Inhibitory effect of traditional oriental medicine-derived monoamine oxidase B inhibitor on radioresistance of non-small cell lung cancer

Son, Bong Soo; Jun, Se Young; Seo, Hyunduk; Youn, HyeSook; Yang, Hee Jung; Kim, Wanyeon; Kim, Hyung Kook; Kang, ChulHee; Youn, BuHyun

doi:10.1038/srep21986

Cited by 42 publications

(30 citation statements)

References 49 publications

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“…24 Briefly, cells (1 × 10 4 in serum-free RPMI-1640 medium) subjected to the indicated treatments for 72 h were seeded into the upper chambers of a 24-well Transwell chamber (Corning, Corning, NY, USA) fitted with a 5 μm pore-size insert. The lower chamber was filled with RPMI-1640 medium containing 2% FBS.…”

Section: Methodsmentioning

confidence: 99%

TFAP2C-mediated upregulation of TGFBR1 promotes lung tumorigenesis and epithelial–mesenchymal transition

Kim

Lee

et al. 2016

Exp Mol Med

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TFAP2C (transcription factor-activating enhancer-binding protein 2C) expression has been positively correlated with poor prognosis in patients with certain types of cancer, but the mechanisms underlying TFAP2C-mediated tumorigenesis in non-small-cell lung cancer (NSCLC) are still unknown. We previously performed a microarray analysis to identify TFAP2C regulation genes, and TGFBR1 (transforming growth factor-β receptor type 1) was found to be upregulated by TFAP2C. We observed that TFAP2C or TGFBR1 overexpression led to oncogenic properties, such as cell viability, proliferation and cell cycle progression. TGFBR1 upregulation induced by TFAP2C also promoted cell motility and migration, leading to malignant development. We also found that PAK1 (p21 protein (Cdc42/Rac)-activated kinase 1) signaling was involved in TFAP2C/TGFBR1-induced tumorigenesis. These results were confirmed by an in vivo xenograft model and patient tissue samples. This study shows that TFAP2C promoted tumor progression by upregulation of TGFBR1 and consequent activation of PAK1 signaling.

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Section: Methodsmentioning

confidence: 99%

TFAP2C-mediated upregulation of TGFBR1 promotes lung tumorigenesis and epithelial–mesenchymal transition

Kim

Lee

et al. 2016

Exp Mol Med

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“…The isolation of RNA, synthesis of cDNA and real-time RT-PCR were performed as previously described [28]. To isolate total RNA from A549 and NCI-H441 cells, Trizol® reagent (Thermo Fisher Scientific, Grand Island, NY) was utilized and RNA quality was assessed by agarose gel electrophoresis (visual absence of significant 18s and 28s rRNA degradation).…”

Section: Rna Extraction and Real-time Qrt-pcrmentioning

confidence: 99%

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

Lee

Kim

Kang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Radiotherapy is applied to patients with inoperable cancer types including advanced stage non-small cell lung cancer (NSCLC) and radioresistance functions as a critical obstacle in radiotherapy. This study was aimed to investigate the mechanism of radioresistance regulated by surfactant protein B (SP-B). Methods: To investigate the role of SP-B in radioresistance, ΔSFTPB A549 cell line was established and SP-B expression was analyzed. In response to ionizing radiation (IR), the change of SP-B expression was analyzed in A549 and NCI-H441 cell lines. Conditioned media (CM) from NSCLC cells were utilized to evaluate the downstream signaling pathway. The in vivo effects of SP-B were assessed through mouse xenograft model with intratumoral injection of CM. Results: In response to IR, NSCLC cell lines showed decreased SP-B regulated by the TGF-β signaling and decreased SP-B stimulated cell survival and epithelial-mesenchymal transition. Treatment with CM from irradiated cells activated sPLA 2 , enhanced protein kinase Cδ-MAPKs signaling pathway, and increased arachidonic acid production. We confirmed the in vivo roles of SP-B through mouse xenograft model. Conclusion: Our results revealed that down-regulation of SP-B was involved in the radiation-induced metastatic conversion of NSCLC and provided evidence that SP-B acted as a suppressor of NSCLC progression.S. Lee and D. Kim contributed equally to this work.

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“…It has previously been established that Salvia miltiorrhiza Bunge is widely used in Traditional Chinese Medicine for the treatment of cardiovascular disease, and tanshinol extracted from S. miltiorrhiza Bunge has been identified to be the primary active component (10). Tanshinol has now been widely applied in various human diseases including cancer (11), chronic kidney disease (12) and heart disease (13). Previous data have demonstrated that tanshinol may decrease oxidative stress to avoid deleterious effects on tissue (14).…”

Section: Introductionmentioning

confidence: 99%

Tanshinol upregulates the expression of aquaporin�5 in lung tissue of rats with sepsis

Yang

Dong

2018

Oncol Lett

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Aquaporin 5 (AQP-5) is a water channel protein that is closely associated with non-small cell lung cancer tissues. The present study aimed to investigate the mechanism of tanshinol treatment on AQP-5 in the lung tissue of rats with sepsis. Animals in a rat sepsis model were randomly divided into six groups including blank control (ctrl), sham operation (SO), model (sepsis), low dose tanshinol (5 mg/kg/day; Tan-L), moderate dose tanshinol (10 mg/kg/day; Tan-M) and high dose tanshinol (20 mg/kg/day; Tan-H) groups. After 7 days of administration, the expression level of AQP-5 mRNA was detected by reverse transcription-quantitative polymerase chain reaction. The levels of interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were measured by ELISA. Hematoxylin and eosin staining was used for histopathological observation. The expression levels of AQP-5, P38 and phosphorylated (P)-P38 protein in lung tissues were detected by western blot analysis. The expression levels of AQP-5 in the sepsis group were significantly decreased compared with those in ctrl and SO groups (P<0.01), while the levels of TNF-α, IL-6 and p-P38 were significantly increased in sepsis group compared with those in ctrl and SO groups (P<0.01). Following tanshinol intervention, the expression levels of AQP-5 were significantly increased, while the levels of TNF-α, IL-6 and p-P38 were decreased compared with those in sepsis group. Tanshinol may upregulate the expression of AQP-5 by inhibiting the inflammatory cytokines and phosphorylation of P38, therefore protecting the lung tissue of rats with sepsis.

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Inhibitory effect of traditional oriental medicine-derived monoamine oxidase B inhibitor on radioresistance of non-small cell lung cancer

Cited by 42 publications

References 49 publications

TFAP2C-mediated upregulation of TGFBR1 promotes lung tumorigenesis and epithelial–mesenchymal transition

TFAP2C-mediated upregulation of TGFBR1 promotes lung tumorigenesis and epithelial–mesenchymal transition

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

Tanshinol upregulates the expression of aquaporin�5 in lung tissue of rats with sepsis

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