scholarly journals Effect and Mechanism of Transthyretin Over-Expression on Proliferation and Cell Cycle of Lung Cancer A549 Cells

2021 ◽  
Author(s):  
Deqing Zhu ◽  
Xuan Li ◽  
Hao Gong ◽  
Jing Li ◽  
Xike Lu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Mrna Expression ◽  
Quantitative Polymerase Chain Reaction ◽  
Statistical Significance ◽  
A549 Cells ◽  
Control Group ◽  
Over Expression

Background: The effects of transthyretin (TTR) over-expression on the proliferation and cell cycle of nonsmall cell lung cancer (NSCLC) A549 cells and its possible mechanism were verified. Methods: A total of 196 LC patients and 20 healthy controls were enrolled at Tianjin Hospital, Tianjin, China between Apr 2017 and Oct 2017. The serum TTR content was detected by ELISA. Through lentiviral transfection method, NSCLC cells were divided into non-transfected group (group A), negative control group (group B) transfected with empty vector and experimental group (group C) transfected with TTR overexpression. Cell proliferation was detected by CCK-8 method, TTR mRNA expression was detected by realtime quantitative polymerase chain reaction (RT-qPCR), and TTR protein expression was tested by Western blot (WB). Cell cycle was detected by flow cytometry, Wnt3a/β-catenin protein expression was detected by WB, and mRNA expression was detected by RT-qPCR. Results: The serum TTR content in early, middle and late LC group was remarkably lower than that in healthy group (P<0.05). Compared with late stage, TTR content in early and middle stages of LC group was higher, and the difference was statistically marked (P < 0.05). The absorbance value of group C was lower than that of groups A and B, indicating that the cell proliferation activity dramatically decreased, with statistically marked difference (P<0.05). LC A549 cells in group C were obviously blocked in G2M, with statistical significance (P<0.05). Conclusion: TTR over-expression can inhibit the proliferation of NSCLC A549 cells, and the expression is related to Wnt3a/β-catenin pathway. TTR in serum of patients was helpful for diagnosing LC and has certain clinical value.  

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.

scholarly journals SUZ12 Participates in PNH Cloning Proliferation By Regulating Histone H3K27me3 Methylation Level

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 1106-1106
Author(s):  
Rong Fu ◽  
Yingying Chen ◽  
Zonghong Shao ◽  
Hui Liu ◽  
Lijie Zeng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Peripheral Blood ◽  
Methylation Level ◽  
Cell Model ◽  
Gene Mutations ◽  
Control Group ◽  
Mrna And Protein Expression ◽  
And Control

Abstract Paroxysmal nocturnal hemoglobinuria (PNH) is a disease of hematopoietic stem cell membrane defects due to acquired PIG-Amutation. Our previous study found some secondary gene mutations in PNH patients by WES. However, it is not clear exactly which mutations are associated with the disease. So, 97 target genes were selected as a target gene panel and tested in 23 PNH patients by DNA sequencing of specific target regions. We found that all PNH patients had other gene mutations except PIG-Amutations, including TTN, NCOR2, CPS1, MUC4, SUZ12, LFNG, CELSR2, JAK2, SETBP1 and KMT2D (Figure1A). Through harmful analysis, KEGG enrichment, GO enrichment analysis and protein interaction analysis, we screened out the secondary mutant gene SUZ12 that may be involved in the cloning proliferation of PNH. We detected the mRNA and protein expression levels of SUZ12 and H3K27me3 methylation in PNH patients and health volunteers, the results showed that the mRNA and protein expression levels of SUZ12 and H3K27me3 methylation in peripheral blood CD59 -cells of PNH patients were higher than those in CD59 + cells of PNH patients and healthy controls (Figure1B). The relative expression level of SUZ12 in peripheral blood CD59 -cells of PNH patients was correlated with (r=0.4162, p=0.0385), CD59 -erythrocyte ratio (r=0.4636, p=0.0196), CD59 -monocyte ratio (r=0.4052, p=0.0495), Flaer -monocyte ratio (r=0.6769, p=0.0004) and Flaer -granulocytic ratio (r=0.6146, p=0.0018), indicating that SUZ12 may be involved in abnormal PNH cloning and proliferation by regulating H3K27me3. To verify the role of SUZ12 in the proliferation of PNH cloning, we used CRISPR/Cas9 to knockdown PIG-A expression in THP-1 cells to construct A PNH cell model, the expression level of PIG-A protein in the cell model was significantly decreased, and the proportion of CD59 - cells accounted was stable at 95%. Then lentivirus transfection was used to knockdown the expression of SUZ12 in PNH cell model. The results showed when the SUZ12 expression was knockdown, the methylation level of histone H3K27me3 was decreased, the cell proliferation activity was decreased, apoptosis was increased, and the cell cycle was arrested at G0/G1 phase. The proportion of CD59 + cells increased gradually from 3 weeks after transfection, and significantly increased at 4 weeks after transfection, while no changes were observed in the empty virus group and control group (Figure1C). Four weeks after lentivirus transfection, the expression of PIG-A protein recovered in SUZ12 knockdown group compared with empty virus group and control group (Figure1D). In conclusion, SUZ12 mutation leads to the overexpression of SUZ12, which can affect cell proliferation, apoptosis and cell cycle by regulating the methylation level of histone H3K27me3, thereby promoting the proliferation of PNH abnormal cloning and participating in the pathogenesis of PNH. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

