scholarly journals Alkaloid Extract of Moringa oleifera Lam. Exerts Antitumor Activity in Human Non-Small-Cell Lung Cancer via Modulation of the JAK2/STAT3 Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jing Xie ◽  
Lin-jie Peng ◽  
Ming-rong Yang ◽  
Wei-wei Jiang ◽  
Jia-ying Mao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Moringa Oleifera ◽  
A549 Cells ◽  
Cycle Arrest ◽  
And Migration ◽  
Related Proteins ◽  
Moringa Oleifera Lam ◽  
Proliferation And Migration

Lung cancer is one of the most common malignant tumors diagnosed worldwide. Moringa oleifera Lam. is a valuable medicinal plant native to India and Pakistan. However, the antilung cancer activity of M. oleifera alkaloid extract (MOAE) is unknown. The present study aimed to evaluate the regulatory effect of MOAE on A549 cells by examination of the proliferation, apoptosis, cell cycle, and migration of cells and to elucidate the possible mechanism of action of MOAE. We tested five types of cancer cells and four types of lung cancer cells and found MOAE exerted the strongest growth inhibitory effect against A549 cells but had low toxicity to GES-1 cells (human gastric mucosal epithelial cells). Simultaneously, MOAE induced apoptosis and increased the expression of the apoptosis-related proteins caspase-3 and caspase-9 in A549 cells. Furthermore, MOAE induced cell cycle arrest in the S phase through a decrease in the expression of the proteins cyclin D1 and cyclin E and an increase in the expression of the protein p21. MOAE also inhibited the migratory ability of A549 cells and decreased the expression of the migration-related proteins, matrix metalloproteinase (MMP) 2 and MMP9. In addition, the phosphorylation level of JAK2 and STAT3 proteins was decreased in MOAE-treated A549 cells. Furthermore, AZD1480 (a JAK inhibitor) and MOAE inhibited the proliferation and migration of A549 cells and induced cell apoptosis, and the effects of MOAE and AZD1480 were not additive. These results indicated that MOAE inhibits the proliferation and migration of A549 cells and induces apoptosis and cell cycle arrest through a mechanism that is related to the inhibition of JAK2/STAT3 pathway activation. Thus, this extract has potential for preventing and treating lung cancer.

scholarly journals TRIM59 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer Cells by Upregulating Cell Cycle Related Proteins

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0142596 ◽  
Author(s):  
Weihua Zhan ◽  
Tianyu Han ◽  
Chenfu Zhang ◽  
Caifeng Xie ◽  
Mingxi Gan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
And Migration ◽  
Related Proteins ◽  
Proliferation And Migration

scholarly journals TIFA Promotes Cell Survival and Migration in Lung Adenocarcinoma

2018 ◽  
Vol 47 (5) ◽  
pp. 2097-2108 ◽  
Author(s):  
Wanfu Men ◽  
Wenya Li ◽  
Jungang Zhao ◽  
Yu Li
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
Cycle Arrest ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Background/Aims: TNF-α receptor-associated factor (TRAF)-interacting protein with a forkhead-associated (FHA) domain (TIFA) may mediate the impact of TRAF on the development of lung cancer. The current study was conducted to investigate the expression of TIFA in lung adenocarcinoma and its potential role in the regulation of cancer cell proliferation and migration, and its influence on patient survival. Methods: Specimens of lung adenocarcinoma tissues and their adjacent normal lung tissues were obtained from 116 patients who underwent surgical resection of lung cancer. The expression of TIFA in the lung tissues was examined by immunohistochemistry, immunoblotting, and real-time RT-PCR in four different lung cancer cell lines and one normal bronchial epithelial cell line (BEAS-2B). TIFA was silenced by RNAi technique, and cell proliferation was then assessed by the CCK8 method. Furthermore, cell migration was determined by wound-healing trans-well and wound-healing migration assays. Additionally, cell-cycle arrest and apoptosis were assessed by flow cytometry analysis. Results: TIFA was positively detected in 63 (54.3%) out of 116 lung adenocarcinoma specimens, which was significantly higher than the respective rate established in normal tissues adjacent to the tumor (30.1%, p < 0.05). The overall survival rate was significantly lower in the patients with positive TIFA expression than that in the patients with negative TIFA expression (p < 0.05). TIFA was also highly expressed in the lung cancer cell lines (H1299, H1975, and HCC827) tested. It is noteworthy that siRNA suppressed the expression of TIFA, which contributed to the attenuation of cell proliferation and migration, but promoted cell-cycle arrest and apoptosis. Furthermore, the silencing of TIFA caused upregulation of p53, p21, and cleaved-caspase-3, but downregulation of Bcl-2, cyclin D1, and CDK4, as well as phosphorylation of IKKß, IκB, and p65. Conclusions: TIFA may serve as a biomarker in the prediction of lung adenocarcinoma. Furthermore, TIFA may modulate lung cancer cell survival and proliferation through regulating the synthesis of apoptosis-associated proteins.

