جستجوی مقالات مرتبط با کلیدواژه « non-small cell lung cancer » در نشریات گروه « پزشکی »

To investigate the risk factors of Programmed Cell Death Protein 1 (PD-1), Programmed Cell Death Ligand 1(PD-L1) inhibitor associated acute kidney injury (AKI) in patients with primary non-small cell lung cancer (NSCLC) and construct a predictive model.

120 NSCLC patients were selected as the research subjects and their clinical data were collected. Patients were divided into AKI and Non-AKI (N-AKI) group based on the development of AKI. Exploring the risk factors of PD-1P/D-L1 inhibitor related AKI in NSCLC patients using multivariate logistic regression analysis and visualized the logistic regression analysis to obtain a nomogram model. Meanwhile, evaluate the predictive value of the model.

The results of multivariate analysis showed that the presence of extrarenal immune related adverse reactions (irAEs) is a risk factor for PD-1/PD-L1 inhibitor related AKI in NSCLC patients; At the same time, the risk of developing PD-1/PD-L1 inhibitor related AKI in NSCLC patients increases with increasing serum creatinine (SCr) and C-reactive protein (CRP) levels, decreasing baseline estimated glomerular filtration rate (eGFR) levels (P < .05). The analysis results of receiver operator characteristic curve (ROC), calibration curve, and decision curve show that the model has good discrimination and accuracy, and can achieve a high clinical benefit rate.

Primary NSCLC patients with extrarenal irAEs, high levels of SCr and CRP, and low levels of eGFR have a higher risk of AKI after PD-1/PD-L1 inhibitor treatment. Establishing a predictive model with high accuracy is more conducive to early detection of high-risk patients.

The To measure regulatory T cells (Tregs) expression in driver-gene-negative advanced non-small cell lung cancer (NSCLC) as well as its effect on the therapeutic efficacy and prognosis of immune checkpoint inhibitors (ICIs).

Fifty patients with advanced non-small cell lung cancer without driving genes who were receiving treatment with a monoclonal antibody targeting the programmed death receptor-1 (PD-1) made up the study group. 30 healthy subjects in the same period were chosen into the control group. Flow cytometry was used to identify CD4highCD25+Foxp3+Treg cells in peripheral blood of all participants. Relation between CD4highCD25+Foxp3+Treg cells and tumor markers were explored, and efficacy and prognosis in patients before and after therapy was analyzed.

The fraction of CD4highCD25+Foxp3+Treg cells in the study group was higher (P<0.05). Following three rounds of PD-1 monoclonal antibody treatment, patients' CD4highCD25+Foxp3+Treg cells proportion was lower than before treatment (P<0.01), and showed a positive correlation with tumor markers (P<0.05). The fraction of CD4highCD25+Foxp3+Treg cells in the CR+PR group decreased in both the second and third cycles after treatment compared to the SD+PD group (P<0.01), but no change was found before or during the first cycle (P>0.05). CD4highCD25+Foxp3+Treg cells proportion in the death group presented higher relative to the survival group (P<0.05). CD4highCD25+Foxp3+Treg cells predicted the area under the ROC curve was 0.8134, with significant difference (P<0.05).

CD4highCD25+Foxp3+Treg cells proportion in peripheral blood of NSCLC patients shows increased, and has predictive value for therapeutic efficacy of ICIs and prognosis of driver-gene-negative advanced NSCLC patients.

 Non-small cell lung cancer (NSCLC) patients with COVID-19 have an excessive chance of morbidity and mortality. The fecal-nasopharyngeal microbiota compositions of NSCLC patients were assessed in this study.

 In total, 234 samples were collected from 17 NSCLC patients infected with COVID-19, 20 NSCLC patients without confirmed COVID-19, 40 non NSCLC patients with COVID-19, and 40 healthy individuals.

 In lung microbiota, the abundance of Streptococcus spp. in NSCLC patients with confirmed COVID-19 was significantly higher than the two control groups. Pseudomonas aeruginosa and Staphylococcus aureus were listed as the most frequent pulmonary bacterial groups that colonized COVID-19 patients. In fecal specimens, the numbers of Bacteroidetes, Firmicutes, and Actinobacteria phyla were significantly higher amongst NSCLC patients with COVID-19. NSCLC patients infected with COVID-19 showed lower levels of Lactobacillus spp., Akkermansia muciniphila, and Bifidobacterium spp. The counts of Streptococcus spp., in NSCLC patients with COVID-19 were significantly higher than those of healthy individuals (8.49±0.70 log CFU/g wet feces vs 8.49±0.70 log CFU/g wet feces). Prevotella spp. were enriched in the gut and respiratory tracts of COVID-19 patient groups. The unbiased analysis showed an increment in Enterococcus spp., Streptococcus spp., and Prevotella spp.

