Lighting up endogenous H2O2 in the tumor microenvironment using a dual-mode nanoprobe for long afterglow and MR bioimaging.

Persistent luminescent nanoparticles (PLNPs) are excellent luminescent materials, and near-infrared PLNPs are efficiently applied for biosensing and bioimaging due to their advantages of no excitation, excellent light stability and long afterglow. However, due to interference from the complex environment within organisms, single-mode imaging methods often face limitations in selectivity, sensitivity, and accuracy. Therefore, it is desirable to construct a dual-mode imaging probe strategy with higher specificity and sensitivity for bioimaging. Magnetic resonance imaging (MRI) has been widely used in the field of bioimaging due to its advantages of high resolution, non-radiation and non-invasiveness. Here, by combining near-infrared PLNPs and manganese dioxide (MnO2) nanosheets, a sensitive and convenient dual-mode "turn on" bioimaging nanoprobe ZGC@MnO2 has been developed for long afterglow imaging and MRI of endogenous hydrogen peroxide (H2O2) in the tumor microenvironment (TME). The monitoring of H2O2 has garnered significant attention due to its crucial role in human pathologies. For the dual-mode "turn on" bioimaging nanoprobe, the near-infrared PLNPs of quasi-spherical ZnGa2O4:Cr (ZGC) nanoparticles were synthesized as luminophores, and MnO2 nanosheets were utilized as a fluorescence quencher, carrier and H2O2 recognizer. H2O2 in the TME could reduce MnO2 nanosheets to Mn2+ for MRI, and ZGC nanoparticles were released for long afterglow imaging. Finally, the ZGC@MnO2 nanoprobe exhibited a rapid response, an excellent signal-to-noise ratio and a limit of detection of 3.67 nM for endogenous H2O2 in the TME. This dual-mode approach enhances the detection sensitivity for endogenous H2O2, thereby facilitating the research of endogenous H2O2-associated diseases and clinical diagnostics.

Neoadjuvant savolitinib targeted therapy for stage IIIB-N3 lung adenocarcinoma harboring mesenchymal-epithelial transition exon 14 skipping mutation: a case report and literature review.

Savolitinib is a selective inhibitor that specifically targets the phosphorylation of mesenchymal-epithelial transition (MET) kinase. It has demonstrated significant inhibitory effects on the proliferation of tumor cells with METex14 skipping mutation, making it a promising treatment option. While it is the first approved small-molecule inhibitor specifically targeting MET kinase in China, there is limited information about its efficacy as neoadjuvant therapy for patients with supraclavicular lymph node metastasis (N3). In this case report, we presented the successful outcome of a 48-year-old male patient who was diagnosed with stage IIIB (T2bN3M0) lung adenocarcinoma originating from the left upper lobe. The patient exhibited the METex14 skipping alteration. Following two months of neoadjuvant savolitinib treatment, the patient achieved partial remission, with a significant reduction in the size of the primary tumor and metastatic lymph nodes. Postoperative pathological confirmation revealed a pathological complete response, and subsequent imaging examinations, including computed tomography scan and circulating tumor DNA-based molecular residual disease detection, showed no sign of recurrence at 7 months after surgery. Based on this case, neoadjuvant and adjuvant savolitinib therapy may be considered as a favorable alternative to chemotherapy for marginally resectable nonsmall cell lung cancer patients with METex14 skipping mutation.

Involvement of plasminogen activator inhibitor-1 in p300/p53-mediated age-related atrial fibrosis.

Plasminogen activator inhibitor-1 (PAI-1), a key regulator of the fibrinolytic system, is also intimately involved in the fibrosis. Although PAI-1 may be involved in the occurrence of atrial fibrillation (AF) and thrombosis in the elderly, but whether it participated in aging-related atrial fibrosis and the detailed mechanism is still unclear. We compared the transcriptomics data of young (passage 4) versus senescent (passage 14) human atrial fibroblasts and found that PAI-1 was closely related to aging-related fibrosis. Aged mice and senescent human and mouse atrial fibroblasts underwent electrophysiological and biochemical studies. We found that p300, p53, and PAI-1 protein expressions were increased in the atrial tissue of aged mice and senescent human and mouse atrial fibroblasts. Curcumin or C646 (p300 inhibitor), or p300 knockdown inhibited the expression of PAI-1 contributing to reduced atrial fibroblasts senescence, atrial fibrosis, and the AF inducibility. Furthermore, p53 knockdown decreased the protein expression of PAI-1 and p21 in senescent human and mouse atrial fibroblasts. Our results suggest that p300/p53/PAI-1 signaling pathway participates in the mechanism of atrial fibrosis induced by aging, which provides new sights into the treatment of elderly AF.