scholarly journals Moringa oleifera Alkaloids Inhibited PC3 Cells Growth and Migration Through the COX-2 Mediated Wnt/β-Catenin Signaling Pathway

2020 ◽  
Vol 11 ◽  
Author(s):  
Jing Xie ◽  
Feng-xian Luo ◽  
Chong-ying Shi ◽  
Wei-wei Jiang ◽  
Ying-yan Qian ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Moringa Oleifera ◽  
Prostate Cancer Cells ◽  
Cycle Arrest ◽  
Pc3 Cells ◽  
Cox 2 ◽  
And Migration ◽  
Proliferation And Migration

Moringa oleifera Lam. (M. oleifera) is valuable plant distributed in many tropical and subtropical countries. It has a number of medicinal uses and is highly nutritious. M. oleifera has been shown to inhibit tumor cell growth, but this effect has not been demonstrated on prostate cancer cells. In this study, we evaluated the inhibitory effect of M. oleifera alkaloids (MOA) on proliferation and migration of PC3 human prostate cancer cells in vitro and in vivo. Furthermore, we elucidated the mechanism of these effects. The results showed that MOA inhibited proliferation of PC3 cells and induced apoptosis and cell cycle arrest. Furthermore, MOA suppressed PC3 cell migration and inhibited the expression of matrix metalloproteinases (MMP)-9. In addition, MOA significantly downregulated the expression of cyclooxygenase 2 (COX-2), β-catenin, phosphorylated glycogen synthase 3β, and vascular endothelial growth factor, and suppressed production of prostaglandin E2 (PGE2). Furthermore, FH535 (β-catenin inhibitor) and MOA reversed PGE2-induced PC3 cell proliferation and migration, and the effects of MOA and FH535 were not additive. In vivo experiments showed that MOA (150 mg/kg) significantly inhibited growth of xenograft tumors in mice, and significantly reduced the protein expression levels of COX-2 and β-catenin in tumor tissues. These results indicate that MOA inhibits the proliferation and migration, and induces apoptosis and cell cycle arrest of PC3 cells. Additionally, MOA inhibits the proliferation and migration of PC3 cells through suppression of the COX-2 mediated Wnt/β-catenin signaling pathway.

scholarly journals Metabolomics analysis reveals aminoquinazolin derivative 9d-induced oxidative stress and cell cycle arrest in A549 cells

RSC Advances ◽  
2017 ◽  
Vol 7 (22) ◽  
pp. 13149-13158 ◽  
Author(s):  
Wenrui Liu ◽  
Feng Jin ◽  
Dan Gao ◽  
Lu Song ◽  
Chao Ding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
A549 Cells ◽  
Cycle Arrest ◽  
A549 Lung ◽  
Metabolomics Analysis ◽  
Tof Ms