129 microRNA-183~96~182 CLUSTER PROMOTE BOVINE GRANULOSA CELL PROLIFERATION THROUGH COORDINATED REGULATION OF FOXO1

2016 ◽  
Vol 28 (2) ◽  
pp. 194
Author(s):  
S. Gebremedhn ◽  
D. Salilew-Wondim ◽  
M. Hoelker ◽  
F. Rings ◽  
C. Neuhoff ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Statistical Significance ◽  
Flow Cytometric Analysis ◽  
Cell Counting ◽  
G1 Arrest ◽  
Mirna Cluster ◽  
Mrna And Protein Expression ◽  
Coordinated Regulation

Among other microRNA clusters, we previously showed that the miR-183~96~182 cluster (miR-183, miR-96, and miR-182) is abundantly expressed in bovine granulosa cells (bGC) of preovulatory dominant follicles obtained at the follicular phase of the bovine oestrous cycle. Moreover, this miRNA cluster are validated to coordinately target the Fork head O1 (FOXO1), a subfamily of transcription factors that regulate genes involved in cell proliferation, apoptosis, cell cycle arrest, and metabolism. However, the functional involvement of miR-183~96~182 cluster in bGC function by regulation of FOXO1 is not yet determined. Here, we aimed to investigate the function of miR-183~96~182 cluster in bGC using in vitro cell culture model. For this, bGC were aspirated from ovarian follicles (Ø 3–5 mm) obtained from local abattoir. Cells were plated in 24-well plate (2.5 × 105 cells well–1) in DMEM/F-12 (Sigma, Germany) supplemented with 10% FBS (GIBCO, Grand Island, NY) and 1% penicillin/streptomycin (GIBCO) and incubated at 37°C in 5% CO2. Transfection of bGC with miRNA mimics, inhibitors, FOXO1-siRNA, and appropriate controls (Exiqon, Vedbæk, Denmark) was performed using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). Cell proliferation was determined using Cell Counting Kit-8 (CCK-8; Dojindo Molecular Technology, Kumamoto, Japan). Cell cycle distribution was determined with flow cytometric analysis. Total RNA was isolated using miRNeasy mini kit (Qiagen, Hilden, Germany), quantification of target gene was performed using qPCR, and data were analysed using ΔΔCT method. Differences in the mean expression values between treatments were analysed with two-tailed Student’s t-test and statistical significance was defined at P ≤ 0.05. Results showed that a sponge effect was observed upon inhibition in individual miRNA of the cluster, which could be attributed to the partial sequence similarity among cluster members. Both FOXO1 mRNA and protein expression were significantly reduced upon transfection of bGC with miR-183~96~182 cluster mimics, while miR-183~96~182 cluster inhibition increased both FOXO1 mRNA and protein expression. Transfection of bGC with miR-183~96~182 mimics promoted cell proliferation, while inhibition tends to slow down proliferation. Furthermore, the proportion of bGC under G0/G1 arrest markedly declined (P < 0.05), while the S and G2/M phases increased in response to miR-183~96~182 mimicking. Selective knockdown of FOXO1 with FOXO1-siRNA significantly reduced FOXO1 mRNA and protein expression. Interestingly, knockdown of FOXO1 showed similar phenotypic effects such as that of miR-183~96~182 mimics transfection, which resulted in elevated bGC proliferation and reduction in the proportion of cells under G0/G1 arrest. In conclusion, overexpression of miR-183~96~182 cluster promote bGC proliferation and G0/G1 to S and G2/M cell cycle transition through coordinated regulation of genes in the FOXO1 signaling axis.

scholarly journals Knockdown of RAD54B expression reduces cell proliferation and induces apoptosis in lung cancer cells

