Grifolin Inhibits Proliferation, Migration, and Invasion of Lung Cancer A549 Cells by Regulating miRNA-1251-5p

2020 ◽  
Vol 12 (3) ◽  
pp. 376-382
Author(s):  
Xiao Liu ◽  
Yuanlan Chen ◽  
Zhijiao Jiang
Keyword(s):  
Lung Cancer ◽  
Matrix Metalloproteinase ◽  
Cellular Proliferation ◽  
A549 Cells ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Control Group ◽  
Inhibitory Influence ◽  
Proliferation Inhibition ◽  
Inhibition Rate

To investigate the effect and molecular mechanism of grifolin on the proliferation, transfer, and infiltration of lung cancer (LC) cells. A control group, low grifolin group, midium grifolin group and high grifolin group, anti-miRNA-NC group, anti-miRNA-1251-5p group, grifolin + miRNA-NC group, and grifolin + miRNA-1251-5p group were established based on LC A549 cells. MTT was employed to detect cellular proliferation inhibition rate; Transwell assay was used to detect cellular transfer and infiltration; Western blot was used to test Cyclin D1, cyclin-dependent kinase inhibitor 1A (p21), matrix metalloproteinase 2 (MMP-2), and matrix metalloproteinase 9 (MMP-9) protein expression; and finally RT-qPCR was employed to test miRNA-1251-5p expression. After treatment with different concentrations of grifolin, an increase in proliferation inhibition rate of A549 cells, a decrease in migrating and invading cells, a decrease in CyclinD1, MMP-2, and MMP-9 expression, an increase in p21 expression, and a decrease in miRNA-1251-5p expression in a manner of concentration dependence was observed (P < 0.05). Inhibiting miRNA-1251-5p expression led to an increase in cellular proliferation inhibition rate, a decrease in migrating and invading cells, a decrease in CyclinD1, MMP-2, and MMP-9 expression, and an increase in p21 expression (P < 0.05). Overexpression of miRNA-1251-5p reversed the inhibitory influence of grifolin on the proliferation, transfer, and infiltration of A549 cells. Grifolin likely inhibits the proliferation, transfer, and infiltration of LC A549 cells by down-regulating miRNA-1251-5p.

scholarly journals Rose (Rosa gallica) Petal Extract Suppress Proliferation, Migration, and Invasion of Human Lung Adenocarcinoma A549 Cells through via the EGFR Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (21) ◽  
pp. 5119
Author(s):  
Won-Chul Lim ◽  
Hyo-Kyung Choi ◽  
Kyung-Tack Kim ◽  
Tae-Gyu Lim
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Cancer Cell ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Egfr Signaling Pathway ◽  
Rosa Gallica

We sought to investigate the effect of rose petal extract (RPE) on the proliferation, migration, and invasion of cancer cells. RPE significantly inhibited the growth of lung and colorectal cancer cell lines, with rapid suppression of A549 lung cancer cells at low concentrations. These effects occurred concomitantly with downregulation of the cell proliferation mediators PCNA, cyclin D1, and c-myc. In addition, RPE suppressed the migration and invasion of A549 cells by inhibiting the expression and activity of matrix metalloproteinase-2 and matrix metalloproteinase-9 (MMP-2 and -9). We hypothesize that the suppressive activity of RPE against lung cancer cell proliferation and early metastasis occurs via the EGFR-MAPK and mTOR-Akt signaling pathways. These early results highlight the significant potency of RPE, particularly for lung cancer cells, and warrant further investigation.

scholarly journals Normobaric hyperoxia inhibits the progression of lung cancer by inducing apoptosis

2018 ◽  
Vol 243 (9) ◽  
pp. 739-748 ◽  
Author(s):  
Sei Won Kim ◽  
In Kyoung Kim ◽  
Jick Hwan Ha ◽  
Chang Dong Yeo ◽  
Hyeon Hui Kang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
A549 Cells ◽  
Migration And Invasion ◽  
Control Group ◽  
Normobaric Hyperoxia ◽  
Human Lung Cells ◽  
Hyperoxia Exposure