An UPLC/Q-TOF MS based metabolomics approach was established to study the probable antitumor mechanism of aminoquinazolin derivative 9d, which could induce oxidative stress and cell cycle arrest in A549 lung cancer cells.

scholarly journals A novel EZH2/NXPH4/CDKN2A axis is involved in regulating the proliferation and migration of non-small cell lung cancer cells

2021 ◽  
Author(s):  
Zeng Yang ◽  
Bo Wei ◽  
Anbang Qiao ◽  
Popo Yang ◽  
Wenhui Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Transcriptional Activation ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Arrest ◽  
And Migration ◽  
Proliferation And Migration

Abstract NXPH4 is discovered to be a neuropeptide-like glycoprotein, belonging to the Neurexophilins (Nxphs) family. NXPH4 shares a similar domain structure with NXPH1, which, however, is poorly understood in terms of its function. Bioinformatics analysis and experimental verification in this study confirmed the abnormal high expression of NXPH4 in non-small cell lung cancer (NSCLC) tissues and cells. Knockdown of NXPH4 by siRNA can inhibit the proliferation and migration of cells, resulting in significant cell cycle arrest in S1 phase. Furthermore, in NSCLC cells, NXPH4 was regulated by transcriptional activation of Enhancer of zeste homolog 2 (EZH2) in its upstream. While downstream, NXPH4 could interact with CDKN2A and downregulate its protein stability, thus participating in the cell cycle regulation through interacting with cyclinD-CDK4/6-pRB-E2F signaling pathway. To sum up, the present study reveals a regulatory pathway of EZH2/NXPH4/CDKN2A in NSCLC, providing possible reference for understanding the function of NXPH4 in tumors.

scholarly journals Berbamine Inhibits Cell Proliferation and Migration and Induces Cell Death of Lung Cancer Cells via Regulating c-Maf, PI3K/Akt, and MDM2-P53 Pathways

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Lili Liu ◽  
Zhiying Xu ◽  
Binbin Yu ◽  
Li Tao ◽  
Ying Cao
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Colony Formation ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
And Migration ◽  
Proliferation And Migration

Berbamine (BBM) is a natural product isolated from Berberis amurensis Rupr. We investigated the influence of BBM on the cell viability, proliferation, and migration of lung cancer cells and explored the possible mechanisms. The cell viability and proliferation of lung cancer cells were evaluated by MTT assay, EdU assay, and colony formation assay. Migration and invasion abilities of cancer cells were determined through wound scratch assay and Transwell assay. Cell death was evaluated by cell death staining assay and ELISA. The expressions of proteins were evaluated using western blot assay. A xenograft mouse model derived from non-small-cell lung cancer cells was used to detect the effect of BBM on tumor growth and metastasis in vivo. Both colony formation and EdU assays results revealed that BBM (10 μM) significantly inhibited the proliferation of A549 cells ( P < 0.001 ). BBM (10 μM) also significantly inhibited the migration and invasion ability of cancer cells in wound scratch and Transwell assays. Trypan blue assay and ELISA revealed that BBM (20 μM) significantly induced cell death of A549 cells. In xenograft mouse models, the tumor volume was significantly smaller in mice treated with BBM (20 mg/kg). The western blotting assay showed that BBM inhibited the PI3K/Akt and MDM2-p53 signaling pathways, and BBM downregulated the expression of c-Maf. Our results show that BBM inhibits proliferation and metastasis and induces cell death of lung cancer cells in vitro and in vivo. These effects may be achieved by BBM reducing the expression of c-Maf and regulating the PI3K/Akt and MDM2-p53 pathways.

scholarly journals Biochanin A Induces S Phase Arrest and Apoptosis in Lung Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Yan Li ◽  
Haiyang Yu ◽  
Fengfeng Han ◽  
Mengmeng Wang ◽  
Yong Luo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Lung Cancer Cells ◽  
Biochanin A ◽  
Dependent Manner ◽  
Cycle Arrest ◽  
Related Proteins ◽  
Dose Dependent

