Circular RNA COL1A1 promotes Warburg effect and tumor growth in nasopharyngeal carcinoma.

OBJECTIVE: Circular RNAs (circRNAs), pivotal in the pathogenesis and progression of nasopharyngeal carcinoma (NPC), remain a significant point of investigation for potential therapeutic interventions. Our research was driven by the objective to decipher the roles and underlying mechanisms of hsa_circ_0044569 (circCOL1A1) in governing the malignant phenotypes and the Warburg effect in NPC. METHODS: We systematically collected samples from NPC tissues and normal nasopharyngeal epithelial counterparts. The expression levels of circCOL1A1, microRNA-370-5p (miR-370-5p), and prothymosin alpha (PTMA) were quantitatively determined using quantitative polymerase chain reaction (qPCR) and Western blotting. Transfections in NPC cell lines were conducted using small interfering RNAs (siRNAs) or vectors carrying the pcDNA 3.1 construct for overexpression studies. We interrogated the circCOL1A1/miR-370-5p/PTMA axis's role in cellular functions through a series of assays: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide for cell viability, colony formation for growth, Transwell assays for migration and invasion, and Western blotting for protein expression profiling. To elucidate the molecular interactions, we employed luciferase reporter assays and RNA immunoprecipitation techniques. RESULTS: Our investigations revealed that circCOL1A1 was a stable circRNA, highly expressed in both NPC tissues and derived cell lines. A correlation analysis with clinical pathological features demonstrated a significant association between circCOL1A1 expression, lymph node metastasis, and the tumor node metastasis staging system of NPC. Functionally, silencing circCOL1A1 led to substantial suppression of cell proliferation, migration, invasion, and metabolic alterations characteristic of the Warburg effect in NPC cells. At the molecular level, circCOL1A1 appeared to modulate PTMA expression by acting as a competitive endogenous RNA or 'sponge' for miR-370-5p, which in turn promoted the malignant characteristics of NPC cells. CONCLUSION: To conclude, our findings delineate that circCOL1A1 exerts its oncogenic influence in NPC through the modulation of the miR-370-5p/PTMA signaling axis.

Differential Circulating Fungal Microbiome in Prostate Cancer Patients Compared to Healthy Control Individuals.

BACKGROUNDS: Infection and inflammation play an important role in prostate cancer (PCa) etiology and pathogenesis. However, the environmental drivers for PCa are not fully understood. METHODS: In a cross-sectional study, we analyzed circulating fungal microbiome in plasma samples from age and race-matched healthy control men (n = 34) and preoperative PCa patients (n = 31). RESULTS: The fungal community in the plasma exhibited differences between individuals with PCa and healthy controls according to the beta diversity; there was no difference in the alpha diversity. Moreover, the relative abundance of several fungi differed between the two study groups from the class to species levels. The most significant differences were Filobasidiales family, Pyronemataceae family, and Cryptococcus ater species, which were enriched in PCa patients compared to controls. The increased Bipolaris genus was associated with low prostate-specific antigen (PSA) levels, increased Sordariomycetes class was associated with severe pathological stage, and decreased Phoma herbarum species was associated with disease relapse, compared to corresponding controls. Several fungi from class to species levels were increased in the controls compared to patients. CONCLUSION: This is the first study to show plasma distinct fungal microbiome and its associations with PSA levels, relapse, and pathology stages in PCa patients.

Chronic cannabis smoking-enriched oral pathobiont drives behavioral changes, macrophage infiltration, and increases ß-amyloid protein production in the brain.

