Search

To solve the problem of transmission line galloping monitoring for optical power grounded waveguides (OPGWs) in external field environments, we propose a low-noise monitoring array based on adjacent sensors with low reflectivity fiber Bragg grating (FBG). We analyze the interference signal models for adjacent FBG sensors, and based on them, a noise suppression method by using adaptive filter input is constructed. Then we simulate the noise suppression effect of the proposed algorithm under different noise conditions. Finally, we deploy the low-noise OPGW transmission line galloping monitoring system based on low reflectivity FBGs in China's western autonomous prefecture with a 220 kV transmission line. The experimental results show that, after adaptive filtering using adjacent sensors, the average noise power spectral density is reduced by 6.5 dB, and the algorithm optimizes the monitoring intensity spectrum. Oscillation events of about 100 m can be clearly observed within the monitoring interval. It creates certain conditions for further improving the typical event classification data processing and pattern recognition database for OPGWs and demonstrates promising prospects for engineering applications. [ABSTRACT FROM AUTHOR]

Plakophilin 3 (PKP3) affects cell signal transduction and cell adhesion and performs a crucial function in tumorigenesis. The current investigation evaluated the predictive significance and underlying processes of PKP3 within pancreatic cancer (PC) tissues. The assessment of differences in PKP3 expression was conducted through an analysis of RNA-seq data acquired from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Additionally, clinical samples were collected to validate the findings. The predictive significance of PKP3 was investigated by analyzing survival data derived from TCGA and clinical specimens. PKP3′s biological function was assessed via phenotypic experiments after the suppression of PKP3 expression within PC cells. Functional enrichment analysis, encompassing KEGG, GO, and GSEA, was employed to assess the underlying mechanism of PKP3. Immune infiltration analysis was conducted in the present investigation to determine the association between PKP3 and tumor-infiltrating immune cells (TICs). In PC tissues, PKP3 expression was abnormally upregulated and correlated with a negative prognosis in individuals with PC. PKP3 can promote the progression, migration, and invasive capacity of PC cells and is relevant to the regulation of the PI3K–Akt and MAPK signaling pathways. Immune infiltration analysis demonstrated that PKP3 impeded CD8+ T-cell infiltration and immune cytokine expression within the tumor microenvironment. The PKP3 protein was identified as a prospective independent predictive indicator and represents a viable approach for immunotherapy in the context of PC. PKP3 may impact prognosis by broadly inhibiting immune cell infiltration and promoting the activation of tumor-associated signaling pathways. [ABSTRACT FROM AUTHOR]

Tumor-associated macrophages M2 (TAM2), which are highly prevalent infiltrating immune cells in the stroma of pancreatic cancer (PC), have been found to induce an immunosuppressive tumor microenvironment, thus enhancing tumor initiation and progression. However, the immune therapy response and prognostic significance of regulatory genes associated with TAM2 in PC are currently unknown. Based on TCGA transcriptomic data and single-cell sequencing data from the GEO database, we identified TAM2-driven genes using the WGCNA algorithm. Molecular subtypes based on TAM2-driven genes were clustered using the ConsensusClusterPlus algorithm. The study constructed a prognostic model based on TAM2-driven genes through Lasso-COX regression analysis. A total of 178 samples obtained by accessing TCGA were accurately categorized into two molecular subtypes, including the high-TAM2 infiltration (HMI) cluster and the low-TAM2 infiltration (LMI) cluster. The HMI cluster exhibits a poor prognosis, a malignant tumor phenotype, immune-suppressive immune cell infiltration, resistance to immunotherapy, and a high number of genetic mutations, while the LMI cluster is the opposite. The prognostic model composed of six hub genes from TAM2-driven genes exhibits a high degree of accuracy in predicting the prognosis of patients with PC and serves as an independent risk factor. The induction of TAM2 was employed as a means of verifying these six gene expressions, revealing the significant up-regulation of BCAT1, BST2, and MERTK in TAM2 cells. In summary, the immunophenotype and prognostic model based on TAM2-driven genes offers a foundation for the clinical management of PC. The core TAM2-driven genes, including BCAT1, BST2, and MERTK, are involved in regulating tumor progression and TAM2 polarization, which are potential targets for PC therapy. [ABSTRACT FROM AUTHOR]