Lung cancer is among the most common malignancies with a poor 5-year survival rate reaching only 16%. Thus, new effective treatment modalities and drugs are urgently needed for the treatment of this malignancy. In this study, we conducted the first investigation of the effects of Biochanin A on lung cancer and revealed the mechanisms underlying its potential anticancer effects. Biochanin A decreased cell viability in a time-dependent and dose-dependent manner and suppressed colony formation in A549 and 95D cells. In addition, Biochanin A induced S phase arrest and apoptosis and decreased mitochondrial membrane potential (ΔΨm) in A549 and 95D cells in a dose-dependent manner. Our results of subcutaneous xenograft models showed that the growth of Biochanin A group was significantly inhibited compared with that of control groups. Finally, P21, Caspase-3, and Bcl-2 were activated in Biochanin A-treated cells and Biochanin A-treated xenografts which also demonstrated that Biochanin A induced cell cycle arrest and apoptosis in lung cancer cells by regulating expression of cell cycle-related proteins and apoptosis-related proteins. In conclusion, this study suggests that Biochanin A inhibits the proliferation of lung cancer cells and induces cell cycle arrest and apoptosis mainly by regulating cell cycle-related protein expression and activating the Bcl-2 and Caspase-3 pathways, thus suggesting that Biochanin A may be a promising drug to treat lung cancer.

Antrodia cinnamomea Inhibits Growth and Migration of Lung Cancer Cells through Regulating p53-Bcl2 and MMPs Pathways

2020 ◽  
Vol 48 (08) ◽  
pp. 1941-1953
Author(s):  
Yi Tan ◽  
Michael Johnson ◽  
Jiong Zhou ◽  
Yi Zhao ◽  
Mohammad Amjad Kamal ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Protein Expression ◽  
Mrna Expression ◽  
Cancer Cells ◽  
A549 Cells ◽  
Mrna Levels ◽  
Antrodia Cinnamomea ◽  
Qrt Pcr ◽  
And Migration

Antrodia cinnamomea has been shown to possess antitumor activity. This study investigated the effects and mechanisms of Antrodia cinnamomea extract (ACE) on growth and migration of human non-small cell lung cancer A549 cells. The effect of ACE on cell viability was determined by MTT assay and fluorescent live-cell imaging. The apoptotic effect of ACE was determined by cell cycle distribution using flow cytometry. A P53-mediated apoptosis pathway was identified by measuring protein expression of p53 and Bcl-2 with Western blotting. Additionally, mRNA expression of p53 and Bcl-2 and Bax was detected by qRT-PCR. The effect of ACE on cancer cell migration was confirmed by a wound-healing assay. Expression of MMP-2 and MMP-9 at the protein and gene levels was determined by western blot and qRT-PCR analysis. This study demonstrates the inhibitory effect of ACE on A549 cell proliferation in a dose-response manner with an [Formula: see text]. It was determined that ACE concentration at [Formula: see text] induced cell cycle arrest at S phase in A549 cells. The apoptosis-regulating protein p53 expression was enhanced and also associated with the downregulation of Bcl-2 in ACE treatment cells. The mRNA expression of p53 and Bcl-2 associated with Bxa was consistent with protein expression. The inhibition of migration of cancer cells treated with ACE was clearly evident. At the same time, suppression of expression of MMP-2 and MMP-9 at protein and mRNA levels was observed. The findings of this study highlight ACE as a potential agent of adjuvant therapy for lung cancer.

