Quantitative expression of human drug transporter proteins in lung tissues: Analysis of regional, gender, and interindividual differences by liquid chromatography–tandem mass spectrometry

Sakamoto, Atsushi; Matsumaru, Takehisa; Yamamura, Norio; Uchida, Yasuo; Tachikawa, Masanori; Ohtsuki, Sumio

doi:10.1002/jps.23606

Cited by 76 publications

(92 citation statements)

References 53 publications

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“…It is known that several different ABC and SLC transporters are expressed in lung tissue (e.g., multidrug resistance-associated protein 1 [ABCC1] and ABCG2), where they control pulmonary absorption of inhaled drugs as well as transport of drugs from epithelial cells to the circulating blood (26). We found no influence of Abcb1a/b and Abcg2 on the distribution of 11 C-erlotinib to the lung (Supplemental Fig.…”

Section: Discussionmentioning

confidence: 77%

Breast Cancer Resistance Protein and P-Glycoprotein Influence In Vivo Disposition of ¹¹C-Erlotinib

et al. 2015

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Section: Discussionmentioning

confidence: 77%

Breast Cancer Resistance Protein and P-Glycoprotein Influence In Vivo Disposition of ¹¹C-Erlotinib

et al. 2015

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“…However, they also have some limitations in that they are frequently used as a single cell type in monolayer culture, they may have an atypical phenotype (e.g., derived from adenocarcinomas) and their tight junctions may not be representative of the target tissue. Furthermore, their drug transporters may not be typical of normal lung epithelium, although these have been recently evaluated in five commercially available immortalized lung cell lines (Calu-3, BEAS2-B, NCI-H292, NCI-H441 and A549) by liquid chromatography-tandem mass spectrometrybased approaches (Sakamoto et al, 2015), allowing comparison with data from primary lung cells (Sakamoto et al, 2013). Although immortalized, ideally these cells should be used within a defined range of passages to ensure that their phenotypic characteristics remain consistent.…”

Section: Cell Lines (Standardization and Validation)mentioning

confidence: 99%

Non-animal models of epithelial barriers (skin, intestine and lung) in research, industrial applications and regulatory toxicology

Gordon

Daneshian

Bouwstra

et al. 2015

ALTEX

122

103

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SummaryModels of the outer epithelia of the human body -namely the skin, the intestine and the lung -have found valid applications in both research and industrial settings as attractive alternatives to animal testing. A variety of approaches to model these barriers are currently employed in such fields, ranging from the utilization of ex vivo tissue to reconstructed in vitro models, and further to chip-based technologies, synthetic membrane systems and, of increasing current interest, in silico modeling approaches. An international group of experts in the field of epithelial barriers was convened from academia, industry and regulatory bodies to present both the current state of the art of non-animal models of the skin, intestinal and pulmonary barriers in their various fields of application, and to discuss research-based, industry-driven and regulatory-relevant future directions for both the development of new models and the refinement of existing test methods. Issues of model relevance and preference, validation and standardization, acceptance, and the need for simplicity versus complexity were focal themes of the discussions. The outcomes of workshop presentations and discussions, in relation to both current status and future directions in the utilization and development of epithelial barrier models, are presented by the attending experts in the current report.

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“…In the present study, the celecoxib-treated lymphoma cells exhibited significantly decreased expression of Bcl-2 and increased expression of Bax compared with those that were not treated with celecoxib, suggesting that effect on the Bcl-2/BaX protein ratio may be an important contributing factor to celecoxib-induced apoptosis. Additionally, it has been identified that the abnormal expression of P-gp and MRP1 on the surface of the cell membrane may impair tumor chemosensitivity and lead to MDR by removing chemotherapy drugs from tumor cells (13)(14)(15)(16). Overexpression of P-gp and MRP1 in tumor tissues has been associated with poor response to clinical chemotherapy in T-cell lymphoma (15,17).…”

Section: Discussionmentioning

confidence: 99%

Celecoxib enhances sensitivity to chemotherapy drugs of T‑cell lymphoma

Yang

Zhao

et al. 2018

Oncol Lett

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Abstract. Celecoxib is a newly-identified nonsteroidal anti-inflammatory drug, which has been used to treat fever in clinical practice. Celecoxib has been demonstrated to suppress the viability of various human tumor cells. However, the effect of celecoxib on response of T-cell lymphoma to chemotherapy agents remains unclear. The aim of the present study was to investigate the effect of celecoxib on chemosensitivity of human T-cell lymphoma, and to address the underlying mechanism of action. The cytotoxicity of CDDP, epirubicin and VCR on Jurkat and Hut-78 cells treated with celecoxib was assessed by MTT assay, and the half-maximal inhibitory concentration (IC 50 ) value was calculated by Origin 75 software. The effect of celecoxib on apoptosis and intracellular concentration of Rhodamine-123 in Jurkat and Hut-78 cells was analyzed by flow cytometry. The expression of transcription factor p65 (p65), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), multidrug resistance 1 (MDR1) and multidrug resistance-associated protein 1 (MRP1) at mRNA and protein levels were detected by reverse transcription quantitative polymerase chain reaction and western blotting, respectively. Proliferation suppression rates and apoptosis levels were significantly increased in Jurkat and Hut-78 cells combined with celecoxib compared with those without celecoxib, when treated with CDDP, epirubicin and VCR. The IC 50 values of the chemotherapy agents were lower in Jurkat and Hut-78 cells treated with celecoxib compared with those that were not.The apoptosis level, expression of Bax and the intracellular concentration of Rhodamine-123 were increased, whereas the expression of p65, Bcl-2, MDR1 and MRP1 were decreased, in celecoxib-treated Jurkat and Hut-78 cells compared with those without celecoxib treatment. These results indicated that celecoxib may enhance the sensitivity of T-cell lymphoma to chemotherapy drugs by inhibiting the expression of multidrug resistance (MDR)-associated proteins via downregulating the activity of the nuclear factor-κB signaling pathway, suggesting that celecoxib may improve the curative effect of chemotherapy drugs in T-cell lymphoma.

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Quantitative expression of human drug transporter proteins in lung tissues: Analysis of regional, gender, and interindividual differences by liquid chromatography–tandem mass spectrometry

Cited by 76 publications

References 53 publications

Breast Cancer Resistance Protein and P-Glycoprotein Influence In Vivo Disposition of ¹¹C-Erlotinib

Breast Cancer Resistance Protein and P-Glycoprotein Influence In Vivo Disposition of ¹¹C-Erlotinib

Non-animal models of epithelial barriers (skin, intestine and lung) in research, industrial applications and regulatory toxicology

Celecoxib enhances sensitivity to chemotherapy drugs of T‑cell lymphoma

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Quantitative expression of human drug transporter proteins in lung tissues: Analysis of regional, gender, and interindividual differences by liquid chromatography–tandem mass spectrometry

Cited by 76 publications

References 53 publications

Breast Cancer Resistance Protein and P-Glycoprotein Influence In Vivo Disposition of 11C-Erlotinib

Breast Cancer Resistance Protein and P-Glycoprotein Influence In Vivo Disposition of 11C-Erlotinib

Non-animal models of epithelial barriers (skin, intestine and lung) in research, industrial applications and regulatory toxicology

Celecoxib enhances sensitivity to chemotherapy drugs of T‑cell lymphoma

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Product

Resources

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Breast Cancer Resistance Protein and P-Glycoprotein Influence In Vivo Disposition of ¹¹C-Erlotinib

Breast Cancer Resistance Protein and P-Glycoprotein Influence In Vivo Disposition of ¹¹C-Erlotinib