Prognostic Value of the Lung Immune Prognostic Index for Metastatic Non-Small Cell Lung Cancer Patients: A Chinese Cohort Study.

Background: Most cancer-related deaths around the globe are caused by lung cancer. The present treatments for metastatic non-small cell lung cancer (mNSCLC) are cytotoxic chemotherapy (CCT), targeted therapy (TT) and immunotherapy, but the benefit of the same regime varies greatly. Hence, it is important to identify biomarkers to predict the efficacy of modalities. Previous literature suggested certain parameters might be predictive factors. Nevertheless, the utility of these parameters is limited due to the types of solid tumors. Purpose: The study aimed to examine whether the lung immune prognostic index (LIPI) was related to outcomes of CCT, immune checkpoint inhibitors (ICIs) and TT for mNSCLC patients. Materials and Methods: A retrospective cohort study between September 2012 and May 2020 was conducted on 350 Chinese mNSCLC patients, including 147 patients receiving ICIs, 103 TT, and 100 CCT. The data were examined to analyze the prognostic value of LIPI among various treatments. Main Outcomes and Measures: The associations between PFS and good, intermediate, or poor prognostic LIPI scores in ICIs, TT, and CCT were determined, respectively. Results: In univariable analyses, there was a relevance between a good LIPI score and better PFS among patients receiving ICIs (HR, 0.81; 95% CI, 0.44-1.51), TT (HR, 0.35; 95% CI, 0.16-1.74), and CCT (HR, 0.39; 95% CI, 0.19-0.80). In multivariable analyses, the intermediate LIPI score was linked to better PFS only in patients receiving TT (HR, 0.31; 95% CI, 0.17-0.92) rather than ICIs (HR, 1.12; 95% CI, 0.66-2.45) or CCT (HR, 1.24; 95% CI, 0.49-4.55). Conclusion: Baseline LIPI value is an important prognostic biomarker for mNSCLC patients treated with TT. Shorter PFS with TT was associated with poor baseline LIPI. Poor LIPI score may be considered as a promising indicator showing which patients are unlikely to respond well to TT. The prognostic value of LIPI can be more clearly determined through prospective clinical study.

Circ_0024108 promotes the progression of esophageal cancer cells.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a serious malignant cancer. The treatment effect of ESCC is relatively poor and needs further improvement. According to reports, circular RNAs (circRNAs) actively participate in human carcinogenesis. More explorations are needed about the action of circRNAs in ESCC. METHODS: Circ_0024108, miR-488-3p, and USP14 was quantified by a qRT-PCR or immunoblotting method. Cell proliferation evaluation was performed by MTT, EdU, and colony formation assays. Evaluation of cell motility and invasiveness was conducted using wound healing assay and transwell assay. The regulatory mechanism of circ_0024108, miR-488-3p, and USP14 was detected by RNA pull-down assay and dual-luciferase reporter assay. RESULTS: Circ_0024108 and USP14 were significantly overexpressed in ESCC, while miR-488-3p was underexpressed. Deficiency of circ_0024108 impeded cell growth, motility, and invasiveness. Circ_0024108 regulated the expression of USP14 in ESCC cells via miR-488-3p. Also, circ_0024108 was present at high levels in serum exosomes from ESCC patients with high specificity and sensitivity. CONCLUSIONS: Taken together, circ_0024108 participated in the progress of ESCC through the miR-488-3p/USP14 axis. Circ_0024108 was differentially expressed in serum exosomes. Circ_0024108 might be a potential biomarker for the diagnosis of ESCC.

