaved form of ferritin appeared when HCE-T cells were incubated with CSE. This aberrant ferritin processing was suppressed by treatment with autophagy inhibitors. Furthermore, the CSE-induced cell death was suppressed by either ferrostatin-1 or deferoxamine (DFO). CSE exposure also promoted the expression of cytokines whereas DFO treatment inhibited the CSE-induced expression of these cytokines. Exposure to HTPs also induced both HCE-T cell death and cleaved ferritin accumulation in a concentration- and time-dependent manner. These results indicated that CSE or HTPs activated the ferroptosis signaling pathway, which contributed to corneal epithelial cell injury.

| S-EPMC8448754 | biostudies-literature

Cytotoxic effects of the cigarette smoke extract of heated tobacco products on human oral squamous cell carcinoma: the role of reactive oxygen species and CaMKK2.

Project description:BackgroundThe increasing prevalence of heated tobacco products (HTPs) has heightened concerns regarding their potential health risks. Previous studies have demonstrated the toxicity of cigarette smoke extract (CSE) from traditional tobacco's mainstream smoke, even after the removal of nicotine and tar. Our study aimed to investigate the cytotoxicity of CSE derived from HTPs and traditional tobacco, with a particular focus on the role of reactive oxygen species (ROS) and intracellular Ca2+.MethodsA human oral squamous cell carcinoma (OSCC) cell line, HSC-3 was utilized. To prepare CSE, aerosols from HTPs (IQOS) and traditional tobacco products (1R6F reference cigarette) were collected into cell culture media. A cell viability assay, apoptosis assay, western blotting, and Fluo-4 assay were conducted. Changes in ROS levels were measured using electron spin resonance spectroscopy and the high-sensitivity 2',7'-dichlorofluorescein diacetate assay. We performed a knockdown of calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) by shRNA lentivirus in OSCC cells.ResultsCSE from both HTPs and traditional tobacco exhibited cytotoxic effects in OSCC cells. Exposure to CSE from both sources led to an increase in intracellular Ca2+ concentration and induced p38 phosphorylation. Additionally, these extracts prompted cell apoptosis and heightened ROS levels. N-acetylcysteine (NAC) mitigated the cytotoxic effects and p38 phosphorylation. Furthermore, the knockdown of CaMKK2 in HSC-3 cells reduced cytotoxicity, ROS production, and p38 phosphorylation in response to CSE.ConclusionOur findings suggest that the CSE from both HTPs and traditional tobacco induce cytotoxicity. This toxicity is mediated by ROS, which are regulated through Ca2+ signaling and CaMKK2 pathways.

| S-EPMC11197199 | biostudies-literature

<sup>210</sup>Po and <sup>210</sup>Pb content in the smoke of Heated Tobacco Products versus Conventional Cigarette smoking.

Project description:210Po is a radioactive component of conventional cigarette tobacco smoke and is a recognized carcinogen. Despite the expanding market of heated tobacco products, no data are available on the activity of 210Po in the smoke of IQOS Heets cigarette. We determined the 210Po activity in the mainstream smoke of thirteen cigarette brands available on the Swiss market using a smoking machine and compared the results to the 210Po activity measured in the mainstream smoke of the IQOS system. In addition, we measured the 210Po and 210Pb loss on heating after uniform heating from 50 to 600 °C for several cigarette brands and the Heets cigarettes. 13.6 ± 4.1% of 210Po activity was found in the mainstream smoke in conventional cigarette smoking (7% for 210Pb). This dropped to 1.8 ± 0.3% in the mainstream smoke of IQOS Heets. Conversely, when the tobacco was heated uniformly at 330 °C, a loss of 210Po of more than 80% was observed for all type of cigarettes. Apparently, IQOS significantly reduced the 210Po and 210Pb activities in the mainstream smoke. However, our results show that only 15% of the Heets tobacco reaches 330 °C with IQOS. While IQOS reduces the 210Po and 210Pb activities in the mainstream smoke compared to conventional cigarettes, it only heats a marginal fraction of the tobacco present in the Heets cigarette. Because smoking is an addiction (mostly due to nicotine), IQOS could possibly deliver an unsatisfactory dose of nicotine to a Heets cigarette smoker, as most of the tobacco is left unaltered.

| S-EPMC9207432 | biostudies-literature

Cancer potencies and margin of exposure used for comparative risk assessment of heated tobacco products and electronic cigarettes aerosols with cigarette smoke.