BACKGROUND: Little is known about chronic cannabis smoking-associated oral microbiome and its effects on central nervous system (CNS) functions. METHODS: In the current study, we have analyzed the saliva microbiome in individuals who chronically smoked cannabis with cannabis use disorder (n = 16) and in non-smoking controls (n = 27). The saliva microbiome was analyzed using microbial 16S rRNA sequencing. To investigate the function of cannabis use-associated oral microbiome, mice were orally inoculated with live Actinomyces meyeri, Actinomyces odontolyticus, or Neisseria elongata twice per week for six months, which mimicked human conditions. FINDINGS: We found that cannabis smoking in humans was associated with oral microbial dysbiosis. The most increased oral bacteria were Streptococcus and Actinomyces genus and the most decreased bacteria were Neisseria genus in chronic cannabis smokers compared to those in non-smokers. Among the distinct species bacteria in cannabis smokers, the enrichment of Actinomyces meyeri was inversely associated with the age of first cannabis smoking. Strikingly, oral exposure of Actinomyces meyeri, an oral pathobiont, but not the other two control bacteria, decreased global activity, increased macrophage infiltration, and increased ß-amyloid 42 protein production in the mouse brains. INTERPRETATION: This is the first study to reveal that long-term oral cannabis exposure is associated oral enrichment of Actinomyces meyeri and its contributions to CNS abnormalities.

Treatment of oil-based drilling cuttings using the demulsification separation-Fenton oxidation method.

In this study, demulsification separation-Fenton oxidation technology was employed as a combined technology to treat total petroleum hydrocarbons (TPH) in oil-based drill cuttings (OBDC). Batch experiments were carried out to optimize the technology parameter. Under the optimal condition, 70% and 51% TPH removal rate was obtained for demulsification technology and Fenton oxidation technology, respectively. Eighty-five percent of TPH removal rate was obtained using combination technology of demulsification separation and Fenton oxidation. Multiple characterizations were used to analyze the physical and chemical properties of treated OBDC. The result of XRD pattern indicated the combination technology had no obvious effect for structure phase of OBDC. The results of FTIR, GC-MS, TG-DTG and SEM were used to characterize the treated OBDC. This paper provides an efficient and feasible combined technology for OBDC treatment, which expands a new strategy for the removal of TPH from solid waste.

Molecular-level variation of dissolved organic matter and microbial structure of produced water during its early storage in Fuling shale gas field, China.

Shale gas-produced water (PW), the waste fluid generated during gas production, contains a large number of organic contaminants and high salinity matrix. Previous studies generally focused on the end-of-pipe treatment of the PW and ignored the early collection process. In this study, the transformation of the molecular composition and microbial community structure of the PW in the transportation and storage process (i.e., from the gas-liquid separator to the storage tank) were investigated. As the PW was transported from the gas-liquid separator to the portable storage tank, the dissolved organic matter (DOM) showed greater saturation, less oxidation, and lower polarity. DOMs with high O/C and low H/C ratios (numbers of oxygen and hydrogen divided by numbers of carbon) were eliminated, which may be due to precipitation or adsorption by the solids suspended in the PW. The values of double-bond equivalent (DBE), DBE/C (DBE divided by the number of carbon), and aromatic index (AI) decreased, likely because of the microbial degradation of aromatic compounds. The PW in the gas-liquid separator presented a lower biodiversity than that in the storage tank. The microbial community in the storage tank showed the coexistence of anaerobes and aerobes. Genera related to biocorrosion and souring were detected in the two facilities, thus indicating the necessity of more efficient anticorrosion strategies. This study helps to enhance the understanding of the environmental behavior of PW during shale gas collection and provides a scientific reference for the design and formulation of efficient transportation and storage strategies to prevent and control the environmental risk of shale gas-derived PW.

3nLcn2, a teleost lipocalin 2 that possesses antimicrobial activity and inhibits bacterial infection in triploid crucian carp.