Opposite evolution of pathogenicity driven by in vivo wzc and wcaJ mutations in ST11-KL64 carbapenem-resistant Klebsiella pneumoniae.

AIMS: To investigate the in vivo evolution of the mucoid-phenotype of ST11-KL64 carbapenem-resistant Klebsiella pneumoniae (CRKP) isolated from the same patients and gain insights into diverse evolution and biology of these strains. METHODS: Whole genome sequencing and bioinformatic analysis were used to determine the mutation involved in the mucoid phenotype of ST11-KL64 CRKP. Gene knockout, bacterial morphology and capsular polysaccharides (CPS) extraction were used to verify the role of wzc and wcaJ in the mucoid phenotypes. Antimicrobial susceptibility, growth assay, biofilm formation, host cell adhesion and virulence assay were used to investigate the pleiotropic role of CPS changes in ST11-KL64 CRKP strains. RESULTS: Mutation of wzc S682N led to hypermucoid phenotype, which had negative impact on bacterial fitness and resulted in reduced biofilm formation and epithelial cell adhesion; while enhanced resistance to macrophage phagocytosis and virulence. Mutations of wcaJ gene led to non-mucoid phenotype with increased biofilm formation and epithelial cell adhesion, but reduced resistance of macrophage phagocytosis and virulence. Using virulence gene knockout, we demonstrated that CPS, rather than the pLVPK-like virulence plasmid, has a greater effect on mucoid phenotypic changes. CPS could be used as a surrogate marker of virulence in ST11-KL64 CRKP strains. CONCLUSIONS: ST11-KL64 CRKP strains sacrifice certain advantages to develop pathogenicity by changing CPS with two opposite in vivo evolution strategies.

Local tumour residue after microwave ablation for lung cancer: a case report.

Thermal ablation has become a novel method for the treatment of pulmonary nodules, but the short-time evaluation of the ablation effect is mainly based on computed tomography images. We report a case of local tumour residue after microwave ablation, which was confirmed by pathology after lobectomy. This case alerts us that thermal ablation should not be the preferred treatment for operable pulmonary nodules.

Ttc39c is a potential target for the treatment of lung cancer.

BACKGROUND: The novel TTC gene, tetratricopeptide repeat domain 39 C (Ttc39c), mainly mediates the interaction between proteins. It is involved in the progression of various tumors. In this study, we determined the effect of Ttc39c on lung adenocarcinoma and found that it might be used as a potential intervention target. METHODS: We performed a difference analysis of Ttc39c samples from the TCGA database. Transwell experiments were conducted to determine the ability of cell metastasis. Celigo and MTT assays were performed to determine the effect of Ttc39c gene subtraction on cell proliferation. FACS was performed to determine the effect of Ttc39c gene subtraction on apoptosis. Clone-formation experiments were conducted to determine the effect of Ttc39c gene subtraction on cloning ability. Transcriptomics, proteomics, and metabolomics were used to elucidate the enrichment pathway of the Ttc39c gene in the progression of lung adenocarcinoma. RESULTS: The expression of Ttc39c increased significantly in lung adenocarcinoma. The proliferation, metastasis, and cloning ability of human lung cancer cells were inhibited, while the apoptosis of cells increased significantly after the depletion of Ttc39c. Our results based on the transcriptomics, proteomics, and metabolomics analyses indicated that Ttc39c might be involved in the progression of lung adenocarcinoma (LUAD) mainly through the metabolic pathway and the p53 pathway. CONCLUSION: To summarize, Ttc39c strongly regulates the proliferation and metastasis of lung adenocarcinoma cells. The main pathways involved in Ttc39c in lung adenocarcinoma include the energy metabolism and p53 pathways.

Interactions between host epithelial cells and Acinetobacter baumannii promote the emergence of highly antibiotic resistant and highly mucoid strains.