Arsenic trioxide inhibits the growth of human lung cancer cell lines via cell cycle arrest and induction of apoptosis at both normoxia and hypoxia

2009 ◽  
Vol 25 (8) ◽  
pp. 505-515 ◽  
Author(s):  
Qu Ge-ping ◽  
Xiu Qing-Yu ◽  
Li Bing ◽  
Liu Yong-an ◽  
Zhang Ling-Zhen
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Lung ◽  
A549 Cells ◽  
Cyclin B ◽  
M Cell ◽  
Cycle Arrest ◽  
Induction Of Apoptosis

Arsenic trioxide (As 2O3) has been established to be an effective agent for treating acute promyleocytic leukemia. Laboratory data suggest that As2O 3 induces apoptosis of several solid tumor cells including lung cancer cells. Regions of tissue hypoxia often arise in aggressive solid tumors, and hypoxic tumors exhibit augmented invasiveness and metastatic ability in several malignancies. Furthermore, hypoxia may impair the treatment efficiency; therefore, we studied the cytotoxic effect of As2O3 on human lung adenocarcinoma cell lines A549 and A549/R (resistant to vincristine, adriamycin and mitomycin etc.) grown under normoxic and hypoxic (1% oxygen) conditions. At both normoxia and hypoxia, 5, 10 and 15 µM As2O3 induced evident growth inhibition and apoptosis in A549 cells as well as A549/R cells after 48 hours of exposure. In contrast, the conventional chemotherapeutic drug vincristine showed lowered efficiency in hypoxic A549 cells. As2O3 induced G2/M cell cycle arrest in both normoxic and hypoxic A549 cells. As2O3 significantly decreased the messenger RNA (mRNA) levels of Cyclin B1 and survivin and the protein levels of Cyclin B1, phospho-CDC2 (Thr 161) and survivin in both normoxic and hypoxic A549 cells. Together, our findings indicated that As2O3 significantly inhibited the proliferation of lung cancer cells via G2/M cell cycle arrest and induction of apoptosis at both normoxia and hypoxia, and the induction of apoptosis was associated with down regulation of survivin.

scholarly journals CD73 Severed as a Potential Prognostic Marker and Promote Lung Cancer Cells Migration via Enhancing EMT Progression

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhao-wei Gao ◽  
Chong Liu ◽  
Lan Yang ◽  
Hao-chuan Chen ◽  
Long-fei Yang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Prognostic Marker ◽  
Prognostic Value ◽  
A549 Cells ◽  
Expression Levels ◽  
Km Plotter ◽  
And Migration ◽  
Cd73 Expression ◽  
Proliferation And Migration

To investigate the expression levels and prognostic value of CD73 in lung cancer. And moreover, to identify the effect and potential mechanism of CD73 on lung cancer cells proliferation and migration. CD73 expression levels in lung cancer were analyzed base on GEPIA2 and GEO database. GEPIA2 and Kaplan-Meier Plotter (KM Plotter) was used to analyzed the correlation between CD73 expression and prognosis. GEO dataset were analyzed via GEO2R. CD73 overexpression cell model was construction via recombinant lentivirus transfection into A549 and NCI-H520 cells. CCK8 assay were used to investigate cells proliferation. Migration and invasion ability were evaluated by scratch and transwell methods. Base on GEPIA2, GSE32683, GSE116959 and GSE37745 dataset, we found that CD73 expression were significant higher in tumor tissues of lung adenocarcinoma (LUAD) compared with that in non-tumor normal tissues and in lung squamous cell carcinoma (LUSC), while there were no significant difference of CD73 expression between LUSC and normal control tissues. Interestingly, a high CD73 level predict poor overall survival (OS) of LUSC. However, GEPIA2 and KM plotter showed the opposite conclusion of prognostic value of CD73 in LUAD. By using cell experiments, we found that CD73 overexpression promoted proliferation and migration of LUAD A549 cells. However, there was no significant effect of CD73 overexpression on LUSC NCI-H520 cells. Furthermore, CD73 overexpression facilitates epithelial to mesenchymal transition (EMT) progression of A549 cells. In conclusion, our results indicated that CD73 expression were increased in LUAD and might be an poor prognostic marker for LUSC patients. CD73 play an important role in LUAD cells proliferation and migration. These data allowed to support CD73 as a therapeutic target for LUAD.

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