Lipocalin 2 (Lcn2) has been identified in mammals, however, the in vivo function of fish Lcn2 is essentially unknown. Triploid crucian carp (3n = 150) of red crucian carp (female, 2n = 100) and allotetraploid (male, 4n = 200) shows better resistance to pathogenic infections. To elucidate the antimicrobial mechanism of triploid crucian carp, we examined the function of a novel Lcn2 from triploid crucian carp (3nLcn2). 3nLcn2 is 183 residues in length and contains a conserved lipocalin domain. Quantitative real time reverse transcription PCR (qRT-PCR) analysis showed that 3nLcn2 expression occurred in multiple tissues and was upregulated by bacterial infection in a time-dependent manner. We found that purified recombinant 3nLcn2 (r3nLcn2) exerted bactericidal activity to Aeromonas hydrophila and Escherichia coli. qRT-PCR detected increased expression of pro-inflammatory cytokines and tight junctions in fish with 3nLcn2 overexpression. Fish administered with 3nLcn2 exhibited enhanced intestinal barrier and resistance against bacterial infection. These results provide the first evidence that 3nLcn2 is a functional lipocalin with antimicrobial activity and plays a positive role in the immune defense during bacterial infection.

Progesterone decreases gut permeability through upregulating occludin expression in primary human gut tissues and Caco-2 cells.

Progesterone plays a protective role in preventing inflammation and preterm delivery during pregnancy. However, the mechanism involved is unknown. Microbial product translocation from a permeable mucosa is demonstrated as a driver of inflammation. To study the mechanism of the protective role of progesterone during pregnancy, we investigated the effect of physiologic concentrations of progesterone on tight junction protein occludin expression and human gut permeability in vitro and systemic microbial translocation in pregnant women in vivo. Plasma bacterial lipopolysaccharide (LPS), a representative marker of in vivo systemic microbial translocation was measured. We found that plasma LPS levels were significantly decreased during 24 to 28 weeks of gestation compared to 8 to 12 weeks of gestation. Moreover, plasma LPS levels were negatively correlated with plasma progesterone levels but positively correlated with plasma tumor necrosis factor-alpha (TNF-α) levels at 8 to 12 weeks of gestation but not at 24 to 28 weeks of gestation. Progesterone treatment increased intestinal trans-epithelial electrical resistance (TEER) in primary human colon tissues and Caco-2 cells in vitro through upregulating tight junction protein occludin expression. Furthermore, progesterone exhibited an inhibitory effect on nuclear factor kappa B (NF-κB) activation following LPS stimulation in Caco-2 cells. These results reveal a novel mechanism that progesterone may play an important role in decreasing mucosal permeability, systemic microbial translocation, and inflammation during pregnancy.

Systemic translocation of Staphylococcus drives autoantibody production in HIV disease.

BACKGROUND: Increased autoreactive antibodies have been reported in HIV disease; however, the mechanism accounting for autoantibody induction in HIV remains unknown. RESULTS: Herein, we show that seasonal influenza vaccination induces autoantibody production (e.g., IgG anti-nuclear antibody (ANA) and anti-double-stranded DNA antibody (anti-dsDNA)) in some viral-suppressed antiretroviral therapy (ART)-treated HIV+ subjects, but not in healthy controls. These autoantibodies were not derived from antigen-specific B cells but from activated "bystander" B cells analyzed by single-cell assay and by study of purified polyclonal ANAs from plasma. To explore the mechanism of autoantibody generation in HIV+ subjects, plasma level of microbial products, gene expression profile of B cells, and B cell receptor (BCR) repertoires were analyzed. We found that autoantibody production was associated with increased plasma level of microbial translocation; the patients with high autoantibodies had skewed B cell repertoires and upregulation of genes related to innate immune activation in response to microbial translocation. By analyzing circulating microbial 16S rDNA in plasma, the relative abundance of Staphylococcus was found to be associated with autoantibody production in HIV+ subjects. Finally, we found that injection of heat-killed Staphylococcus aureus promoted germinal center B cell responses and autoantibody production in mice, consistent with the notion that autoantibody production in HIV+ patients is triggered by microbial products. CONCLUSIONS: Our results showed that translocation of Staphylococcus can promote B cell activation through enhancing germinal center response and induces autoantibody production. It uncovers a potential mechanism linking microbial translocation and autoimmunity in HIV+ disease and provides a strong rationale for targeting Staphylococcus to prevent autoantibody production.