Acinetobacter baumannii is an important nosocomial pathogen. Upon colonizing a host, A. baumannii are subjected to selective pressure by immune defenses as they adapt to the host environment. However, the mechanism of this pathoadaptation is unknown. Here, we established an in vitro system to evolve A. baumannii driven by the continuous selective pressure exerted by epithelial cells, and we used a combination of experimental evolution, phenotypic characterization and multi-omics analysis to address the underlying mechanism. When continuously exposed to selective pressure by pulmonary epithelial cells, A. baumannii showed ptk mutation-mediated mucoid conversion (reduced adhesion and increased anti-phagocytic ability) by enhancement of capsular exopolysaccharide chain length; rsmG mutation-mediated deficiency of 7-methylguanosine modification in the 524th nucleotide of 16S rRNA, which increased ribosome translation efficiency; and rnaseI mutation-mediated changes in outer membrane permeability and efflux pump expression. Together, these mutations altered susceptibility to a variety of antimicrobial agents, including the novel antibiotic cefiderocol, by regulating siderophore and siderophore-receptor biosynthesis. In conclusion, pulmonary epithelial cells modulate A. baumannii pathoadaptation, implicating the host-microbe interaction in the survival and persistence of A. baumannii.

Perioperative Exhaled Nitric Oxide as an Indicator for Postoperative Pneumonia in Surgical Lung Cancer Patients: A Prospective Cohort Study Based on 183 Cases.

Introduction: This study is conducted to investigate the correlation between perioperative fractional exhaled nitric oxide and postoperative pneumonia (POP) and the feasibility of perioperative FeNO for predicting POP in surgical lung cancer patients. Methods: Patients who were diagnosed with non-small-cell lung cancer (NSCLC) were prospectively analyzed, and the relationship between perioperative FeNO and POP was evaluated based on patients' basic characteristics and clinical data in the hospital. Results: There were 218 patients enrolled in this study. Finally, 183 patients were involved in the study, with 19 of them in the POP group and 164 in the non-POP group. The POP group had significantly higher postoperative FeNO (median: 30.0 vs. 19.0 ppb, P < 0.001) as well as change in FeNO (median: 10.0 vs. 0.0 ppb, P < 0.001) before and after the surgery. For predicting POP based on the receiver operating characteristic (ROC) curve, a cutoff value of 25 ppb for postoperative FeNO (Youden's index: 0.515, sensitivity: 78.9%, and specificity: 72.6%) and 4 ppb for change in FeNO (Youden's index: 0.610, sensitivity: 84.2%, specificity: 76.8%) were selected. Furthermore, according to the bivariate regression analysis, FEV1/FVC (OR = 0.948, 95% CI: 0.899-0.999, P=0.048), POD1 FeNO (OR = 1.048, 95% CI: 1.019-1.077, P=0.001), and change in FeNO (OR = 1.087, 95% CI: 1.044-1.132, P < 0.001) were significantly associated with occurrence of POP. Conclusions: This prospective study revealed that a high postoperative FeNO (>25 ppb), as well as an increased change in FeNO (>4 ppb), may have the potential in detecting the occurrence of POP in surgical lung cancer patients.

Smartphones as an Ecological Niche of Microorganisms: Microbial Activities, Assembly, and Opportunistic Pathogens.

Smartphone usage and contact frequency are unprecedentedly high in this era, and they affect humans mentally and physically. However, the characteristics of the microorganisms associated with smartphones and smartphone hygiene habits remain unclear. In this study, using various culture-independent techniques, including high-throughput sequencing, real-time quantitative PCR (RT-qPCR), the ATP bioluminescence system, and electron microscopy, we investigated the structure, assembly, quantity, and dynamic metabolic activity of the bacterial community on smartphone surfaces and the user's dominant and nondominant hands. We found that smartphone microbiotas are more similar to the nondominant hand microbiotas than the dominant hand microbiotas and show significantly decreased phylogenetic diversity and stronger deterministic processes than the hand microbiota. Significant interindividual microbiota differences were observed, contributing to an average owner identification accuracy of 70.6% using smartphone microbiota. Furthermore, it is estimated that approximately 1.75 × 106 bacteria (2.24 × 104/cm2) exist on the touchscreen of a single smartphone, and microbial activities remain stable for at least 48 h. Scanning electron microscopy detected large fragments harboring microorganisms, suggesting that smartphone microbiotas live on the secreta or other substances, e.g., human cell debris and food debris. Fortunately, simple smartphone cleaning/hygiene could significantly reduce the bacterial load. Taken together, our results demonstrate that smartphone surfaces not only are a reservoir of microbes but also provide an ecological niche in which microbiotas, particularly opportunistic pathogens, can survive, be active, and even grow. IMPORTANCE Currently, people spend an average of 4.2 h per day on their smartphones. Due to the COVID-19 pandemic, this figure may still be increasing. The high frequency of smartphone usage may allow microbes, particularly pathogens, to attach to-and even survive on-phone surfaces, potentially causing adverse effects on humans. We employed various culture-independent techniques in this study to evaluate the microbiological features and hygiene of smartphones, including community assembly, bacterial load, and activity. Our data showed that deterministic processes drive smartphone microbiota assembly and that approximately 1.75 × 106 bacteria exist on a single smartphone touchscreen, with activities being stable for at least 48 h. Fortunately, simple smartphone cleaning/hygiene could significantly reduce the bacterial load. This work expands our understanding of the microbial ecology of smartphone surfaces and might facilitate the development of electronic device cleaning/hygiene guidelines to support public health.

