Chemotherapy Immunophenoprofiles in Non‐Small‐Cell Lung Cancer by Personalized Membrane Proteomics

Putri, Denise Utami; Feng, Po Hao; Hsu, Yuu Hueih; Lee, Kang Yun; Jiang, Feng; Kuo, Lu Wei; Chen, Yu‐Ju; Han, Chia Li

doi:10.1002/prca.201700040

Cited by 10 publications

(4 citation statements)

References 52 publications

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“…In brief, lung tissues were lysed and homogenized using a Minilys® personal homogenizer (Bertin, Rockville, MD, USA) to collect clear supernatants as lung tissue lysates. Fifty micrograms of lung tissue proteins from ve randomly selected rats in each group was separately subjected to gel-assisted digestion with trypsin [54], and resulting peptides from the same exposure group were pooled and labeled with one of the tandem mass tag isobaric reagents (ThermoFisher Scienti c). Labeled peptides were then pooled and fractionated by reverse-phase StageTip following a previously reported protocol [55].…”

Section: Quantitative Tissue Proteomics Analysismentioning

confidence: 99%

Air pollution-regulated E-cadherin mediates contact inhibition of proliferation via the hippo signaling pathways in emphysema

Chang

Lee

Laiman

et al. 2022

Chemico-Biological Interactions

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Section: Quantitative Tissue Proteomics Analysismentioning

confidence: 99%

Air pollution-regulated E-cadherin mediates contact inhibition of proliferation via the hippo signaling pathways in emphysema

Chang

Lee

Laiman

et al. 2022

Chemico-Biological Interactions

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“…Fifty micrograms of lung tissue proteins were aliquoted from each of the 5 rats from the 6 exposure groups for our reported gel-assisted digestion with trypsin individually (60). The resulting peptides were vacuum-dried and resuspended in 100 mM TEABC for BCA protein assay.…”

Section: Gel-assisted Digestion Tandem Mass Tag (Tmt) Labeling and Hmentioning

confidence: 99%

Prolonged Exposure to Traffic-related Particulate Matter Showed Distinct Molecular Mechanisms of Lung Injury in Rats

Jheng¹,

Putri²,

Chuang³

et al. 2020

Preprint

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Background: Exposure to particulate matter (PM) pollution has direct impacts on the respiratory organs, yet the molecular alterations underlying PM-induced pulmonary injury remain unclear. In this study, we investigated the effect of PM on lung tissues of SD rats with whole-body exposure to traffic-related PM1 (< 1 mm in aerodynamic diameter) pollutants and compared it with rats exposed to high-efficiency particulate air-filtered gaseous pollutants and clean air control for 3 and 6 months. Lung function and histological examinations as well as quantitative proteomics analysis and functional validation were performed. Results: The rats in 6-month PM1-exposed group showed significant decline in lung function by decreased forced expiratory flow and forced expiratory volume, but the histological analysis revealed an earlier lung damage evidenced by increased congestion and macrophage infiltration in 3-month PM1-exposed rat lungs. The lung tissue proteomics analysis identified 2,673 proteins which highlighted dysregulations on proteins involved in oxidative stress, cellular metabolisms, calcium signaling, inflammatory responses, and actin dynamics. The presence of fine particles specifically enhanced the oxidative stress and inflammatory reactions under sub-chronic exposure of traffic-related PM1 and suppressed the glucose metabolism and actin cytoskeleton signaling which might lead to repair failure and thus lung function decline after chronic exposure of traffic-related PM1. A detailed pathogenic mechanism was proposed to depict the temporal and dynamic molecular regulations associated with PM1-induced lung injury.Conclusion: Our study explored the earlier lung injury prior to lung function decline and proposed potential molecular features for traffic-related PM1-induced lung injury.

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“…Gel-assisted digestion, tandem mass tag (TMT) labeling and high pH reversed phage (RP) StageTip fractionation Fifty micrograms of lung tissue proteins were aliquoted from each of the 5 rats from the 6 exposure groups for our reported gel-assisted digestion with trypsin individually (58). The resulting peptides were vacuum-dried and resuspended in 100 mM TEABC for BCA protein assay.…”

Section: Tissue Lysate Collectionmentioning

confidence: 99%

Differential Lung Proteome Profiles Upon Pulmonary Exposure to Traffic-related Particulate Matter

Jheng¹,

Putri²,

Chuang³

et al. 2020

Preprint

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Abstract Background: Exposure to particulate matter (PM) pollution has direct impacts on the respiratory organs, yet the molecular alterations underlying PM-induced pulmonary injury remain unclear. In this study, we investigated the effect of PM on lung tissues from our previously reported rat model with whole-body exposure to traffic-related PM1 pollutants and compared it with rats exposed to high-efficiency particulate air-filtered gaseous pollutants and clean air control for 3 and 6 months. Lung function and histological examinations as well as quantitative proteomics analysis and functional validation were performed. Results: The rats in 6-month PM1-exposed group showed significant decline in lung function by decreased forced expiratory flow and forced expiratory volume, but the histological analysis revealed an earlier lung damage evidenced by increased congestion and macrophage infiltration in 3-month PM1-exposed rat lungs. The lung tissue proteomics analysis identified 2,673 proteins which highlighted dysregulations on proteins involved in oxidative stress, cellular metabolisms, calcium signaling, inflammatory responses, and actin dynamics. The presence of fine particles specifically enhanced the oxidative stress and inflammatory reactions under sub-chronic exposure of traffic-related PM1 and suppressed the glucose metabolism and actin cytoskeleton signaling which might lead to repair failure and thus lung function decline after chronic exposure of traffic-related PM1. A detailed pathogenic mechanism was proposed to depict the temporal and dynamic molecular regulations associated with PM1-induced lung injury.Conclusion: Our study explored the earlier lung injury prior to lung function decline and proposed several proteins as potential molecular features for traffic-related PM1-induced lung injury.

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Chemotherapy Immunophenoprofiles in Non‐Small‐Cell Lung Cancer by Personalized Membrane Proteomics

Abstract: Without the additional isolation of specific immune cell populations, our study demonstrated that PEM-CIS chemotherapy altered patients' immune system in terms of neutrophils, T cells, and antigen presentation pathways.

Cited by 10 publications

References 52 publications

Air pollution-regulated E-cadherin mediates contact inhibition of proliferation via the hippo signaling pathways in emphysema

Air pollution-regulated E-cadherin mediates contact inhibition of proliferation via the hippo signaling pathways in emphysema

Prolonged Exposure to Traffic-related Particulate Matter Showed Distinct Molecular Mechanisms of Lung Injury in Rats

Differential Lung Proteome Profiles Upon Pulmonary Exposure to Traffic-related Particulate Matter

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