Hypoxia is a critical characteristic of solid tumors with respect to cancer cell survival, angiogenesis, and metastasis. Hyperoxic treatment has been attempted to reverse hypoxia by enhancing the amount of dissolved oxygen in the plasma. In this study, we evaluated the effects of normobaric hyperoxia on the progression of lung cancer to determine whether oxygen toxicity can be used in cancer therapy. Following a tail vein injection of the Lewis lung carcinoma cells, C57BL/6J mice were exposed to a 24-h normobaric hyperoxia/normoxia cycle for two weeks. In addition, A549 lung cancer cells were incubated in a normobaric hyperoxia chamber for a 24-h period. As a result, the size and number of tumors in the lung decreased significantly with exposure to normobaric hyperoxia in the mouse model. Cell viability, colony-forming ability, migration, and invasion all decreased significantly in A549 cells exposed to normobaric hyperoxia and the normal control group exposed to normobaric hyperoxia showed no significant damage. Oxidative stress was more prominent with exposure to normobaric hyperoxia in cancer cells. A549 cells exposed to normobaric hyperoxia showed a significantly higher cell apoptosis ratio compared with A549 cells without normobaric hyperoxia exposure and normal human lung cells (BEAS-2B cells). The Bax/Bcl-2 mRNA expression ratio also increased significantly. Changes in the key regulators of apoptosis were similar between in vivo and in vitro conditions. The p-ERK level decreased, while the p-JNK level increased, after normobaric hyperoxia exposure in A549 cells. This study demonstrated the role of normobaric hyperoxia in inhibiting lung cancer. Normal tissue and cells showed no significant hyperoxic damage in our experimental setting. The anti-tumor effect of normobaric hyperoxia may due to the increased reactive oxygen species activity and apoptosis, which is related to the mitogen-activated protein kinase pathway. Impact statement Normobaric hyperoxia (NBO) is a feasible therapy for cancer with a low complication rate. Although NBO may be beneficial in cancer treatment, very few studies have been conducted; thus, the evidence is thin. This is the first study to clearly demonstrate morphological changes in lung cancer with NBO exposure and to investigate the underlying mechanisms both in vivo and in vitro. This study will arouse interest in NBO treatment and promote further research.

Mechanism of Ampelopsin Inhibiting Proliferation, Remove and Incursion of Colorectal Cancer Through Regulating the Expression of LncRNA ZFPM2-AS1/miR-515-5p

2021 ◽  
Vol 11 (6) ◽  
pp. 1029-1036
Author(s):  
Sheng Yuan ◽  
Dazhong Yu
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Inhibitory Effect ◽  
Expression Level ◽  
Migration And Invasion ◽  
Control Group ◽  
Proliferation Inhibition ◽  
Inhibition Rate ◽  
Colorectal Cancer Cells ◽  
Sw480 Cells

The incidence rate, recurrence and metastasis rate and mortality of colorectal cancer (CRC) are high. Therefore, clinical has been looking for better treatment. Ampelopsin (AMP) has obvious inhibitory effect on some tumors. However, there is no report on the effect and mechanism of AMP on rectal cancer. To investigate the effect and mechanism of AMP on the proliferation, migration and invasion of colorectal cancer cells, at first, different concentrations of Ampelopsis japonica group (10μM, 25 μM, 50 μM), control group (without AMP), pcDNA group, pcDNA-ZFPM2-AS1 group, si-NC group, si-ZFPM2-AS1 group, miR-NC group, miR-515-5p group, AMP+pcDNA group, AMP + pcDNA-ZFPM2-AS1 group were set up. Then the expression levels of miR-515-5p and ZFPM2-AS1 were detected by QRT-PCR, protein expression was detected by Western blot, cell proliferation inhibition rate was detected by MTT method, cell invasion and migration were detected by Transwell and fluorescence activity was detected by double luciferase reporter gene assay. The results show that compared with the control group, the proliferation inhibition rate of SW480 cells in different concentrations of AMP increased and the number of migration and invasion decreased significantly. Moreover, the expression levels of CyclinD1, MMP-2 and MMP-9 were significantly lower than those in the control group, while the expression of p21 was significantly increased. The expression level of miR-515-5pin SW480 cells treated with AMP was significantly increased, while the expression level of ZFPM2-AS1 was significantly decreased. Inhibition of ZFPM2-AS1 expression or miR-515-5p overexpression could inhibit the proliferation, migration and invasion of SW480 cells and then ZFPM2-AS1 overexpression reversed the inhibitory effect of AMP on the proliferation, migration and invasion of SW480 cells. Therefore, AMP affects the proliferation, migration and invasion of colorectal cancer cells by regulating the expression of lncRNA ZFPM2-AS1/miR-515-5p, which provides a new target and new idea for the prevention and treatment of colorectal cancer.