Virgin coconut oil: A comprehensive review of antioxidant activity and mechanisms contributed by phenolic compounds.

Virgin coconut oil (VCO) is obtained by processing mature coconut cores with mechanical or natural methods. In recent years, VCO has been widely used in the food, pharmaceutical, and cosmetic industries because of its excellent functional activities. VCO has biological functions such as antioxidant, anti-inflammatory, antibacterial, and antiviral, and also has potential therapeutic effects on many chronic degenerative diseases. Among these functions, the antioxidant is the most basic and important function, which is mainly determined by phenolic compounds and medium-chain fatty acids (MCFAs). This review aims to elucidate the antioxidant functions of each phenolic compound in VCO, and discuss the antioxidant mechanisms of VCO in terms of the role of phenolic compounds with fat, intestinal microorganisms, and various organs. Besides, the composition of VCO and its application in various industries are summarized, and the biological functions of VCO are generalized, which should lay a foundation for further research on the antioxidant activity of VCO and provide a theoretical basis for the development of food additives with antioxidant activity.

Low level of complement factor H increases the risk of cancer-related death in patients with small-cell lung cancer.

INTRODUCTION: Pulmonary cancer is a kind of deeply invasive tumour which is difficult to treat, and its mortality rate is high. Previous research has shown that activation of complement could contribute to the progression of non-small-cell lung cancer (SCLC). However, little research has been done on SCLC. METHODS: Complement factor H (CFH), complements C3 as well as C4 were measured in patients, and the prognostic impact of different parameters was assessed by log-rank function analysis and Cox multifactor models. Besides, we constructed a predictive model based on complement fractions and validated the accuracy of the model. RESULTS: Among these 242 patients, 200 (82.6%) died. The median survival time was 18.3 months. We found by multifactorial analysis that high levels of CFH decreased the risk of death (HR 0.23, 95% CI 0.10 to 0.57, p<0.001), while elevated complement C4 displayed poor prognosis (HR 2.28, 95% CI 1.66 to 3.13, p<0.001). We screened variables by Cox models and constructed CFH-based prediction models to plot a nomogram by internal validation. The nomogram showed excellent accuracy in assessing the probability of death, yielding an adjusted C-statistics of 0.905. CONCLUSIONS: CFH can be recognised as a biomarker to predict the risk of death in SCLC. The prediction model established based on CFH, C3 and C4 levels has good accuracy in patients' prognostic assessment.

Early Patient-Reported Outcomes After Uniportal vs Multiportal Thoracoscopic Lobectomy.