Increased Preoperative Plasma Level of Microbial 16S rDNA Translocation Is Associated With Relapse After Prostatectomy in Prostate Cancer Patients.

Background: The environmental factors for promoting prostate cancer (PCa) recurrence remain unknown. Methods: A retrospective cross-sectional study was conducted in healthy men (n = 12) and PCa patients undergoing prostatectomy (n = 27). Plasma preoperative level of total cell-free bacterial 16S rDNA, a marker of microbial translocation, was evaluated by qPCR. Plasma levels of prostate-specific antigen (PSA) were evaluated by ELISA. Results: Similar degrees of microbial translocation were found in healthy men and patients. However, the levels of microbial 16S rDNA were increased in patients with cancer relapse (n = 10) compared to patients without relapse (n = 17) after prostatectomy. Furthermore, the levels of microbial 16S rDNA were marginally increased in patients with pT3 or pT4 tumors compared to those with pT 2 or less. The levels of microbial 16S rDNA tended to increase in patients with higher pathologic tumor stage, Gleason score, and margin and lymph node involvements; but these differences did not reach significance. Conclusion: The plasma 16S rDNA levels increased in patients with PCa who have biochemical recurrence and 16S rDNA levels were higher in patients with higher-grade PCa.

Elevated systemic microbial translocation in pregnant HIV-infected women compared to HIV-uninfected women, and its inverse correlations with plasma progesterone levels.

In HIV infection, increased adverse perinatal outcomes reported among HIV-associated pregnancies are not fully understood. Currently, microbial product translocation (MT) from a permeable mucosa is demonstrated as a driver of inflammation, and may contribute to preterm delivery in HIV. Here, our results showed that plasma LPS levels (a representative marker of MT) were increased in HIV-infected women in the first and second trimester. Progesterone levels were significantly decreased in HIV-infected subjects in the first trimester and second trimester. There were significant inverse correlations between plasma LPS and progesterone in the first and second trimester. These results suggested heightened systemic MT and decreased plasma progesterone levels in HIV-infected pregnant women may play a role in increased incidence of preterm delivery.

Overexpression of geranylgeranyl diphosphate synthase contributes to tumour metastasis and correlates with poor prognosis of lung adenocarcinoma.

This study aimed to evaluate the biological role of geranylgeranyl diphosphate synthase (GGPPS) in the progression of lung adenocarcinoma. GGPPS expression was detected in lung adenocarcinoma tissues by qRT-PCR, tissue microarray (TMA) and western blotting. The relationships between GGPPS expression and the clinicopathological characteristics and prognosis of lung adenocarcinoma patients were assessed. GGPPS was down-regulated in SPCA-1, PC9 and A549 cells using siRNA and up-regulated in A549 cells using an adenoviral vector. The biological roles of GGPPS in cell proliferation, apoptosis, migration and invasion were determined by MTT and colony formation assays, flow cytometry, and transwell and wound-healing assays, respectively. In addition, the regulatory roles of GGPPS on the expression of several epithelial-mesenchymal transition (EMT) markers were determined. Furthermore, the Rac1/Cdc42 prenylation was detected after knockdown of GGPPS in SPCA-1 and PC9 cells. GGPPS expression was significantly increased in lung adenocarcinoma tissues compared to that in adjacent normal tissues. Overexpression of GGPPS was correlated with large tumours, high TNM stage, lymph node metastasis and poor prognosis in patients. Knockdown of GGPPS inhibited the migration and invasion of lung adenocarcinoma cells, but did not affect cell proliferation and apoptosis. Meanwhile, GGPPS inhibition significantly increased the expression of E-cadherin and reduced the expression of N-cadherin and vimentin in lung adenocarcinoma cells. In addition, the Rac1/Cdc42 geranylgeranylation was reduced by GGPPS knockdown. Overexpression of GGPPS correlates with poor prognosis of lung adenocarcinoma and contributes to metastasis through regulating EMT.