The signal transducer and activator of transcription (STAT) is a family of intracellular cytoplasmic transcription factors involved in many biological functions in mammalian signal transduction. Among them, STAT3 is involved in cell proliferation, differentiation, apoptosis, and inflammatory responses. Despite the advances in the treatment of pancreatic cancer in the past decade, the prognosis for patients with pancreatic cancer remains poor. STAT3 has been shown to play a pro-cancer role in a variety of cancers, and inhibitors of STAT3 are used in pre-clinical and clinical studies. We reviewed the relationship between STAT3 and pancreatic cancer and the latest results on the use of STAT3 inhibitors in pancreatic cancer, with the aim of providing insights and ideas around STAT3 inhibitors for a new generation of chemotherapeutic modalities for pancreatic cancer. [ABSTRACT FROM AUTHOR]

Methylation of cytosine residues resulting in 5-methylcytosine (5-mC) is an important epigenetic modification associated with tumorigenesis. The present study explored the relationship between methylation, prognosis, and immunotherapy of patients suffering from lung squamous cell carcinoma (LUSC). RNA sequencing data and corresponding clinical information were downloaded, and preprocessed, and unsupervised consistent cluster analysis was used to identify 5-mC-related clusters and gene clusters. 5-mC scores were calculated using principal component analysis, and a Boruta algorithm was used to evaluate the relationship between tumor mutation burden (TMB), immune checkpoint inhibitor response, and prognosis of individual LUSC patients. : Two 5-mC clusters and three gene clusters with different prognoses were identified. Patients with higher 5-mC scores showed worse prognoses, which was confirmed in multiple cohorts. Some immune-related biological functions and pathways were enriched in the high-5-mC score subtype. The 5-mC score is a potential biomarker independent of TMB, which can be a decisive factor regarding immune treatment responses. Further, patients with low 5-mC scores may respond better to immunotherapy. The 5-mC score can thus be used as a potential biomarker for the prognosis of LUSC patients and their response to immunotherapy. [ABSTRACT FROM AUTHOR]

A finite element model of steel frame joints is established using finite element analysis software ANSYS/LS-DYNA. The ideal triangular impact load is used to numerically analyze the dynamic response of steel frame welded joints under blast loading, the main factors affecting this response, and the failure modes of three types of joints, so as to provide reference for the antiexplosive design of steel frame joints. The results show that steel frame joints vibrate violently in the explosive blast direction. Due to the strain rate effect, the strength of steel increases, the material enters the plastic strengthening stage, and there is a certain residual displacement. In addition, displacement and stress caused by blast action in the joint area are large, and the flange shear failure of the beam and column is prone to occur in the joint. Increasing the flange width of the beam and the column cannot improve the antiexplosive performance of the joints, while increasing their thickness can. Furthermore, bolted and welded joints have the highest stiffness and best antiexplosion performance, followed by welded joints, while the antiexplosion performance of bolted joints was the worst. [ABSTRACT FROM AUTHOR]

Introduction: Lung cancer is the malignant tumor with the fastest increase in morbidity and mortality and the greatest threat to human health and life. Long non-coding RNA (lncRNA) is emerging as an important regulator in many cancers. Recently, it was found that lncRNA prostate cancer associated transcript 1 (PCAT-1) was up-regulated in lung cancer, playing oncogenic roles. However, the underlying regulatory mechanism of PCAT-1 remains unknown.Material and Methods: The expression levels of PCAT-1 and miR-324-5p were analyzed by real-time PCR, and RAP1A expression was determined by western blotting. RNA pull-down, luciferase and western blotting assays were used to examine the target relationship between PCAT-1 and miR-324-5p or that between miR-324-5p and RAP1A. The functional effects of PCAT-1 and miR-324-5p were examined using cell viability and cell apoptosis assays.Results: PCAT-1 overexpression remarkably promoted cell proliferation and suppressed cell apoptosis. Mechanistic investigations demonstrated that PCAT-1 can interact with miR-324-5p and repress its expression, thereby increasing the expression of its target RAP1A. Additionally, rescue experiments revealed that PCAT-1 served as an oncogene partly through sponging miR-324-5p and upregulating RAP1A in lung cancer cells.Conclusions: Our findings demonstrate that on account of the dual function of pro-proliferation and anti-apoptosis, PCAT-1/miR-324-5p/RAP1A may be novel candidates for application in the diagnosis, prognosis and therapy of lung cancer. [ABSTRACT FROM AUTHOR]