Project description:Health risk associated with the use of combustible cigarettes is well characterized and numerous epidemiological studies have been published for many years. Since more than a decade, innovative non-combusted tobacco products have emerged like heated tobacco products (HTP) or electronic cigarettes (EC). Long-term effects of these new products on health remain, however, unknown and there is a need to characterize associated potential health risks. The time dedicated to epidemiological data generation (at least 20 to 40 years for cancer endpoint), though, is not compatible with innovative development. Surrogates need, therefore, to be developed. In this work, non-cancer and cancer risks were estimated in a range of HTP and commercial combustible cigarettes based upon their harmful and potentially harmful constituent yields in aerosols and smoke, respectively. It appears that mean lifetime cancer risk values were decreased by more than one order of magnitude when comparing HTPs and commercial cigarettes, and significantly higher margin of exposure for non-cancer risk was observed for HTPs when compared to commercial cigarettes. The same approach was applied to two commercial ECs. Similar results were also found for this category of products. Despite uncertainties related to the factors used for the calculations and methodological limitations, this approach is valuable to estimate health risks associated to the use of innovative products. Moreover, it acts as predictive tool in absence of long-term epidemiological data. Furthermore, both cancer and non-cancer risks estimated for HTPs and ECs highlight the potential of reduced risk for non-combusted products when compared to cigarette smoking.

| S-EPMC7811518 | biostudies-literature

Heated tobacco products and cigarette marketing in nightclubs in Gdansk, Poland: A mixed-methods analysis.

Project description:IntroductionAlthough advertising and promotion of tobacco products in Poland are prohibited, tobacco companies exploit legal loopholes and insufficient enforcement of the laws to conduct their marketing. To reach young adults, advertisements are placed in entertainment and social venues. This aspect of tobacco product marketing in Poland remains under-researched. The main aim of this study was to investigate the occurrence and characteristics of advertising and promotion of tobacco products in nightclubs in Gdansk, a large city in northern Poland.MethodsWe conducted a single-center observational study of nightclubs in Gdansk, between July and October 2022. Two independent observers visited 30 nightclubs and collected information using pre-prepared research form. The occurrences of tobacco branded bar accessories, logo signs, package displays and other forms of advertising and promotion were recorded. Where possible, photographs of visible marketing displays were taken.ResultsAdvertising of tobacco products was present in 2/3 of the nightclubs observed. The most commonly advertised product category were heated tobacco products. Tobacco brand representatives promoted and offered consumers free tobacco product samples. Multi-level marketing activities were observed, including tobacco branded bar accessories, prominent sale points and tobacco brand logo signs.ConclusionsThe majority of nightclubs observed in Gdansk advertise and promote tobacco products. The ban on tobacco advertising and promotion is being violated in nightclubs, where the most commonly advertised products are heated tobacco products. The authorities should take steps to extend the bans to cover private promotion and enforce the law to protect high-risk individuals from smoking initiation and relapse.

| S-EPMC10768186 | biostudies-literature

Particle emissions from heated tobacco products.

Project description:IntroductionThis study determines the particle emissions from five heated tobacco products (HTPs).MethodsAn aethalometer is used for the determination of black carbon (BC) and an aerosol monitor for total particulate matter (PM) concentration and also PM fractions (1, 2.5, 4, and 10 μm) in the mainstream emissions of 5 HTPs: IQOS, LIL, PULZE, ILUMA, and GLO. Fifteen different flavors were used, five sticks per flavor, which were smoked using a peristaltic pump under both ISO and Canadian smoking regimes. The method repeatability was determined using 15 sticks of one flavor for each brand for each smoking regime.ResultsAll HTPs emit particles, and more than 99.7% of the particles emitted are smaller than 1 μm. Both BC and PM emissions show quite low repeatability. Particle emissions increase in relation to the heating temperature and the intensity smoking regime, and are depending on the flavor used. BC corresponds to a small percentage of total PM.ConclusionsAlthough HTPs are promoted as products of reduced risk compared to conventional cigarettes, high particle concentrations are detected in their emissions, depending on the smoking regime, the flavor used, and the operation parameters. PM emissions vary significantly between different brands under the ISO smoking regime, probably due to the heating temperature. In contrast, PM emissions under the Canadian smoking regime do not vary significantly between different brands. This could probably be attributed to the fact that increased puff frequency does not allow the device to cool down between puffs, resulting in an increase in PM emissions for all the brands, but not dependent on the maximum heating temperature of the device. BC emissions only consist of a very small fraction of PM and do not vary significantly between different brands under both smoking regimes.

| S-EPMC10986040 | biostudies-literature

Conditioned Media of Adipose-Derived Stem Cells Suppresses Sidestream Cigarette Smoke Extract Induced Cell Death and Epithelial-Mesenchymal Transition in Lung Epithelial Cells.

Project description:The role of the epithelial-mesenchymal transition (EMT) in lung epithelial cells is increasingly being recognized as a key stage in the development of COPD, fibrosis, and lung cancers, which are all highly associated with cigarette smoking and with exposure to second-hand smoke. Using the exposure of human lung cancer epithelial A549 cells and non-cancerous Beas-2B cells to sidestream cigarette smoke extract (CSE) as a model, we studied the protective effects of adipose-derived stem cell-conditioned medium (ADSC-CM) against CSE-induced cell death and EMT. CSE dose-dependently induced cell death, decreased epithelial markers, and increased the expression of mesenchymal markers. Upstream regulator analysis of differentially expressed genes after CSE exposure revealed similar pathways as those observed in typical EMT induced by TGF-β1. CSE-induced cell death was clearly attenuated by ADSC-CM but not by other control media, such as a pass-through fraction of ADSC-CM or A549-CM. ADSC-CM effectively inhibited CSE-induced EMT and was able to reverse the gradual loss of epithelial marker expression associated with TGF-β1 treatment. CSE or TGF-β1 enhanced the speed of A549 migration by 2- to 3-fold, and ADSC-CM was effective in blocking the cell migration induced by either agent. Future work will build on the results of this in vitro study by defining the molecular mechanisms through which ADSC-CM protects lung epithelial cells from EMT induced by toxicants in second-hand smoke.