2019 ◽  
Vol 47 (11) ◽  
pp. 5650-5659 ◽  
Author(s):  
Chuan Xu ◽  
Di Liu ◽  
Hong Mei ◽  
Jian Hu ◽  
Meng Luo
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Caspase 3 ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Gene And Protein Expression ◽  
Healthy Lung

Objective RAD54 homolog B (RAD54B), a member of the SNF2/SWI2 superfamily, is implicated in homologous recombination, and high RAD54B expression predicts the prognostic outcomes of lung adenocarcinoma. However, its role in lung carcinogenesis was unclear so this was determined in the present study. Methods We evaluated the gene and protein expression of RAD54B in 15 lung adenocarcinoma tissues and matched adjacent healthy lung tissues by real-time PCR, immunohistochemical staining, and western blotting. A549 lung cancer cells were transduced with lentivirus carrying small hairpin RNA (shRNA) against RAD54B (shRAD54B) or control shRNA (shCtrl), and cell proliferation, viability, apoptosis, and caspase 3/7 activity were evaluated. Results RAD54B protein expression was significantly higher in lung adenocarcinoma tissues than in healthy lung tissues. RAD54B gene expression was high in A549 cells but was efficiently knocked down using shRAD54B with an infection efficiency of 80% and a knockdown ratio of 72.2% compared with shCtrl. Suppressing RAD54B expression in A549 cells significantly reduced cell proliferation and caspase 3/7 activity, and significantly increased the apoptotic rate. Conclusions RAD54B exerts an oncogenic role in lung cancer cell proliferation.

scholarly journals APEX1 regulates alternative splicing of key tumorigenesis genes in non-small-cell lung cancer

2020 ◽  
Author(s):  
Li Peng ◽  
Yuwei Liu ◽  
Jing Chen ◽  
Xuebei Du ◽  
Renwei Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Alternative Splicing ◽  
Small Cell Lung Cancer ◽  
Tumor Progression ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Over Expression ◽  
Proliferation And Apoptosis

Abstract Background: Aberrant alternative splicing (AS) contributes to tumor progression. Previous studies have shown that apurinic-apyrimidinic endonuclease-1 (APEX1) is involved in tumor progression. It is unknown whether APEX1 functions in tumor progression by regulation of AS. It is also unknown whether APEX1 can regulate non-small-cell lung cancer (NSCLC) proliferation and apoptosis. Methods: We analyzed APEX1 expression levels in 517 lung NSCLC samples from the TCGA (Cancer Genome Atlas) database. The impact of APEX1 over expression on A549 cell proliferation and apoptosis was detected by the methyl thiazolyl tetrazolium assay and by flow cytometry. The transcriptome of A549 cells with and without APEX1 over expression was determined by Illumina sequencing, followed by analysis of AS. RT-qPCR validated APEX1 in A549 cells. Results: We have successfully applied RNA-seq technology to demonstrate APEX1 regulation of AS. APEX1 expression was shown to be upregulated in NSCLC samples and to reduce cell proliferation and induce apoptosis of A549 cells. Further, APEX1 regulated AS of key tumorigenesis genes involved in cancer proliferation and apoptosis within the MAPK and Wnt signaling pathways. Each of these pathways are involved in lung cancer progression. Validated AS events regulated by APEX1 were located in key tumorigenesis genes; AXIN1 (axis inhibition protein 1), GCNT2 (N-acetyl glucosaminyl transferase 2), and SMAD3 (SMAD Family Member 3). These genes encode signaling pathway transcription regulatory factors. Conclusions: We found that increased expression of APEX1 in NSCLC is an independent prognostic factor related to tumor progression. Therefore, APEX1 regulation of AS may serve as a molecular marker or therapeutic target for NSCLC treatment.

Carbonyl Reductase 3-Antisense RNA 1 Negatively Regulates microRNA-337-3p Expression: Effects on Proliferation, Migration, and Invasion of Lung Cancer Cells

2021 ◽  
Vol 11 (3) ◽  
pp. 433-438
Author(s):  
Shining Lin ◽  
Xiufeng Zhang ◽  
Huifang Shi ◽  
Fahui Wang ◽  
Shan Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Protein Expression ◽  
A549 Cells ◽  
Migration And Invasion ◽  
High Morbidity ◽  
Cancer Cell Proliferation ◽  
Expression Levels ◽  
Cancer Tissues ◽  
E Cadherin