BACKGROUND: Uniportal video-assisted thoracoscopic surgery (U-VATS) can achieve traditional clinical outcomes comparable to those of multiportal video-assisted thoracoscopic surgery (M-VATS). This study aimed to compare patient-reported outcomes between U-VATS and M-VATS for lung cancer lobectomy in the early postoperative period. METHODS: This comparative analysis used data from a longitudinal prospective study (Perioperative Symptom Study of Lung Cancer [CN-PRO-Lung 1]). Symptom severity, functional status, and quality of life were compared between groups using generalized estimation equation models. Symptom severity and functional status were reported as proportion of patients with clinically meaningful severe scores on 0- to 10-point scales assessed using the MD Anderson Symptom Inventory-Lung Cancer module. RESULTS: Of the 174 patients included, 102 (58.6%) underwent U-VATS lobectomy and 72 (41.4%) underwent M-VATS lobectomy. After adjusting for confounders, patients in the U-VATS group reported less severe pain (P = .02), fatigue (P = .001), constipation (P = .01), coughing (P = .003), shortness of breath (P < .001), and disturbed sleep (P = .007) during the 6-day postoperative hospitalization than did patients in the M-VATS group. Moreover, fewer patients reported severe impairment in walking (P = .033) or their capacity to enjoy life (P = .027) in the U-VATS group. Meanwhile, there were no significant between-group differences in the quality of life scores, operative time, chest tube duration, length of hospital stay, or early complication rate (grade II or higher) (all P > .05). CONCLUSIONS: U-VATS may produce fewer severe symptoms and better functional status than M-VATS for lung cancer lobectomy in the early postoperative period.

Toward improvements for enhancement the productivity and color value of Monascus pigments: a critical review with recent updates.

Monascus pigments are a kind of high-quality natural edible pigments fermented by Monascus filamentous fungi, which have been widely used in food, cosmetics, medicine, textiles, dyes and chemical industries as active functional ingredients. Moreover, Monascus pigments have a good application prospect because of a variety of biological functions such as antibacterial, antioxidation, anti-inflammatory, regulating cholesterol, and anti-cancer. However, the low productivity and color value of pigments restrict their development and application. In this review, we introduced the categories, structures, biosynthesis and functions of Monascus pigments, and summarized the current methods for improving the productivity and color value of pigments, including screening and mutagenesis of strains, optimization of fermentation conditions, immobilized fermentation, mixed fermentation, additives, gene knockout and overexpression technologies, which will help to develop the foundation for the industrial production of Monascus pigments.

Value of Peak Expiratory Flow Rate in Evaluating Cough Ability in Patients Undergoing Lung Surgery.

Introduction: Postoperative ineffective cough is easy to occur after thoracic surgery, and it is also a risk factor for postoperative pulmonary complications (PPCs). Objectives: To explore the value of peak expiratory flow rate (PEF) in evaluating cough ability in patients undergoing lung surgery and evaluate the effectiveness of chest wall compression during the expiratory phase by PEF. Methods: From September 2020 to May 2021, the researchers collected the data of patients who underwent lung surgery. Eventually, 153 patients who met the criteria were included, 102 cases were included in the effective cough group and 51 cases were included in the ineffective cough group. The receiver working curve (ROC curve) was used to analyze whether PEF could evaluate cough ability. At the same time, the researchers collected the pulmonary function data of the first 30 patients of the ineffective cough group while compressing the chest wall during the expiratory phase to evaluate the effectiveness of chest wall compression. Results: The area under the curve (AUC) of postoperative PEF to evaluate the postoperative cough ability was 0.955 (95% CI: 0.927-0.983, P < 0.001). The values of PEF (127.17 ± 34.72 L/min vs. 100.70 ± 29.98 L/min, P < 0.001, 95% CI: 18.34-34.59) and FEV1 (0.72 (0.68-0.97) L vs. 0.64 (0.56-0.82) L, P < 0.001) measured while compressing the chest wall were higher than those without compression. Conclusions: PEF can be used as a quantitative indicator of cough ability. Chest wall compression could improve cough ability for patients who have ineffective cough.

RSPH14 regulates the proliferation, cell cycle progression, and apoptosis of non-small cell lung cancer cells.

Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer, and it is characterized by a high incidence. It is important to understand the molecular mechanisms that determine the progression and metastasis of NSCLC in order to develop more effective therapies and identify novel diagnostic indicators of NSCLC. RSPH14 has been reported to be related to multiple human diseases, including duodenal adenocarcinoma and meningiomas, but the role of RSPH14 in NSCLC remains unclear. The present study aimed to investigate the molecular function and clinical significance of RSPH14 in NSCLC. Analyses of public datasets and clinical samples demonstrated that RSPH14 expression was upregulated in NSCLC samples compared with normal samples. In addition, high RSPH14 expression was associated with a shorter overall survival time in patients with NSCLC. Notably, RSPH14 knockdown suppressed the proliferation and cell cycle progression and enhanced the apoptosis of NSCLC cells. Mechanically, tandem mass tag analysis demonstrated that RSPH14 can affect multiple processes, including the AMPK signaling pathway, calcium ion import regulation, glucose transmembrane transporter activity, and glucose transmembrane transport. Taken together, the results of the present study suggest that RSPH14 may be a promising prognostic factor and therapeutic target for NSCLC.

Knockdown of GBAS regulates esophageal cancer cell viability and apoptosis.

Esophageal cancer (EC) is the sixth leading cause of cancer­related mortality worldwide, with the incidence gradually increasing each year. Therefore, further clarifying the mechanism underlying the development of EC may be beneficial for identifying novel biomarkers and targets for its treatment. The present study aimed to determine the functional roles of glioblastoma­amplified sequence (GBAS), a newly identified gene that has been reported to play crucial roles in multiple types of cancer, including in the malignant behavior of EC cells, such as cell viability, colony formation, cell apoptosis and cell cycle progression. The results of the present study revealed that, in vitro, the knockdown of GBAS significantly suppressed cell viability and colony formation in TE­1 and KYSE­150 cell lines, using a Celigo cell count analysis and colony formation assay respectively, whereas the apoptotic rate of EC cells was significantly increased by the knockdown of GBAS using Annexin V APC staining. Furthermore, following GBAS knockdown, the cell cycle progression of TE­1 and KYSE­150 cells was arrested in the G1 phase using PI staining. In conclusion, the findings of the present study suggested that GBAS may serve a role in EC by regulating cell viability, apoptosis and cell cycle progression.

MiR-326 mediates malignant biological behaviors of lung adenocarcinoma by targeting ZEB1.

MiR-326 functions as an antioncogene in the several types of cancer. However, the underling mechanisms through which miRNA-326 regulates the anti-carcinogenesis of lung adenocarcinoma have remained elusive. The aim of this study was to explore the role and regulatory mechanism of miR-326 in cell proliferation, invasion, migration and apoptosis in lung adenocarcinoma. Quantitative real-time PCR (qRT-PCR) was used to detect the expression pattern of miR-326 in human bronchial epithelial cells (HBES-2B), 4 kinds of lung adenocarcinoma cell lines (H23, H1975, H2228, H2085) and 20 lung adenocarcinoma tissues. Then, H23 cells were infected with miR-326 mimics, miR-326 inhibitors and si-ZEB1 to build up-regulated miR-326 cell lines, down-regulated ZEB1(zinc-finger-enhancer binding protein 1)cell lines, simultaneous down-regulated ZEB1 and miR-326 cell lines. Moreover, CCK-8 assay, transwell invasion assay, wound healing assay and flow cytometry assay were employed to examine the effects of miR-326 and ZEB1 on the proliferation, invasion, migration and apoptosis abilities of H23 cells. Western blot was performed to explore the effects of miR-326 and ZEB1 on the expression of invasion and migration related proteins N-cadherin, E-cadherin, MMP7, MMP13, SLUG and apoptotic proteins PARP, BAX. On the mechanism, a dual-luciferase reporter gene was used to measure the target relationship between miR-326 and ZEB1. MiR-326 expression was significantly downregulated in lung adenocarcinoma tissues and cells. Overexpression of miR-326 significantly inhibited the malignant behaviors of H23 cells. Mechanically, luciferase reporter assay showed that ZEB1 was a direct target of miR-326. MiR-326 mimic downregulated the expression of ZEB1. Furthermore, knocking down ZEB1 strongly inhibited the proliferation, invasion and migration of H23 cells but promoted apoptosis. MiR-326 could target ZEB1 to inhibit the proliferation, invasion and migration of lung adenocarcinoma cells and promote apoptosis, which is a potential therapeutic target for lung adenocarcinoma.