scholarly journals Sinomenine Inhibits Migration and Invasion of Human Lung Cancer Cell through Downregulating Expression of miR-21 and MMPs

2020 ◽  
Vol 21 (9) ◽  
pp. 3080 ◽  
Author(s):  
Kun-Hung Shen ◽  
Jui-Hsiang Hung ◽  
Yi-Ching Liao ◽  
Shu-Ting Tsai ◽  
Ming-Jiuan Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Matrix Metalloproteinase ◽  
Cell Invasion ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
E Cadherin

Sinomenine is an alkaloid derived from Sinomenium acutum. Recent studies have found that sinomenine can inhibit various cancers by inhibiting the proliferation, migration and invasion of tumors and inducing apoptosis. This study aims to investigate the effect and mechanism of sinomenine on inhibiting the migration and invasion of human lung adenocarcinoma cells in vitro. The results demonstrate that viabilities of A549 and H1299 cells were inhibited by sinomenine in a dose-dependent manner. When treated with sub-toxic doses of sinomenine, cell migration and invasion are markedly suppressed. Sinomenine decreases the mRNA level of matrix metalloproteinase-2 (MMP-2), MMP-9, and the extracellular inducer of matrix metalloproteinase (EMMPRIN/CD147), but elevates the expression of reversion-inducing cysteine-rich proteins with kazal motifs (RECK) and the tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2. In addition, sinomenine significantly increases the expression of the epithelial marker E-cadherin but concomitantly decreases the expression of the mesenchymal marker vimentin, suggesting that it suppresses epithelial–mesenchymal transition (EMT). Moreover, sinomenine downregulates oncogenic microRNA-21 (miR-21), which has been known to target RECK. The downregulation of miR-21 decreases cell invasion, while the upregulation of miR-21 increases cell invasion. Furthermore, the downregulation of miR-21 stimulates the expression of RECK, TIMP-1/-2, and E-cadherin, but reduces the expression of MMP-2/-9, EMMPRIN/CD147, and vimentin. Taken together, the results reveal that the inhibition of A549 cell invasion by sinomenine may, at least in part, be through the downregulating expression of MMPs and miR-21. These findings demonstrate an attractive therapeutic potential for sinomenine in lung cancer anti-metastatic therapy.

Propofol Inhibits Lung Cancer Invasion and Metastasis by Attenuating Icam-1/ Mmp-9 Axis

2021 ◽  
Vol 7 (4) ◽  
pp. 597-603
Author(s):  
Xin Huang ◽  
Guangbin Liang ◽  
Jian Mo ◽  
Weiming Liang ◽  
Fengmin Ge ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Treatment Group ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Inhibitory Influence ◽  
Invasion And Metastasis ◽  
Intercellular Adhesion Molecule 1 ◽  
Metalloproteinase 9