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide. This study aims to understand the underlying mechanism of lncRNA, actin filament-associated protein 1 antisense RNA 1(AFAP1-AS1) in mediating chemotherapeutic resistance in NSCLC. The levels of AFAP1-AS1 in NSCLC tissues and cells were determined using RT-PCR. The protein levels of RRM2, EGFR, and p-AKT were analyzed using Western blotting. Binding between AFAP1-AS1 and miR-139-5p was confirmed using dual luciferase reporter and RNA immunoprecipitation (RIP) assays, and binding between miR-139-5p and RRM2 was confirmed by a dual luciferase reporter assay. NSCLC cell proliferation, apoptosis, and colony formation were examined using MTT, flow cytometry, and colony formation assays, respectively. It was found that AFAP1-AS1 expression was upregulated in NSCLC tissues and cells. In addition, AFAP1-AS1 bound to and downregulated the expression of miR-139-5p, which was reduced in NSCLC tissues. Knockdown of AFAP1-AS1 and overexpression of miR-139-5p inhibited NSCLC cell proliferation, colony formation and chemotherapy resistance and increased cell apoptosis. Additionally, AFAP1-AS1 upregulates RRM2 expression via sponging miR-139-5p. Furthermore, AFAP1-AS1 enhanced NSCLC cell proliferation and chemotherapy resistance through upregulation of RRM2 by inhibiting miR-139-5p expression. Moreover, RRM2 promoted cellular chemotherapy resistance by activating EGFR/AKT. Finally, knockdown of AFAP1-AS1 significantly suppressed tumor growth and chemoresistance in nude mice. In conclusion, AFAP1-AS1 promoted chemotherapy resistance by supressing miR-139-5p expression and promoting RRM2/EGFR/AKT signaling pathway in NSCLC cells. [ABSTRACT FROM AUTHOR]

Purpose: Non-small-cell lung cancer (NSCLC) is the one of the most common malignancies worldwide, and occurs at a higher frequency in male individuals. Little is known about the role of the long intergenic noncoding RNA for kinase activation (LINK-A) in NSCLC, so in the present study we assessed its potential role on cell proliferation in NSCLC. Methods: Expression levels of LINK-A in NSCLC tissues and cell lines were detected by quantitative reverse-transcription polymerase chain reaction. LINK-A was knocked down and overexpressed separately in A549 cells and NCI-H1299 cells. The effect of LINK-A expression on cell proliferation was determined by MTT assay. The correlation between LINK-A and hexokinase II (HKII) expression was investigated by Western blot and HKII Activity Assay. Glucose consumption and lactate production assay were used to investigate the aerobic glycolysis in NSCLC cells. The effect of LINK-A in vivo was determined by xenograft assay. Results: LINK-A expression levels were increased in NSCLC tissues compared with normal tissues. Moreover, LINK-A expression was positively correlated with NSCLC clinicopathological characteristics and survival rate, while knockdown of LINK-A reduced NSCLC cell proliferation. LINK-A expression was also positively correlated with HKII, and NSCLC cells with low LINK-A expression were found to have significantly reduced HKII protein expression, accompanied by a reduction in enzyme activity levels. Both in vitro and in vivo experiments showed that LINK-A expression affected glucose consumption and lactate production through regulation of HKII expression. Conclusion: These data suggest that the functions of LINK-A in NSCLC might play a key role in tumor progression and that LINK-A could be a promising predictive biomarker and potential therapeutic target for NSCLC. [ABSTRACT FROM AUTHOR]