Increased systemic microbial translocation is associated with depression during early pregnancy.

Plasma level of microbial translocation is a marker of mucosal permeability. Increased mucosal permeability ignites elevated microbial translocation and as a consequence of systemic inflammation. Pregnant women with depression have higher levels of inflammatory markers relative to pregnant women without depression, however, no studies have reported whether systemic microbial translocation will change in depressed women during pregnancy. In this study, we examined the plasma LPS level of depressed women during pregnancy. The results showed that the plasma LPS level was significantly increased in depressed mothers during their 8-12 weeks gestation compared to healthy controls. Compared to 8-12 weeks gestation, the plasma LPS levels were significantly decreased at 24-28 weeks gestation and 6-8 weeks postpartum in both depressed subjects and healthy controls. Furthermore, the plasma levels of pro-inflammatory cytokines (TNF-α and MCP/CCL2) associated with microbial translocation were significantly increased in depressed subjects during 8-12 weeks gestation compared to healthy controls. These results indicate that the level of microbial translocation is increased in depressed women during early pregnancy.

Prospective Study of Stereotactic Body Radiation Therapy for Thymoma and Thymic Carcinoma: Therapeutic Effect and Toxicity Assessment.

Stereotactic body radiation therapy (SBRT) is an important modality in treatment of tumors. We hypothesized that SBRT can achieve excellent local control with limited toxicity in patients with thymic tumors. A single-institution prospective study was performed with 32 patients who underwent SBRT of thymoma and thymic carcinoma between 2005 and 2014. Thirty-two patients including 39 target lesions were analyses in this study. Almost half of the patients (46.9%) were type C by histopathology and more than half (56.3%) were classified into stage IVA or IVB. The median dose of SBRT for gross tumor volume (GTV) was 56 Gy (range 49-70 Gy). Results showed that the response rate was 96.9% after SBRT and the median tumor shrinkage rate was 62.2% (range 3.8-100%). For the patients with both stage II-III and type A-B (n = 6), the median PFS was 28 months. In-field failure was only observed in 4 patients, and outside-field failure was seen in 2 patients. The local control rate was 81.25%. Patients treated with SBRT had an excellent local control with mild toxicities, which suggests that SBRT is feasible for the patients with thymic tumors who are unable to undergo either surgery or conventionally fractionated radiation therapy.

The effect of plasma auto-IgGs on CD4+ T cell apoptosis and recovery in HIV-infected patients under antiretroviral therapy.

Although effective antiretroviral therapy (ART) suppresses HIV viral replication, prevents AIDS-related complications, and prolongs life, a proportion of patients fails to restore the patients' CD4+ T cell number to the level of healthy individuals. Increased mortality and morbidity have been observed in these patients. In the current study, we have investigated the role of auto-IgGs in CD4+ T cell apoptosis and recovery in a cross-sectional study. All HIV+ subjects were on viral-suppressive ART treatment with a different degree of CD4+ T cell reconstitution. Total auto-IgG binding on CD4+ T cell surfaces and its associated apoptosis and CD4+ T cell recovery were analyzed by flow cytometry ex vivo. Total IgGs from plasma were tested for their binding capacities to CD4+ T cell surfaces and their mediation to CD4+ T cell death through NK cell cytotoxicity in vitro. HIV+ subjects had increased surface binding of auto-IgGs on CD4+ T cells compared with healthy controls, and IgG binding was associated with elevated CD4+ T cell apoptosis in HIV+ subjects but not in healthy controls. Plasma IgGs from HIV+ subjects bound to CD4+ T cells and induced cell apoptosis through NK cytotoxicity in vitro. Soluble CD4 (sCD4) preincubation prevented NK cell-mediated CD4+ T cell death. Our results suggest that plasma autoantibodies may play a role in some HIV+ patients with poor CD4+ T cell recovery under viral-suppressive ART.

Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues.

Females have a higher prevalence of most autoimmune diseases; however, the mechanism is unknown. In this study, we examined the expression of tight junction protein zonula occludens 1 (ZO-1) and estrogen receptor (ER)-α/ß in human primary gut tissues by immunohistochemistry, immunofluorescence and qPCR. The expression of ZO-1 and ER-ß but not ER-α was present in both male and female gut tissues. There was no sex difference in ER-ß expression, but ZO-1 expression was decreased in females compared to males. In vitro, estrogen treatment decreased ZO-1 mRNA and protein expression, ZO-1 promoter activity, IL-6 production, and NF-κB activation in human primary gut tissues or the Caco-2 cells, but increased the ER-ß expression in Caco-2 cells. Consistently, plasma IL-6 levels in females were reduced relative to males in vivo. Our finding indicates that estrogen may play a role in gut tight junction expression and permeability.

Protein regulator of cytokinesis-1 expression: prognostic value in lung squamous cell carcinoma patients.

BACKGROUND: Protein regulator of cytokinesis-1 (PRC1) has been shown to participate in the completion of cytokinesis, and it is dysregulated in cancer processes. However, its relevance in lung squamous cell carcinoma (SCC) remained largely unknown. We aimed to study the expression pattern of PRC1 and assess its clinical significance in lung SCC. METHODS: PRC1 protein expression in human lung SCC and adjacent normal lung tissues was detected by immunohistochemistry. PRC1 expression was assessed in association with clinicopathological features and clinical outcomes of lung SCC patients. RESULTS: In lung SCC tissues, PRC1 protein expression was significantly higher than those in paired normal lung tissues. The lung SCC patients with PRC1 overexpression had an advanced pathological stage (TNM stage), positive lymph node metastasis, and a shorter overall survival (OS) time more frequently than patients with low PRC1 expression. Additional, PRC1 expression was also shown to be poor as a prognostic factor for OS in patients with lung SCC. CONCLUSIONS: Our study indicated that aberrant expression of PRC1 may point to biochemical recurrence in lung SCC. This highlights its potential as a valuable prognostic marker for lung SCC.

PRC1 contributes to tumorigenesis of lung adenocarcinoma in association with the Wnt/ß-catenin signaling pathway.

BACKGROUND: Protein regulator of cytokinesis-1 (PRC1) belongs to the microtubule-associated proteins (MAPs) family, and is involved in cytokinesis. Recent investigations suggest PRC1 involvement in human carcinogenesis, including breast carcinoma, hepatocellular carcinoma and etc. However, whether PRC1 contributes to lung adenocarcinoma tumorigenesis remains unknown. METHODS: Quantitative reverse-transcription polymerase chain reaction (qRT-PCR), Western blotting and Immunohistochemical staining (IHC) were used to evaluate and contrast the PRC1 expression profile in lung adenocarcinoma and adjacent normal lung tissues. We examined the clinical use of PRC1 in lung adenocarcinoma prognosis. Additionally, the tumorigenesis impact of PRC1 in lung adenocarcinoma cells was verified via in vitro and in vivo metastasis and tumorigenesis assays. Notably, Next Generation Sequencing (NGS) was performed to investigate the molecular mechanism underlying the oncogenic role of PRC1 in lung adenocarcinoma. RESULTS: PRC1 mRNA and protein expressions were upregulated in lung adenocarcinoma tissues compared to adjacent normal lung tissues. PRC1 protein overexpression correlated with lymph node metastasis and was an independent poor prognostic factor for lung adenocarcinoma patients. Our data implied that PRC1 depletion limited the proliferation and invasion of lung adenocarcinoma cells in vitro and lowered tumor development and lung metastasis in vivo. Remarkably, limiting PRC1 substantially prompted G2/M phase cell cycle arrest and apoptosis. Mechanistically, by conducting NGS on PRC1-depleted A549 cells and control cells, we discovered that PRC1 expression was significantly correlated with the Wnt signaling pathway. CONCLUSIONS: This investigation offers confirmation that PRC1 is a prognostic and promising therapeutic biomarker for people with lung adenocarcinoma and takes on a key part in the activation of the Wnt/ß-catenin pathway in lung adenocarcinoma development.