Objective: To investigate the effect of propofol on invasion and metastasis of A549 cells and the expression of intercellular adhesion molecule 1 (ICAM-1) / matrix metalloproteinase-9 (MMP-9) axis.Methods: A549 cells were treated with gradient doses of propofol (25, 50, 100 ng/ml) and different times (12, 24 h). The influences of propofol on ICAM-1 mRNA of A549 cells were observed by qRT-PCR, and the roles of different concentrations of propofol on ICAM-1 and MMP-9 protein and invasion ability were detected by Western Blot and Transwell assay, respectively.Results: The maximum inhibitory influence of propofol was achieved in group 100μg/ml for 24 h. ICAM-1 and MMP-9 protein in the treatment group with 25, 50 and 100μg/ml propofol for 24 h were significantly lower than those in the control group. The number of migrated and invaded cells in the 25, 50 and 100 ng/ml propofol treatment group for 24 h was significantly lower than that in the blank group.Condusion: ICAM-1 protein and MMP-9 protein in human lung cancer A549 cells could be down-regulated after treatment with 50 and 100μg/ml propofol, and the invasion and metastasis ability of A549 cells could be attenuated through ICAM-1/MMP-9 axis.

Inhibitory Effect of Poria cocos Polysaccharides on Proliferation, Migration, and Invasion of Lung Cancer Cells, A549

2021 ◽  
Vol 20 (1) ◽  
pp. 147-152
Author(s):  
Hongyan Jiang ◽  
Zhong Duanmu
Keyword(s):  
Lung Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Inhibitory Effect ◽  
Lung Cancer Cells ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Inhibition Of Proliferation ◽  
Poria Cocos

We have investigated the inhibitory effect of polysaccharides of Poria cocos on the proliferation, migration, and invasion of A549 lung cancer cells. The results showed that compared to the control group, the proliferation, migration, and invasion ability of all the treatment groups were inhibited, and the expression levels of ki-67 protein, matrix metalloproteinase-2, and matrix metalloproteinase-9 were also inhibited (P < 0.05). Moreover, polysaccharides of P. cocos significantly inhibited the expression of nuclear factor-kappa B (NF-κB) signaling pathway related genes p-p65 and p-IκB (P < 0.05). In conclusion, the mechanism of the inhibition of proliferation, migration, and invasion of lung cancer A549 cells by the polysaccharides of P. cocos may involve the inhibition of the NF-κB signaling pathway.

Targeting DNAJC19 overcomes tumor growth and metastasis in NSCLC by regulating AKT1 signaling.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e15024-e15024
Author(s):  
Tao Ren
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
A549 Cells ◽  
Nsclc Cell ◽  
Mechanistic Study ◽  
Migration And Invasion ◽  
Clinical Samples ◽  
Control Group ◽  
Cell Functions ◽  
Study Results

e15024 Background: Some driver oncogenes are still unknown in non-small cell lung cancer (NSCLC). DNAJC19, known as a major component of the translocation machinery of mitochondrial membranes, is a disease-associated protein. Herein, we reported the role of DNAJC19 in NSCLC cell growth and metastasis. Methods: Immunohistochemistry (IHC) was performed to investigate DNAJC19 expression in NSCLC clinical samples. For knockdown or overexpression assays in A549 or NCI-H1299 lung cancer cells, lentiviral vectors were used. After assessment of cell functions, DNAJC19-knockdown A549 cells were further applied to establish mice xenograft and metastasis tumor models. STRING database, western, PCR, immunoprecipitation and IHC were performed for the mechanistic study. Results: Expression of DNAJC19 was higher in tumors than non-cancerous adjacent tissues. Survival analysis found that low DNAJC19 levels were correlated with increased progression-free survival rate. ShRNA-mediated knockdown of DNAJC19 markedly inhibited cell growth, viability, migration and invasion. Moreover, RNA-seq analysis explored that PI3K/AKT signaling pathway was involved in molecular events when A549 cells treated with shDNAJC19. And then DNAJC19 knockdown also decreased AKT1 expression in A549 cells. In addition, cellular functions were greatly rescued in DNAJC19-knockdown A549 cells by exotic overexpression of AKT1. Furthermore, tumor xenograft growth and metastasis were markedly repressed in the shDNAJC19 group than control group. As expected, DNAJC19 and AKT1 expression levels in xenograft mice samples were also lower in the shDNAJC19 group than in the shCtrl group. Conclusions: DNAJC19 greatly promotes NSCLC cell growth and metastasis via regulating AKT1 signaling, providing a novel therapeutic target for NSCLC patients.

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