Lung cancer, a malignant tumor, is associated with high morbidity and mortality worldwide. We studied the influence and mechanism of CBR3-AS1 on lung cancer cell proliferation, migration, and infiltration. The expression of CBR3-AS1 and miRNA-337-3p were higher and lower (P < 0.05), respectively, in lung cancer tissues than in paracancerous tissues. After inhibiting the expression of CBR3-AS1, the OD value of A549 cells, cloning formation numbers, migrating and invasive numbers, N-cadherin protein expression levels were lower. The G0-G1 cell cycle periods was longer. The S cell cycle periods was shorter. The E-cadherin protein expression levels higher (P < 0.05 in all cases). CBR3-AS1 negatively regulated miRNA-337-3p expression in A549 cells (P < 0.05). After inhibiting the expression of CBR3-AS1 and miRNA-337-3p, the OD value of A549 cells was lower, cloning formation numbers, migrating and invasive numbers, N-cadherin protein expression levels were lower. The G0-G1 cell cycle periods was longer. The S cell cycle periods was shorter. The E-cadherin protein expression levels was higher (P < 0.05 in all cases). CBR3-AS1 expression was increased in lung cancer tissues, and interference with CBR3-AS1 expression could inhibit the proliferation, migration, and infiltration of lung cancer A549 cells by negatively regulating miRNA-337-3p.

The Effect of MicroRNA-92a (miR-92a) on Non-Small Cell Lung Cancer (NSCLC) Cell Biological Behaviors and Janus Protein-Tyrosine Kinase 1 (JAK1)/Signal Transducer and Activator of Transcription (STAT3) Signaling

2021 ◽  
Vol 11 (8) ◽  
pp. 1582-1587
Author(s):  
Jianghong Yi ◽  
Jie Zhao ◽  
Pengfei Xiao ◽  
Minghui Gao
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Protein Tyrosine Kinase ◽  
A549 Cells ◽  
Small Cell ◽  
Signal Transducer ◽  
Small Cell Lung ◽  
Stat3 Signaling

Our study investigates miR-92a’s effect on the biological behaviors of non-small cell lung cancer (NSCLC) cells and Janus protein-tyrosine kinase (JAK)/signal transducer and activator of transcription (STAT) signal transduction. A549 cells were divided into KB group (no transfection), NC group (negative control transfection), and SY group (transfection with miR-92a inhibitor) followed by analysis of the expression of miR-92a, JAK1, and STAT3 by qRT-PCR, cell proliferation, invasion and apoptosis as well as JAK1/STAT3 protein expression. The miR-92a, JAK1, and STAT3 expression in SY group were significantly lower than NC group and KB group (P <0.05), indicating the successful transfection. The A549 cell proliferation in SY group was significantly decreased compared with NC and KB group (P <0.05). Cell apoptosis rate in SY group was 25.23±2.31%, which was significantly higher than that in NC (8.15±0.82%) and KB group (8.08±0.79%). The number of cell invasion in SY group was significantly reduced (88.6±7.32) compared with NC group (189.71±15.37) and KB group (181.32±14.62) (F = 937.8, P <0.001). SY group showed significantly lower JAK1/STAT3 protein expression than NC and KB group. In conclusion, silencing miR-92a can inhibit proliferation, migration, and invasion of A549 cells, which may be related to JAK1/STAT3 signaling pathway.

Treatment with Radix Euphorbiae Ebracteolatae Significantly Decreases the Expression of E6 and L1, and Increases the Expression of p53 and Rb in HPV18-infected Human Foreskin Keratinocytes

2019 ◽  
Vol 19 (1) ◽  
pp. 20-31
Author(s):  
Xiang He ◽  
Xufeng He ◽  
Ping Xu ◽  
Lili Yang ◽  
Xin Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Mrna Expression ◽  
Molecular Mechanisms ◽  
Control Group ◽  
Inhibition Of Proliferation ◽  
Tnf Α ◽  
Ree Group ◽  
Vitamin A Acid ◽  
Plantar Warts

