• Toxicological Research
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• v.18 no.4
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• pp.411-416
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• 2002

Apoptosis, or programmed cell death, is a genetically regulated pathway that is altered in many cancers. Overexpression of bcl-2 leads to resistance to apoptosis and promotes tumorigenesis. To determine the effect of bcl-2 antisense treatment in human lung cancer cell lines, a 20 mer full phosphorothioate oligonucleotide (ODN) targeted at the coding region of the bcl-2 mRNA was synthesized. Western blot analyses were used to examine bcl-2 protein level in five human non-small cell lung cancer (NSCLC) cell lines (NCI-H226, SK-MES-1 NCI-H358, NCI-H522 and NCI-Hl 299) and four human small cell lung cancer (SCLC) cell lines (NCI-H69, NCI-H4l7, HCC-2108 and SW2). Three out of five NSCLC (NCI-H226, SK-MES-1 and NCI-Hl 299) and all of SCLC cell lines expressed Bcl-2 protein. Treatment of these cell with antisense ODN for 48 hours reduced their viability and Bcl-2 protein level. As a conclusion, bcl-2 antisense treatment appears reduction of the Bcl-2 protein levels and cytotoxic effect including apoptosis in human lung cancer cell lines.

• BMB Reports
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• v.56 no.10
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• pp.557-562
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• 2023

Dysregulation of the E3 ubiquitin ligase Parkin has been linked to various human cancers, indicating that Parkin is a tumor suppressor protein. However, the mechanisms of action of Parkin remain unclear to date. Thus, we aimed to elucidate the mechanisms of action of Parkin as a tumor suppressor in human lung and colorectal cancer cells. Results showed that Parkin overexpression reduced the viability of A549 human lung cancer cells by inducing G2/M cell cycle arrest. In addition, Parkin caused DNA damage and ATM (Ataxia telangiectasia mutated) activation, which subsequently led to p53 activation. It also induced the p53-mediated upregulation of p21 and downregulation of cyclin B1. Moreover, Parkin suppressed the proliferation of HCT-15 human colorectal cancer cells by a mechanism similar to that in A549 lung cancer cells. Taken together, our results suggest that the tumor-suppressive effects of Parkin on lung and colorectal cancer cells are mediated by DNA damage/p53 activation/cyclin B1 reduction/cell cycle arrest.

• BMB Reports
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• v.49 no.11
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• pp.623-628
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• 2016

GPR78 is an orphan G-protein coupled receptor (GPCR) that is predominantly expressed in human brain tissues. Currently, the function of GPR78 is unknown. This study revealed that GPR78 was expressed in lung cancer cells and functioned as a novel regulator of lung cancer cell migration and metastasis. We found that knockdown of GPR78 in lung cancer cells suppressed cell migration. Moreover, GPR78 modulated the formation of actin stress fibers in A549 cells, in a RhoA- and Rac1-dependent manner. At the molecular level, GPR78 regulated cell motility through the activation of $G{\alpha}q$-RhoA/Rac1 pathway. We further demonstrated that in vivo, the knockdown of GPR78 inhibited lung cancer cell metastasis. These findings suggest that GPR78 is a novel regulator for lung cancer metastasis and may serve as a potential drug target against metastatic human lung cancer.

• Genomics & Informatics
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• v.19 no.1
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• pp.3.1-3.12
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• 2021

Functional interpretation of noncoding genetic variants associated with complex human diseases and traits remains a challenge. In an effort to enhance our understanding of common germline variants associated with lung cancer, we categorize regulatory elements based on eight major cell types of human lung tissue. Our results show that 21.68% of lung cancer-associated risk variants are linked to noncoding regulatory elements, nearly half of which are cell type-specific. Integrative analysis of high-resolution long-range chromatin interactome maps and single-cell RNA-sequencing data of lung tumors uncovers number of putative target genes of these variants and functionally relevant cell types, which display a potential biological link to cancer susceptibility. The present study greatly expands the scope of functional annotation of lung cancer-associated genetic risk factors and dictates probable cell types involved in lung carcinogenesis.

• Parasites, Hosts and Diseases
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• v.59 no.3
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• pp.291-296
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• 2021

Alveolar echinococcosis (AE) is considered as a fatal zoonosis caused by the larvae of Echinococcus multilocularis. The lungs and brain are the most common metastatic organs. We report a human case of hepatic alveolar echinococcosis accompanied by lung and brain metastasis. In particular, the patient had a history of tuberculosis and the lung lesions were easily misdiagnosed as lung abscesses. The lesions of liver and lung underwent radical resection and confirmed as alveolar echinococcosis by pathological examination. The patient had no surgical complications after operation and was discharged after symptomatic treatment. Unfortunately, the patient later developed multiple intracerebral AE metastases. We required the patient to take albendazole orally for life and follow up.