 Eventually, it was found that compared to control groups, COVID-19 patients with NSCLC showed diminished gut bacteria diversity and increase in Lactobacillus spp., A. muciniphila, and Bifidobacterium spp. The overgrowth of Enterococcus spp., Streptococcus spp., and Prevotella spp. could be potential predictive biomarkers in the gut-lung axis of NSCLC patients with COVID-19.

Non-small cell lung cancer (NSCLC) stands as a prominent contributor to cancer-related fatalities on aglobal scale, necessitating the search for novel therapeutic agents. SP-8356, a derivative of (1S)-(–)-verbenone, hasshown promise as an anticancer agent in preclinical studies. However, specific mechanisms underlying its effects inNSCLC remain to be elucidated. The aim of this research was to explore the in vitro anti-NSCLC effects of SP-8356,elucidate its mechanisms of action, and assess its efficacy in inhibiting tumor formation in a murine model. In this experimental study, NSCLC cell lines were treated with various concentrations of SP-8356. Cell viability and proliferation were assessed using MTT and colony formation assays, respectively. Cell cycledistribution was analyzed by flow cytometry, and apoptosis was evaluated by determining apoptotic protein expression.Western blot analysis was conducted to assess protein expression levels of the both p53 and MDM2. Additionally, weevaluated efficacy of the SP-8356 in inhibiting tumor formation of the nude mouse model. SP-8356 demonstrated a concentration-dependent inhibition of cell proliferation in the NSCLC cell lines. Flowcytometric analysis showed that SP-8356 led to cell cycle arrest at the G2/M phase, indicating its potential influenceon regulating the cell cycle. SP-8356 treatment was associated with the downregulation of CDK1 and Cyclin B1.Additionally, SP-8356 significantly enhanced apoptosis in NSCLC cells. SP-8356 treatment was associated with thedownregulation of Bcl-2, while Bax expression was upregulated. Mechanistically, SP-8356 led to accumulation of thep53 protein levels within the NSCLC cells. This accumulation was mediated through inhibition of its negative regulator,MDM2. Using a nude mouse model demonstrated that SP-8356 effectively inhibited tumor formation in vivo. Our findings shed light on the molecular mechanisms underlying anticancer activity of SP-8356 andhighlight its potential as a promising therapeutic candidate for NSCLC treatment.

DDR1 signaling plays a critical role in various cellular functions. Increased DDR1 expression has been shown in different human cancers.t-DARPP is a truncated isoform of DARPP-32, and its upregulation promotes cell survival and migration. Most lung cancer patients have NSCLC, and their survival rate is low. Therefore, it is necessary to study new and effective targeted therapies. Increased t-DARPP expression in NSCLC patients is associated with patient survival and can act as a prognostic marker correlated with increasing stages of NSCLC. The current study aimed to evaluate alteration in DDR1 expression and its effects on t-DARPP expression in NSCLC.

Two human lung adenocarcinoma cell lines, A549 and Calu-3, were treated with collagen type I and transfected with DDR1 siRNA. The relative expression of DDR1 and t-DARPP was evaluated using qRT-PCR.

The results indicated that collagen type I could stimulate DDR1 expression in NSCLC cells. Also, DDR1 upregulation resulted in a significant increase in t-DARPP expression. In contrast, suppression of DDR1 expression significantly decreased t-DARPP expression.

Our findings propose that modification in the expression of DDR1, caused by collagen type I and siRNA, might influence the expression of t-DARPP in NSCLC that is linked to NSCLC progression. Moreover, this alteration could potentially serve as an innovative target for therapeutic intervention.

To investigate the use of uniportal video-assisted thoracoscopic surgery (U-VATS) in the treatment of non-small cell lung cancer (NSCLC).

A total of 82 patients with early NSCLC in our hospital from May 2019 to January 2021 were enrolled to this study. Forty-one patients treated with spontaneous breathing U-VATS were the research group (RG), and 41 with conventional thoracoscopy were the control group (CG). Fasting peripheral blood was drawn from patients before (T0), one (T1) and three days after surgery (T2), respectively. White blood cells (WBC), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), matrix metalloproteinase-9 (MMP-9) and T-lymphocyte subsets were measured in the blood. In addition, we counted the conversion rate to open chest and tracheal intubation in the RG, and compared the operation time, intraoperative bleeding, chest drainage, chest tube retention time, antibiotic application time, postoperative hospital stays and complications between groups. Finally, a 1-year prognostic follow-up was performed to record overall survival, chemotherapy rate, and recurrent metastasis rate.

