scholarly journals Bioactive Secondary Metabolites from Marine Streptomyces griseorubens f8: Isolation, Identification and Biological Activity Assay

2021 ◽  
Vol 9 (9) ◽  
pp. 978
Author(s):  
Wenzhi Yang ◽  
Guangjie Liang ◽  
Yang Sun ◽  
Zhijin Gong
Keyword(s):  
Staphylococcus Aureus ◽  
Anticancer Agents ◽  
A549 Cells ◽  
Klebsiella Aerogenes ◽  
Proteus Vulgaris ◽  
Invasion And Migration ◽  
Bioactive Natural Products ◽  
Streptomyces Griseorubens ◽  
Marine Streptomyces ◽  
And Migration

Marine actinomycetes are a potential source of a wide variety of bioactive natural products. Herein, four cyclic dipeptides, namely, cyclo(L-Val-L-Pro) (compound 1), cyclo(L-Pro-L-Leu) (compound 2), cyclo(L-Pro-L-Tyr) (compound 3) and cyclo(L-Pro-L-Phe) (compound 5), and an N-acetyltyramine (compound 4) were first isolated and identified as products of the marine Streptomyces griseorubens f8. Compounds 3 and 5 exhibit antibacterial activity against Staphylococcus aureus, Klebsiella aerogenes and Proteus vulgaris. The minimum inhibitory concentrations (MICs) against Staphylococcus aureus, Klebsiella aerogenes and Proteus vulgaris are 160 µg/mL, 100 µg/mL, 120 µg/mL for the compound 3 and 180 µg/mL, 130 µg/mL 150 µg/mL for the compound 5, respectively. In addition, compounds 1, 2, 3 and 5 was first found to have the ability to inhibit the invasion and migration of A549 cells (lung cancer cells), which exhibited the potentiality for these compounds to be used as novel anticancer drugs. This study provides a novel production strain for compounds 1, 2, 3 and 5, and four potential promising anticancer agents.

scholarly journals miR-103 Functions as a Tumor Suppressor by Directly Targeting Programmed Cell Death 10 in NSCLC

2018 ◽  
Vol 26 (4) ◽  
pp. 519-528 ◽  
Author(s):  
Dong Yang ◽  
Jian-Jun Wang ◽  
Jin-Song Li ◽  
Qian-Yu Xu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Tumor Size ◽  
Apoptotic Cell ◽  
A549 Cells ◽  
Invasion And Migration ◽  
Metastatic Capacity ◽  
And Migration

Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. Absence of miR-103 has recently been identified to be associated with metastatic capacity of primary lung tumors. However, the exact role of miR-103 in NSCLC and the molecular mechanism are unclear. In the present study, we showed that miR-103 expression was reduced in NSCLC tissues and cells. miR-103 expression was negatively correlated with tumor size and stage. The overall survival was longer in patients with higher miR-103 level than in those with lower miR-103 expression. miR-103 inhibited cell proliferation in A549 cells, decreased tumor weight and volume, and prolonged survival of tumor-implanted nude mice. miR-103 increased apoptotic cell death in A549 cells. Furthermore, miR-103 decreased the invasion and migration abilities in A549 cells, as evidenced by Transwell and wound healing results. Downregulation of miR-103 significantly reduced the level of programmed cell death 10 (PDCD10). We found a significant decrease in the relative luciferase activity of the reporter gene in A549 cells cotransfected with the miR-103 mimic and pGL3-PDCD10 WT 3′-UTR, but not pGL3-PDCD10 mut 3′-UTR. We showed that overexpression of PDCD10 significantly inhibited miR-103-induced inhibition of cell proliferation, increased apoptosis, and decreased invasion and migration in A549 cells. Moreover, we found that PDCD10 expression was increased in NSCLC tissues and cells. PDCD10 expression was positively correlated with tumor size and stage. Overexpression of PDCD10 increased cell proliferation and inhibited apoptosis in A549 cells. The data demonstrated that dysregulation of the miR-103/PDCD10 signal may be a novel therapeutic target for the treatment of NSCLC.

S16020 pyridocarbazole derivatives display high activity to lung cancer cells

2021 ◽  
Vol 21 ◽  
Author(s):  
Gabriela Chabowska ◽  
Helena Moreira ◽  
Beata Tylińska ◽  
Ewa Barg
Keyword(s):  
Cell Viability ◽  
Anticancer Agents ◽  
Topoisomerase Ii ◽  
Wide Spectrum ◽  
A549 Cells ◽  
Biological Evaluation ◽  
Dna Intercalation ◽  
P Glycoprotein ◽  
Low Toxicity ◽  
And Migration

Background: Despite the dynamic development of medicine, globally cancer diseases remain the second leading cause of death. Therefore, there is a strong necessity to improve chemotherapy regimens and search for new anticancer agents. Pyridocarbazoles are compounds with confirmed antitumor properties based on multimodal mechanisms, i.a. DNA intercalation and topoisomerase II-DNA complex inhibition. One of them, S16020, displayed a wide spectrum of activity. Objective: The aim of the study was to investigate the antitumor potency of six S16020 derivatives, synthesized according to the SAR (structure-activity relationship) method. Methods: The biological evaluation included influence on cancer cell viability, proliferation, and migration, as well as P-glycoprotein activity. NHDF, A549, MCF-7, LoVo, and LoVo/DX cell lines were used in the study. Results: All derivatives displayed low toxicity to normal (NHDF) cells at 1 and 2 µM (≤ 20% of cell growth inhibition). The highest reduction in cell viability was noted in A549 cells which was accompanied by significant disruption of cells proliferation and motility. Compound 1 exhibited the strongest cytotoxic, antiproliferative, and antimigratory effects, higher than the reference olivacine. A significant reduction in P-glycoprotein activity was found for derivatives 6 and 1. Conclusion: S16020 derivatives could be considered as potential candidates for new anticancer drugs.