Although pulmonary fibrosis (PF) causes respiratory failure and death, effective therapies for PF have not been developed. Oxymatrine (OMT), an active ingredient in the Chinese herb Sophora flavescens, exerts antifibrotic effects; however, its effect on PF remains unclear. The present study aimed to determine whether OMT decreases transforming growth factor-β1 (TGF-β1)-induced PF in human lung cancer A549 cells by inhibiting apoptosis and targeting the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway. To construct a PF cell model, A549 cells were stimulated with TGF-β1. The experimental groups were as follows: control (untreated cells grown in complete medium), TGF-β1 (cells treated with 5 ng/ml TGF-β1), OMT (cells treated with 5 ng/ml TGF-β1 and 0.25, 0.50, or 1.00 mg/ml OMT), and OMT + LY294002 (cells treated with 5 ng/ml TGF-β1, 1.0 mg/ml OMT. and 25 µmol/l LY294002). The effects of OMT on cell morphology (via electron microscopy), apoptosis (via Annexin V-PI staining), mitochondrial apoptosis signaling [using JC-1 method to analyze mitochondrial membrane potential (MMP)], and Bcl-2, as well as Bax expression (via western blotting and reverse transcription-quantitative polymerase chain reaction), were analyzed. OMT significantly protected cells against TGF-β1-induced PF by inhibiting apoptosis. The specific manifestations were cell injury, as evidenced by morphological changes and decreased MMP. Following OMT treatment, the expression of the pro-apoptotic protein Bax increased, whereas that of the anti-apoptotic protein Bcl-2 decreased. The PI3K/AKT-specific inhibitor LY294002 significantly inhibited the ameliorative effects of OMT on TGF-β1-induced apoptosis. Collectively, OMT attenuated TGF-β1-mediated mitochondrial apoptosis of alveolar epithelial cells by activating the PI3K/AKT signaling pathway. Therefore, OMT may be a promising drug for PF treatment. [ABSTRACT FROM AUTHOR]

Transparent conductive oxide (TCO) p-type Li-doped NiO thin films were deposited on the (0001) sapphire substrates by magnetron sputtering technique with a high purity NiO:LiO ceramic target. We systematically investigated the structural, electrical and optical properties of NiO:Li thin films annealed in different conditions. We found that annealing in different conditions greatly affects the physical properties of NiO:Li thin films. Compared with the NiO:Li thin film annealed in oxygen, the hole concentration of NiO:Li thin film annealed in nitrogen at the same processing temperature is obviously lower. Annealed in oxygen at 500 °C, NiO:Li films show excellent crystal quality with single (111) orientation, high hole concentrations. When the annealing temperature increased, the transmittance of NiO:Li thin films become better for wavelength range from ultraviolet (UV) to visible with a significant absorption edge near 350 nm. [ABSTRACT FROM AUTHOR]

Insecticyanin is a blue pigment found in the epidermis and hemolymph of the tobacco hornworm, Manduca sexta. Two distinct full-length eDNA species were isolated and shown to encode the two major isoelectric forms of insecticyanin, the a form (INS-a) and b form (INS-b). Sequence analysis of the two cDNA clones, pE1-11 and pE3-12, reveals that both contain an 618-bp open reading frame which predicts an 189-amino-acid protein and an 17-amino-acid signal peptide. Comparison of the deduced INS-a and INS-b proteins show 13 amino acid differences, of which six are conserved. Three amino acid substitutions are also found between the deduced INS-b sequence and the sequenced INS-b protein isolated from the hemolymph. Isolation and characterization of live genomic clones revealed that pE1-11 and pE3-12 come from two different genes. Both INS-a and INS-b genes have four exons interrupted by three introns at the same positions. The two genes share 93% nucleotide similarity in the coding region. Moreover, the 'TATA box' and 'CAAT box' are completely conserved in the putative promoter regions of the two genes. Primer extension revealed that both INS-a and INS-b genes begin their transcription at position -52 relative to their translation initiation codon, ATG. We conclude that the two genes are the result of gene duplication. [ABSTRACT FROM AUTHOR]

β-Ga2O3 films were grown on sapphire (0001) substrates with various O/Ga (VI/III) ratios by metal organic chemical vapor deposition. The effects of VI/III ratio on growth rate, structural, morphological, and Raman properties of the films were systematically studied. By varying the VI/III ratio, the crystalline quality obviously changed. By decreasing the VI/III ratio from 66.9 × 103 to 11.2 × 103, the crystalline quality improved gradually, which was attributed to low nuclei density in the initial stage. However, crystalline quality degraded with further decrease of the VI/III ratio, which was attributed to excessive nucleation rate. [ABSTRACT FROM AUTHOR]