At T1, WBC, IL-6, TNF-α, and MMP-9 were lower in the RG than in the CG, while immune function was better in the RG at T1 and T2 (P<0.05). Complication rates were lower in the RG than in the CG when compared (P>0.05). The prognosis of 1-year overall survival, chemotherapy rate, and recurrence rate were not different between the two groups (P>0.05).

Spontaneous breathing U-VATS can effectively reduce the inflammation and enhance the stability of immune function in NSCLC patients undergoing surgery.

To evaluate treatment outcomes and toxicity of pulmonary SBRT for intrathoracic recurrence in patients with locally advanced NSCLC treated as a combination of surgery, radiotherapy or chemotherapy.

A total of 46 patients with NSCLC who received thoracic SBRT for local or non local intrapulmonary recurrent lesions in our department from 2009 to 2019 were retrospectively enrolled in this study. The patients received median 43.4 Gy (25 Gy -60 Gy) radiotherapy using the CyberKnife radiosurgery system in median 3.6 fractions (range, 1-8).Univariate and multivariate Cox regression analyses were performed on the factors predicting outcomes.

The median follow up time after SBRT was 23.5 months. Treatment of the primary tumor consisted of surgical resection, radiochemotherapy, and systemic therapy in 25, 8 and 13 patients, respectively. İsolated local recurrence, intrathoracic recurrence and distant metastasis were detected in 5 (10.9%), 12 (26.1%) and 8 (17.4%) patients, respectively. Kaplan-Meier analysis of 2 year OS, PFS and LC for all tumors treated after SBRT were; 51%, 56% and 91%, respectively. In parameters related to patient and treatment; no statistical significance was found affecting local control and survival.(p>0.05). Grade 2 radiation pneumonitis and chest wall pain were observed in 2 (4.3%) and 1 (2.1 %) patients. Grade 3 toxicity was detected in 3 ( 6.5%) cases.

Pulmonary SBRT for recurrent NSCLC is a good treatment option with favourable LC and promising survival. SBRT can be an effective treatment modality in the treatment of patients with local/limited pulmonary relapses with acceptable toxicity rates.

Activating mutations in the epidermal growth factor receptor (EGFR) are initially responsive to tyrosine kinase inhibitors (TKIs), but responses to TKIs is not permanent and drug resistance eventually happens for almost all patients. Subsequent studies found different resistance mechanisms, among which (EGFR) T790M mutation is the most important mechanism of TKI treatment failure. Using cell- free DNA (cfDNA) is a new way for diagnosing resistance mutations in EGFR. The aim of present study is to determine cfDNA-identified recurrence mutation rate and their association with clinical outcome in lung Adenocarcinoma patients.
Patients who were diagnosed with metastatic adenocarcinoma of the lung and acquired resistance to TKIs were enrolled. The incidence of T790M positivity, overall survival (OS) and median duration of TKI treatment before progression was calculated. Polymerase chain reaction (PCR) and sequencing were used to identify the T790M mutation in cfDNA.
The incidence of T790M mutations was higher in men, younger cases (<59 years), in patients with L858R primary mutation and never smokers although they were not significantly different (P-values= 041, 0.316, 0.316 and 0.158, respectively). There was significant longer OS in the Del19 subgroup than the L858R subgroup (p = 0.014). In multivariable analysis, significant longer OS was associated with younger age (<59 years) and primary EGFR mutation exon 19 (P- values= 0.028 and 0.050, respectively).
T790M mutations frequency may differ by ethnicity, genetic factors and EGFR primary mutations. Detecting T790M mutations in plasma is considered as an indicator of treatment with third generation EGFR-TKIs.

Lung cancer is the leading cause of cancer deaths worldwide. Pharmacogenomics plays an important role in tailoring cancer patients’ treatment. Pemetrexed is widely used in first- and second-line chemotherapy of non-small cell lung cancer (NSCLC); however, there is no available predictive biomarker for pemetrexed treatment. The present study aimed to investigate the role of polymorphisms in thymidylate synthase and SLC19A1 polymorphisms with clinical outcome in patients with advanced NSCLC treated in first-line with pemetrexed or pemetrexed plus cisplatin.