scholarly journals Low-Dose Radiation Promotes Invasion and Migration of A549 Cells by Activating the CXCL1/NF-κB Signaling Pathway

2020 ◽  
Vol Volume 13 ◽  
pp. 3619-3629
Author(s):  
Jing Li ◽  
Dong-ming Wu ◽  
Rong Han ◽  
Ye Yu ◽  
Shi-hua Deng ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Low Dose ◽  
A549 Cells ◽  
Low Dose Radiation ◽  
Invasion And Migration ◽  
And Migration ◽  
Dose Radiation

scholarly journals PRDX6 Overexpression Promotes Proliferation, Invasion, and Migration of A549 Cells in vitro and in vivo

2021 ◽  
Vol Volume 13 ◽  
pp. 1245-1255
Author(s):  
Hao Li ◽  
Donghua Zhang ◽  
Bo Li ◽  
Honghua Zhen ◽  
Wenping Chen ◽  
...  
Keyword(s):  
A549 Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Neutrophil Extracellular Traps Facilitate A549 Cell Invasion and Migration in a Macrophage-Maintained Inflammatory Microenvironment

2022 ◽  
Vol 2022 ◽  
pp. 1-11
Author(s):  
Lemeng Zhang ◽  
Huifang Yi ◽  
Jianhua Chen ◽  
Haitao Li ◽  
Yongzhong Luo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
A549 Cell ◽  
Cell Invasion ◽  
A549 Cells ◽  
Neutrophil Extracellular Traps ◽  
Invasion And Metastasis ◽  
Inflammatory Microenvironment ◽  
Invasion And Migration ◽  
Extracellular Traps ◽  
And Migration

Introduction. The biological functions of neutrophil extracellular traps (NETs) in tumorigenesis have drawn an increasing amount of attention. This study explored the relationship between NETs and the inflammatory microenvironment in lung cancer cell invasion and metastasis. Methods. NETs were quantified using myeloperoxidase (MPO–DNA) and immunofluorescence staining. Cytokine levels were measured using ELISA kits. THP-1 and A549 cells were used for in vitro experiments. Transwell and Matrigel assays were used to assess the invasion and migration abilities of the cells. Results. Neutrophil infiltration and NET formation were observed in the lung cancer tissues. Compared with healthy controls, the level of MPO–DNA complexes in lung cancer patients increased remarkably and was positively correlated with peripheral blood neutrophil counts, smoking status, and poor prognosis. Increased circulating NET levels were also positively correlated with the levels of inflammatory cytokines, including IL-1β, IL-6, IL-18, and TNF-α. Neutrophils isolated from patients with lung cancer are more prone to NET release. NETs can promote the invasion and migration ability of THP-1 and A549 cell in coculture systems, while pretreatment with NET inhibitors can effectively reduce NET-induced invasion and metastasis. The ability of NETs to promote invasion and metastasis is partly dependent on macrophages. Conclusion. Taken together, our study demonstrated that NETs facilitate A549 cell invasion and migration in a macrophage-maintained inflammatory microenvironment.

scholarly journals Hydrogen gas represses the progression of lung cancer via down-regulating CD47

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Jinghong Meng ◽  
Leyuan Liu ◽  
Dongchang Wang ◽  
Zhenfeng Yan ◽  
Gang Chen
Keyword(s):  
Lung Cancer ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Hydrogen Gas ◽  
Cell Counting ◽  
Dependent Manner ◽  
Expression Levels ◽  
Invasion And Migration ◽  
Tumor Tissues ◽  
And Migration

Abstract Hydrogen gas (H2) has been identified to play an anti-tumor role in several kinds of cancers, but the molecular mechanisms remain largely unknown. In our previous study, our project group found that H2 could decrease the expression of CD47 in lung cancer A549 cells via the next-generation sequencing, indicating that CD47 might be involved in H2-mediated lung cancer repression. Therefore, the present study aimed to explore the effects of CD47 on H2-induced lung cancer repression. Western blotting and real-time PCR (RT-PCR) assays were used to detect the levels of proteins and mRNAs, respectively. Cell proliferation, invasion, migration and apoptosis were detected by using the cell counting kit-8 (CCK-8), Transwell chambers, wound healing and flow cytometry assays, respectively. The results showed that H2 treatment caused decreases in the expression levels of CD47 and cell division control protein 42 (CDC42) in a dose-dependent manner. Up-regulation of CD47 abolished H2 roles in promoting lung cancer cell apoptosis and repressing cell growth, invasion and migration in both A549 and H1975 cell lines. However, knockdown of CD47 enhanced H2 role in lung cancer inhibition. Moreover, we also observed that H2 treatment induced obvious inhibitions in the expression levels of CDC42 and CD47 in mice tumor tissues, as well as reinforced macrophage-mediated phagocytosis in A549 and H1975 cells. In conclusion, the current study reveals that H2 inhibits the progression of lung cancer via down-regulating CD47, which might be a potent method for lung cancer treatment.

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