• Journal of Pharmacopuncture
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• v.19 no.2
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• pp.114-121
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• 2016

Objectives: Lung cancer remains a deadly disease with unsatisfactory overall survival. Cisplatin, a standard platinum (Pt)-based chemotherapeutic agent, has the potential to inhibit the growth of lung cancer. Its use, however, is occasionally limited by severe organ toxicity. However, until now, no systematic study has been conducted to verify its efficacy with proper experimental support in vivo. Therefore, we examined whether biosynthesized Pt nanoparticles (NPs) inhibited human lung cancer in vitro and in vivo to validate their use in alternative and complementary medicine. Methods: We evaluated the in vitro and the in vivo anticancer efficiencies of biosynthesized Pt NPs in a subcutaneous xenograft model with A549 cells. Severe combined immune deficient mice (SCID) were divided into four groups: group 1 being the vehicle control group and groups 2, 3 and 4 being the experimental groups. Once the tumor volume had reached $70-75mm^3$, the progression profile of the tumor growth kinetics and the body weights of the mice were measured every week for 6 weeks after oral administration of Pt NPs. Doses of Pt NPs of 500, 1,000 and 2,000 mg/kg of body weight were administered to the experimental groups and a dose of honey was administered to the vehicle control group. The efficacy was quantified by using the delay in tumor growth following the administration of Pt NPs of A549 human-lung-cancer xenografts growing in SCID mice. Results: The in vitro cytotoxicity evaluation indicated that Pt NPs, in a dose-dependent manner, inhibited the growth of A549 cells, and the in vivo evaluation showed that Pt NPs at the mid and high doses effectively inhibited and delayed the growth of lung cancer in SCID mice. Conclusion: These findings confirm the antitumor properties of biosynthesized Pt NPs and suggest that they may be a cost-effective alternative for the treatment of patients with lung cancer.

• Environmental Analysis Health and Toxicology
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• v.18 no.1
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• pp.15-19
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• 2003

Metallothionein gene expression activity of cadmium was investigated in a human lung epithelial cell line. Cells, grown to near confluence, were exposed to 0∼10 ${\mu}$M Cd metal for 6 hours. Cadmium did not cause morphological alteration in lung epithelial cells that are characteristic of cell damages such as cell shrinkage, detachment of the cell from its neighbors, cytoplasmic and chromatic condensation. However, metallothionein genes of MT-1 and MT-2 were rapidly induced in the treated cell measured by RT-PCR. Regarding the induction pattern of motallothionein mRNA, MT-1 mRNA was induced in a dependent manner. MT-2 mRNA induction, which was measured using oligo primers based on cDNA of human reticulocytes, seemed to be slightly increased in low doses but decreased at high concentration used in the experiment.

• Korean Journal of Plant Resources
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• v.28 no.3
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• pp.305-311
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• 2015

This study investigated in vitro antioxidant, anti-inflammatory and cytotoxicity on human lung epithelial A549 cells of different solvent extracts from Jerusalem artichoke (Helianthus tuberosus L.) tuber. The EtOH extract contained amounts of phenolics (22.20 tannic acid equivalent ㎎/ɡ) and exhibited the highest antioxidant activity and anti-inflammatory activity. Several methods were employed for measure the antioxidant activity: 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity (IC₅₀ = 206.79 ㎍/㎖), reducing power activity (21.26 ascorbic acid equivalent ㎎/ɡ) and total antioxidant activity (19.05 ascorbic acid equivalent ㎎/ɡ). Meantime, the EtOH extract inhibited the NO production completely with a concentration of 800 ㎍/㎖. Besides, the H₂O extract exhibited more potent effect on human lung epithelial A549 cells. This study suggested that Jerusalem artichoke tuber had antioxidant, anti-inflammatory and cytotoxicity on human lung epithelial A549 cells.

• Journal of Biomedical Engineering Research
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• v.11 no.2
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• pp.195-202
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• 1990

The hypothesis of asymmetric resistance to explain the phenomenon of lung hyperinflation (LHI) during hlgh frequency ventilation (HFV) was quantitatively studied. LHI was predicted by modeling the ism-volume pressure-flow (IVPF) data from 5 human subjects using the empirical Rohrer's equation. Non-steadiness during HFV was compensated by em- ploying recently proposed volume-frequency diagram. Tidal volume and ventilation frequency were 100 ml and 20 Hz, respectively. Airflow pattern was a symmetric sinusoid. The predic- tion results of mean pressure drop across the airways were averaged for those 5 subjects, and compared with zero by one-sided student's t-test. A marginally significant (P<0.1) increase in mean pressure drop was observed during HFV at low lung volumes (below FRC) , which could increase mean lung volume up to one liter When the lung volume was above FRC, no significant LHI (P >0.25) was resulted. LHI seemed to be inversely related to the lung volume. These results recommend to clinically apply HFV only at lung volumes above FRC.

• BMB Reports
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• v.51 no.12
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• pp.642-647
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• 2018

Ubiquitin-conjugating enzyme E2S (UBE2S), a family of E2 protein in the ubiquitination process, is involved in development of various cancers. However, its role in lung adenocarcinoma, has not been well elucidated. In this report, we attempted to investigate expression and function of UBE2S in lung adenocarcinoma. Up-regulation of UBE2S at mRNA, and protein level, was observed in human cancer tissues and lung adenocarcinoma cells. Higher UBE2S expression correlated with poorer prognosis of lung adenocarcinoma patients. UBE2S expression was efficiently suppressed by lentivirus-mediated shRNA strategy in A549 cells, and UBE2S silencing led to reduced cell proliferation, colony formation, and enhanced apoptosis. Inverse results were observed, in UBE2S over-expressed H1299 cells. Microarray analysis indicated that a large number of genes were regulated by UBE2S, and p53 signaling pathway may be critical, to the role of UBE2S in cancer development. Together, UBE2S could be a potential target for lung adenocarcinoma.