Background:Radix Euphorbiae Ebracteolatae (REE) was recently reported to be significantly superior to vitamin A acid ointment in treating multiple plantar warts. However, the effects of REE on HPV18 remain unclear. Therefore, the current study aimed to investigate the effects of REE on the proliferation of HPV18, and explore possible molecular mechanisms underlying the effects.Methods:HFK and HFK-HPV18 were treated with water-extracted single or compound REE, ethanol-extracted single or compound REE, TNF-α and IFN for 3 days, respectively. In addition, the organotypic rafts containing HFK-HPV18 and HFK were treated with REE, IFN and TNF-α for 7 days, respectively. Cell proliferation rates were measured with Brdu. mRNA expression of E6, L1, p53 and Rb was detected by qPCR. Protein expression of p53, Rb and L1 was detected by Western blot.Results:Compared to HFK group, HFK-HPV18 group had significantly higher expression of E6 and L1. Compared to the control group, HFK-HPV18 treated with REE, TNF-α and IFN displayed significantly lower proliferation rates. The mRNA expression of E6 was markedly lower, and mRNA expression of p53 and Rb was significantly higher after treatment of REE in HFK-HPV18 or in organotypic rafts containing HFK-HPV18. Treatment with REE markedly increased the protein expression of p53 and Rb, and decreased the protein expression of L1 in HFK-HPV18 or in organotypic rafts containing HFK-HPV18. Among all formula of REE, the inhibition of proliferation rates and expression of E6 and L1, and the increase in expression of p53 and Rb in HFK-HPV18 was highest in ethanol-extracted compound REE group.Conclusions:The proliferation rates are significantly lower in HFK-HPV18 treated with REE. The expression of E6 and L1 is markedly lower, and expression of p53 and Rb is significantly higher after REE treatment in HFK-HPV18 or organotypic rafts containing HFK-HPV18. Among all formula of REE, ethanol-extracted compound REE displays the highest protection against HPV18.

scholarly journals Effects of Holothurian Glycosaminoglycan on the Sensitivity of Lung Cancer to Chemotherapy

2020 ◽  
Vol 19 ◽  
pp. 153473542091143
Author(s):  
Cunzhi Lin ◽  
Xinhong Zhu ◽  
Qing Jin ◽  
Aihua Sui ◽  
Jinfeng Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Sea Cucumber ◽  
Caspase 3 ◽  
A549 Cells ◽  
Annexin V ◽  
Inhibitory Effect ◽  
The Body ◽  
Control Group ◽  
Apoptosis Pathway

Sea cucumber is a kind of food. Holothurian glycosaminoglycan (hGAG) is extracted from the body wall of the sea cucumber. Administration of hGAG and cisplatin (DDP) together to treat lung cancer was investigated. Lung adenocarcinoma A549 cells were cultured and divided into 4 groups: control group, hGAG 100 µg/mL group, DDP 3 µg/mL group, and hGAG 100 µg/mL + DDP 3 µg/mL group. Cell inhibition and apoptosis was evaluated by CCK8 and Hoechst33258 staining. Cell cycle was tested by Annexin V-FITC/PI (propidium iodide) double-staining and flow cytometry. The expression of mRNA and protein of Bcl-2, Bax, caspase-3, and survivin were detected by reverse transcriptase-polymerase chain reaction and Western blot, respectively. The results showed that hGAG combined with DDP enhanced the inhibitory effect of DDP on A549 lung cells through apoptosis pathway. The mechanism of apoptosis may be related to the reduction of Bcl-2 and survivin, as well as the ascension of Bax and caspase-3. hGAG could promote A549 cell cycle arrest in G1 and G2 phase and improve the DDP chemotherapy effects on A549 cells.

scholarly journals Effects of Laminaria Japonica Polysaccharides on the Survival of Non-Small-Cell Lung Cancer A549 Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Mengxing Yao ◽  
XiaoJun Qian ◽  
Houying Qin
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Control Group ◽  
Small Cell Lung

Objective. To investigate the effect of Laminaria japonica polysaccharides (LJP) on the survival of non-small-cell lung cancer (NSCLC) A549 cells and its mechanism. Methods. In vitro: the cells were randomly divided into control group, LJP (5 mg/ml) group, LJP (10 mg/ml) group, and LJP (20 mg/ml) group. After corresponding treatment, the survival rate and the expression of proteins related to proliferation, apoptosis, epithelial-mesenchymal transition (EMT), and signaling pathway were detected by CCK8 assay and Western blot, respectively. In vivo: a xenograft model was established to detect the tumor volume and mass and the expression of the above pathway proteins. Results. Compared with the control group, LJP decreased the survival rate of A549 cells (P<0.05), inhibited the protein expression of Ki67 and PCNA (P<0.05), downregulated the expression of Bcl-2 while upregulated the expression of Bax, cl-caspase-3, and cl-caspase-9 (P<0.05), upregulated the expression of E-cadherin, downregulated the expression of vascular endothelial growth factor (VEGF) and N-cadherin (P<0.05), and downregulated β-catenin, transcription factor-4 (TCF4), and c-Myc protein expression levels (P<0.05). In vivo: LJP decreased the volume and mass of the xenograft tumors and downregulated β-catenin, TCF4, and c-Myc protein expression levels compared with the control group (P<0.05). Conclusion. LJP can inhibit the survival of non-small-cell lung cancer A549 cells in vitro, and its mechanism is related to the inhibition of activation of β-catenin/TCF4 pathway activation.

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