Comparison between endobronchial ultrasound-guided transbronchial biopsy and CT-guided transthoracic lung biopsy for the diagnosis of peripheral lung cancer: a systematic review and meta-analysis.

BACKGROUND: With the release of the National Lung Screening Trial results, the detection of peripheral pulmonary lesions (PPLs) is likely to increase. Computed tomography (CT)-guided percutaneous transthoracic needle biopsy (PTNB) and radial probe endobronchial ultrasound (r-EBUS)-guided transbronchial lung biopsy (TBLB) are recommended for tissue diagnosis of PPLs. METHODS: A systematic review of published literature evaluating the accuracy of r-EBUS-TBLB and CT-PTNB for the diagnosis of PPLs was performed to determine point sensitivity and specificity, and to construct a summary receiver-operating characteristic curve. RESULTS: This review included 31 publications dealing with EBUS-TBLB and 14 publications dealing with CT-PTNB for the diagnosis of PPLs. EBUS-TBLB had point sensitivity of 0.69 (95% CI: 0.67-0.71) for the diagnosis of peripheral lung cancer (PLC), which was lower than the sensitivity of CT-PTNB (0.94, 95% CI: 0.94-0.95). However, the complication rates observed with EBUS-TBLB were lower than those reported for CT-PTNB. CONCLUSIONS: This meta-analysis showed that EBUS-TBLB is a safe and relatively accurate tool in the investigation of PLC. Although the yield remains lower than that of CT-PTNB, the procedural risks are lower.

The imaging of small pulmonary nodules.

Lung cancer is the leading cause of cancer death worldwide. The major goal in lung cancer research is the improvement of long-term survival. Pulmonary nodules have high clinical importance, they may not only prove to be an early manifestation of lung cancer, but decide to choose the right therapy. This review will introduce the development and current situation of several imaging examination methods: computed tomography (CT), positron emission tomography/computed tomography (PET/CT), endobronchial ultrasound (EBUS).

NCAPG2 promotes tumour proliferation by regulating G2/M phase and associates with poor prognosis in lung adenocarcinoma.

NCAPG2 is a component of the condensin II complex and contributes to chromosome segregation via microtubule-kinetochore attachment during mitosis. It is well known that NCAPG2 plays a critical role in cell mitosis; however, the role of altered NCAPG2 expression and its transcriptional regulatory function in cancer development remains mostly unknown. Here, for the first time we reported that NCAPG2 was evidently increased in non-small cell lung cancer tissues compared to adjacent normal lung tissues. Clinicopathological data analysis showed that NCAPG2 overexpression was significantly correlated with lymph node metastasis and pathologic-Tumour Nodes Metastasen stages, and was an independent prognostic factor in lung adenocarcinoma patients. Moreover, siRNA-mediated knockdown of NCAPG2 could inhibit tumour cell growth of lung adenocarcinoma cells (A549 and H1299) in vitro and could significantly lead to cell cycle arrest in the G2 phase. Furthermore, we found that NCAPG2 silencing significantly decreased the expression levels of G2/M phase cell cycle-related protein expressions (Cyclin B1, Cdc2) and increased the expression levels of p27 and p21 through Western blot analysis. Taken together, we demonstrated that increased NCAPG2 expression could regulate cell proliferation and identified as a poor prognostic biomarker in lung adenocarcinoma.