Introduction: Tumor-associated macrophage 2 (TAM2) abundantly infiltrates pancreatic ductal adenocarcinoma (PAAD), and its interaction with malignant cells is involved in the regulation of tumor metabolism. In this study, we explored the metabolic heterogeneity involved in TAM2 by constructing TAM2-associated metabolic subtypes in PAAD., Materials and Methods: PAAD samples were classified into molecular subtypes with different metabolic characteristics based on a multi-omics analysis strategy. 20 PAAD tissues and 10 normal pancreatic tissues were collected for proteomic and metabolomic analyses. RNA sequencing data from the TCGA-PAAD cohort were used for transcriptomic analyses. Immunohistochemistry was used to assess TAM2 infiltration in PAAD tissues., Results: The results of transcriptomics and immunohistochemistry showed that TAM2 infiltration levels were upregulated in PAAD and were associated with poor patient prognosis. The results of proteomics and metabolomics indicated that multiple metabolic processes were aberrantly regulated in PAAD and that this dysregulation was linked to the level of TAM2 infiltration. WGCNA confirmed pyruvate and glycolysis/gluconeogenesis as co-expressed metabolic pathways of TAM2 in PAAD. Based on transcriptomic data, we classified the PAAD samples into four TAM2-associated metabolic subtypes (quiescent, pyruvate, glycolysis/gluconeogenesis and mixed). Metabolic subtypes were each characterized in terms of clinical prognosis, tumor microenvironment, immune cell infiltration, chemotherapeutic drug sensitivity, and functional mechanisms., Conclusion: Our study confirmed that the metabolic remodeling of pyruvate and glycolysis/gluconeogenesis in PAAD was closely related to TAM2. Molecular subtypes based on TAM2-associated metabolic pathways provided new insights into prognosis prediction and therapy for PAAD patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Li, Du, Jiang, Dong, Li, Tang, Yi, Zhou and Zhang.)

Background: The dilemma of pancreatic cancer treatment has become a global challenge. For this reason, effective, feasible, and new medical methods are currently much-needed. Betulinic acid (BA) has been valued as a potential therapy for pancreatic cancer. However, the mechanism by which BA exerts an inhibitory effect on the development of pancreatic cancer remains elusive., Methods: A rat model and two cell models of pancreatic cancer were established, and the effect of BA on pancreatic cancer was verified in vivo and in vitro by using MTT, Transwell, flow cytometry, RT-PCR, Elisa and immunohistochemistry. At the same time, miR-365 inhibitors were introduced to test whether BA played a role in mediating miR-365., Results: BA can significantly inhibit the proliferation and invasion of pancreatic cancer cells and promote apoptosis. In vivo experiments, BA can significantly lower the number of cancer cells and tumor volume in the rat model of pancreatic cancer. In vitro , it was found that BA inhibited the protein level and phosphorylation level of AKT/STAT3 by mediating the expression of miR365/BTG2/IL-6. Like BA, miR-365 inhibitors also significantly inhibited cell viability and invasion ability, and inhibited the protein level and phosphorylation level of AKT/STAT3 by changing the expression of BTG2/IL-6, and their combination had a synergistic effect., Conclusion: BA inhibits AKT/STAT3 expression and phosphorylation by modulating miR-365/BTG2/IL-6 expression, and BA inhibits the progression of pancreatic cancer through the aforementioned mechanism., Competing Interests: The authors declare that they have no conflicts of interest to report regarding the present study., (© 2023 Li et al.)

Laryngopharyngeal reflux (LPR) is a common disorder in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). This meta-analysis was carried out to evaluate the LPR prevalence in individuals with OSAHS and to analyze the correlation of LPR positivity with the clinical features of patients with OSAHS. A detailed review of the English and Chinese literature on the occurrence of LPR in patients with OSAHS was performed by employing online search tools such as PubMed, EMBASE, Web of Science, VIP, CNKI, WanFang, etc. Two researchers analyzed the studies for quality according to the STROBE standard checklist. The acquired data were analyzed using Stata 11.0 and R 3.6.1 software. The effect size was estimated and calculated using weighted mean difference (WMD) and correlation coefficients. Moreover, a combined analysis was performed by employing either a random- or fixed-effects model. Ultimately, 27 studies met our inclusion criteria. Our study revealed that the LPR prevalence in OSAHS patients was 49%. We carried out subgroup analyses as per OSAHS severity, ethnicity, and body mass index (BMI). The results suggested that the probability of LPR in European and American patients with OSAHS was higher, and the prevalence of LPR was higher in obese individuals and patients with severe OSAHS. Moreover, apnea-hypopnea index (AHI) and BMI were higher in LPR-positive OSAHS patients than in LPR-negative OSAHS patients, but no significant variation in age was observed in the two groups. Moreover, the reflux symptom index (RSI) scores and the reflux finding score (RFS) exhibited a positive correlation with AHI. The current literature shows a higher incidence of LPR in individuals with OSAHS (49%). The severity of AHI in individuals with OSAHS is associated with the presence of LPR. Patients with OSAHS accompanied by LPR showed higher BMI and AHI as compared to those patients with LPR-negative OSAHS., Competing Interests: The authors declare that they have no competing interests in this work., (© 2022 He et al.)