This cohort study included 40 metastatic lung cancer patients treated with pemetrexed plus cisplatin. We utilized the tetra-primer amplification refractory mutation system-polymerase chain (ARMS-PCR) reaction for genotyping of rs3788189 and rs1051298. TYMS 28-VNTR and rs16430 were genotyped in the patients via PCR amplification and PCR-RFLP, respectively. Fisher's exact test and Kaplan-Meier curve were used for statistical analysis.

We recruited 40 patients in this research with a median age of 58.9 years. The median survival of all the 40 patients was 11.6 months. The overall survival of the patients, as well as their gender, age, and metastatic sites were not found to be statistically associated with rs1051298, rs3788189, TYMS VNTR, and rs16430.

Our study did not identify any associations between the SLC19A1 and TYMS VNTR and rs16430 and clinical outcomes in advanced NSCLC patients. However, further investigation will be conducive to finding effective clinical biomarkers for the treatment of patients with NSCLC.

 Cancer is a global public health problem that affects millions of people every year and the immunotherapy has been a promising alternative for its treatment. The aim of this study was to gather data concerning the efficacy and safety of immunotherapy in the treatment of non-small cell lung cancer (NSCLC), emphasizing pembrolizumb, a humanized antibody. This study also reports the role of immunotherapy in cancer treatments, contemplating the anti-CTLA4, anti-PD-L1 and anti PD-1 action in lymphocyte T cells.

 A bibliographic review was performed using Pubmed, SCIELO and SCOPUS databases, screening the scientific studies published within the last 5 years.

 Seven clinical trials were selected to discuss the benefits of pembrolizumab as NSCLC therapy in untreated and previously treated patients, considering or not the tumor proportion score (TPS). It was found that NSCLC occurs with great frequency in Brazil and worldwide, presenting a poor prognosis due to its late diagnosis in most cases. Immunotherapy is a promising treatment strategy for NSCLC because its benefits overcome its risks compared to other therapies. Besides, the studies evidenced the efficiency of pembrolizumab as monotherapy or in association whit chemotherapy, in the first or second line of treatment and, additionally, patient’s whit TPS ≥ 50% seem to have a greater benefit from the treatment.

 The data collected herein showed that pembrolizumab is a very promising, effective, and safe treatment option against NSCLC. Lastly, it is important to highlight the relevance of review’s studies, since they are easy-to-read materials, collecting relevant information on a subject.

Circular RNAs (circRNAs) are identified as key modulators in cancer biology. Nonetheless, the role of circ_0006427 in non-small cell lung cancer (NSCLC) and its modulatory mechanism are undefined. This study aimed to investigate the potential function and mechanism of circ_0006427 in NSCLC. In this experimental study, circ_0006427, miR-346 and vestigial like family member 4 (VGLL4) mRNA expressions were analyzed in NSCLC tissues and cells, using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Multiplication, migration and invasion of NSCLC cells were examined using the CCK-8 method and Transwell experiment, respectively. Dual-luciferase reporter gene experiments were conducted to identify the paring relationship between circ_0006427 and miR-346. Western blot was employed to determine expressions of VGLL4 and epithelial-mesenchymal transition (EMT) markers on protein levels. Immuno histochemistry (IHC) method was adopted to assess VGLL4 protein expression in NSCLC tissues. Circ_0006427 expression was down-regulated in NSCLC tissues and cells, and circ_0006427 suppressed multiplication, migration, invasion and EMT of NSCLC cells. miR-346 expression was upregulated in NSCLC tissues and cells, and miR-346 worked as a target of circ_0006427. VGLL4 was down-regulated in NSCLC tissues and cells, and knockdown of VGLL4 accelerated multiplication, migration, invasion and EMT of NSCLC cells. Circ_0006427 enhanced VGLL4 expression by competitively binding with miR-346. Circ_0006427/miR-346/VGLL4 axis regulated NSCLC progression.