| S-EPMC8584490 | biostudies-literature

Cigarette smoke, but not novel tobacco vapor products, causes epigenetic disruption and cell apoptosis.

Project description:Heat-Not-Burn (HNB) products, generating vapor without combusting tobacco leaves, have been developed with the expectation that the number and quantity of chemicals in the vapor of these products would be reduced compared with the smoke from conventional combustible cigarettes. However, whether the lower chemical levels correlate with lower toxicity remains to be determined. Here we examined differences in the biological effects of conventional cigarette smoke (CS) and two HNB products, Ploom TECH and Ploom TECH+, using the cultured cancer cell line A549 and the normal bronchial epithelium cell line BEAS-2B. The conventional CS 3R4F extract (0.5%) markedly decreased cell proliferation of both A549 and BEAS-2B cells; however, 0.5% extracts of these commercially available HNB products did not affect cell growth. To determine the cause of decreased cell proliferation, a TUNEL assay was performed, and the results indicated that apoptosis had occurred in both A549 and BEAS-2B cells at 24 h after exposure to 3R4F. To further explore the effect of CS on epigenetics, we performed western blotting to detect histone H2A phosphorylation, which is known to affect transcriptional regulation. Only the 3R4F extract decreased histone H2A phosphorylation in both A549 and BEAS-2B cells. Next, we examined alterations in gene expression after treatment of A549 cells with Ploom TECH, Ploom TECH+, or 3R4F extracts. It was found that 339, 107, and 103 genes were upregulated more than 2 fold in A549 cells treated with 3R4F, Ploom TECH, or Ploom TECH + extracts, respectively. Among the 339 genes that were upregulated in response to 3R4F, we focused on EGR1, FOS, and FOSB, since they were upregulated more than 100 fold, which was confirmed using RT-qPCR. These results suggest that CS, but not HNB products, cause epigenetic disruption and cell apoptosis, possibly by elevating transcription of genes such as EGR1.

| S-EPMC7691555 | biostudies-literature

The Substitution of Fifty Percent of Combustible Tobacco Smoke Exposure With Either Electronic Cigarettes or Heated tobacco Products Did Not Attenuate Acute Lung Injury in an Animal Model.

Project description:BackgroundTo reduce the harmful health effects of combustible cigarette smoke (CS), some (CS) users attempt to substitute CS with electronic cigarettes (ECIG) and/or heated tobacco products (HTP). In this animal study, we evaluated the acute effects of substituting CS consumption with ECIG or HTP thus mimicking the dual users' approach, on the lungs of a mouse model.MethodsC57BL/6 mice were divided into Control, ECIG, HTP, CS, ECIG + CS, HTP + CS, and HTP + ECIG groups. Animals were exposed for 3 hours in AM and PM sessions to either air, CS, ECIG, or HTP for seven days. Lung injury was assessed by: wet to dry (W/D) ratio, albumin concentration in bronchoalveolar lavage fluid, expression of IL-1β, IL-6, and TNF-α, histopathology examination, reactive oxygen species (ROS) production, and assessment of cellular apoptosis.ResultsW/D ratio was significantly increased in mice exposed to CS only. Albumin leak and expression of IL-1β, IL-6, and TNF-a were elevated in CS, ECIG + CS, and HTP + CS. Histological examination revealed significant inflammatory cells infiltration, as well as collagen deposit in CS, ECIG + CS, HTP + CS. ROS production was significantly increased in CS, ECIG + CS, HTP + CS. Finally, cell death was also significantly increased in CS, ECIG + CS, and HTP + CS.ConclusionIn this animal model, substituting 50% of daily CS exposure by either ECIG or HTP exposure did not result in significant attenuation of acute lung injury.

| S-EPMC10256882 | biostudies-literature

Cigarette smoke extract-treated alveolar macrophage-derived extracellular vesicles

Project description:This project is based upon the fundamental observation that alveolar macrophage-derived extracellular vesicles (AM-EVs), when internalized by neighboring epithelial cells, inhibit their infection by influenza virus. This inhibitory activity of AM-EVs is abolished when AMs are treated with cigarette smoke extract (CSE). We chose to survey the AM-EV proteome in an effort to identify candidate proteins whose abundance within EVs was downregulated by CSE treatment of AMs, thus explaining the ability of CSE to abrogate the inhibitory activity against influenza.

2020-06-09 | PXD019528 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data