Early and accurate diagnosis and treatment of pancreatic cancer (PC) remain challenging endeavors globally. Late diagnosis lag, high invasiveness, chemical resistance, and poor prognosis are unresolved issues of PC. The concept of metabolic reprogramming is a hallmark of cancer cells. Increasing evidence shows that PC cells alter metabolic processes such as glucose, amino acids, and lipids metabolism and require continuous nutrition for survival, proliferation, and invasion. Glucose metabolism, in particular, regulates the tumour microenvironment (TME). Furthermore, the link between glucose metabolism and TME also plays an important role in the targeted therapy, chemoresistance, radiotherapy ineffectiveness, and immunosuppression of PC. Altered metabolism with the TME has emerged as a key mechanism regulating PC progression. This review shed light on the relationship between TME, glucose metabolism, and various aspects of PC. The findings of this study provide a new direction in the development of PC therapy targeting the metabolism of cancer cells., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Dong, Li, Li, Wang, Chen, Shi, He, Chen and Zhou.)

Introduction: Lung cancer is the malignant tumor with the fastest increase in morbidity and mortality and the greatest threat to human health and life. Long non-coding RNA (lncRNA) is emerging as an important regulator in many cancers. Recently, it was found that lncRNA prostate cancer associated transcript 1 (PCAT-1) was up-regulated in lung cancer, playing oncogenic roles. However, the underlying regulatory mechanism of PCAT-1 remains unknown., Material and Methods: The expression levels of PCAT-1 and miR-324-5p were analyzed by real-time PCR, and RAP1A expression was determined by western blotting. RNA pull-down, luciferase and western blotting assays were used to examine the target relationship between PCAT-1 and miR-324-5p or that between miR-324-5p and RAP1A. The functional effects of PCAT-1 and miR-324-5p were examined using cell viability and cell apoptosis assays., Results: PCAT-1 overexpression remarkably promoted cell proliferation and suppressed cell apoptosis. Mechanistic investigations demonstrated that PCAT-1 can interact with miR-324-5p and repress its expression, thereby increasing the expression of its target RAP1A. Additionally, rescue experiments revealed that PCAT-1 served as an oncogene partly through sponging miR-324-5p and upregulating RAP1A in lung cancer cells., Conclusions: Our findings demonstrate that on account of the dual function of pro-proliferation and anti-apoptosis, PCAT-1/miR-324-5p/RAP1A may be novel candidates for application in the diagnosis, prognosis and therapy of lung cancer., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2019 Termedia & Banach.)

The present study aimed to investigate the effect of various concentrations of etoposide (VP-16) on the E3 ubiquitin-protein ligase Mdm2 (Mdm2)-retinoblastoma (Rb) signaling pathway in the cellular senescence of A549 lung adenocarcinoma cells. A549 cells were randomly divided into the following four groups: Control group (no treatment), group 1 (1 µmol/l VP-16), group 2 (5 µmol/l VP-16) and group 3 (25 µmol/l VP-16). Each group was cultured for 48 h after treatment prior to observation of the alterations to cellular morphology. The cell cycle distribution of each group was also detected by flow cytometry. In addition, the activity of cellular senescence-associated β-galactosidase, and the expression of Mdm2 and phosphorylated (p-) Rb protein, was measured. The percentage of senescent cells was significantly higher following VP-16 treatment compared with the control group. The percentage of G 1 phase cells, and p-Rb protein and Mdm2 protein expression were also significantly different following VP-16 treatment compared with the control group. VP-16 increased the activity of β-galactosidase in the A459 cells. VP-16 also decreased the expression level of Mdm2 and p-Rb protein and inhibited cell cycle progression in G 1 . These results indicate that VP-16 induces the cellular senescence of A549 cells via the Mdm2-Rb signaling pathway. However, further investigations are required to validate the mechanisms underlying these effects of VP-16.