Cancer stem cells are a subpopulation of tumor cells with self-renewal capacity that promote tumorigenesis, resistance to chemotherapy, and metastasis. Sox2, Oct4, and Nanog are three pluripotent transcription factors expressed in embryonic stem cells and cancer stem cells. This study aimed to evaluate the expression of Sox2, Nanog, and Oct4, and analyze their clinical significance in human non-small-cell lung cancer (NSCLC). Expression of Sox2, Nanog, and Oct4 was assayed in cancer tissues and their corresponding paracancerous tissues from 30 patients with NSCLC. RT-PCR was used to analyze the expression of these genes. The correlation between the expression of these three genes and clinical parameters including disease stage, smoking, lymph node, and cancer subgroups (adenocarcinoma and squamous) were analyzed. All three genes were expressed simultaneously in 76.6% of tumor samples. A significant correlation was observed between the expression of Sox2, Nanog, and Oct4 in the cancer tissues in comparison to the paracancerous tissues (P<0.000). Expression of Sox2 and Oct4 gene had a positive correlation with the stage of cancer (Sox2 P=0.01, Oct4 P=0.0007), while the expression profile of Nanog showed a significant positive correlation with sex (P=0.0063), smoking (P=0.0253), tumor stages (P=0.0003), and tumor type (P=0.0085). Evaluating the expression of Sox2, Nanog, and Oct4 genes in NSCLC might have some implications for diagnosis and prognosis; they might be also promising treatment targets. The correlations between prognosis and pathological features and Nanog overexpression in NSCLC suggest Nanog is a potential indicator of the early stage of NSCLC.

Tuberculosis (TB) and non-small cell lung cancer (NSCLC) are two major contributors to mortality and morbidity worldwide. In this regard, TB and NSCLC have similar symptoms, and TB has symptoms that are identical to malignancy; therefore, sometimes it is mistakenly diagnosed as lung cancer. Moreover, patients with active pulmonary TB are at a higher risk of dying due to lung cancer. In addition, several signaling pathways involved in TB and NSCLC have been identified. Also, the miRNAs are biological molecules shown to play essential roles in the above-mentioned diseases through targeting the signaling pathways’ genes. Most of the pathways affected by miRNAs are immune responses such as autophagy and apoptosis in TB and NSCLC, respectively. Several studies have separately investigated the expression of miRNAs profile in patients with NSCLC and infectious TB. In this critical review, we attempted to gather common miRNAs between TB and NSCLC and to explain the involved-pathways, which are affected by miRNAs in both TB and NSCLC. Results of this critical review show that the expressions of miR-155, miR-146a, miR-125b, miR-30a, miR-29a, and miR-Let7 have significantly changed in TB and NSCLC. The data suggest that miRNAs expression may provide a new method for screening or differential diagnosis of NSCLC and TB.

Dysregulation of long non-coding RNAs (lncRNAs) is associated with the progression of non-small cell lung cancer (NSCLC). This study aimed to investigate the role of long intergenic non-protein coding RNA 174 (LINC00174) in NSCLC.

In this experimental study, LINC00174 expression in NSCLC tissues and cell lines was investigated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Besides, cell counting kit-8 (CCK-8), 5-bromo-2'-deoxyuridine (BrdU). Transwell and Flow Cytometry assays were applied to detect the regulatory function of LINC00174 on the growth, migration and apoptosis of NSCLC cells. Bioinformatics analysis, dual luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay predicted and verified the targeting relationship between LINC00174 and miR-31-5p, and between miR-31-5p and the 3´-untranslated region (3´UTR) of large tumor suppressor kinase 2 (LATS2), respectively. Western blotting was performed to detect the regulatory function of LINC00174 and miR-31-5p on LATS2 protein expression.

Compared with that in normal lung tissues, LINC00174 expression in NSCLC tissues and cell lines was reduced. LINC00174 expression was negatively associated with the TNM stage of the patients. Functional experiments showed that LINC00174 overexpression inhibited NSCLC cell multiplication and migration, and induced apoptosis. Furthermore, LINC00174 targeted miR-31-5p and repressed its expression. Additionally, LINC00174 upregulated LATS2 expression through competitively binding to miR-31-5p.

LINC00174, as a competitive endogenous RNA, elevates LATS2 expression by adsorbing miR-31-5p, thereby inhibiting the viability and migration of NSCLC cells, and promoting apoptosis.

This study aimed to investigate the impact of image preprocessing steps, including Gray Level Discretization (GLD) and different Interpolation Algorithms (IA) on 18F-Fluorodeoxyglucose (18F-FDG) radiomics features in Non-Small Cell Lung Cancer (NSCLC).

One hundred and seventy-two radiomics features from the first-, second-, and higher-order statistic features were calculated from a set of Positron Emission Tomography/Computed Tomography (PET/CT) images of 20 non-small cell lung cancer delineated tumors with volumes ranging from 10 to 418 cm3 regarding five intensity discretization schemes with the number of gray levels of 16, 32, 64, 128, and 256, and four Interpolation algorithms, including nearest neighbor, tricubic convolution and tricubic spline interpolation, and trilinear were used. Segmentation was based on 3D region growing-based. The Intraclass Correlation Coefficient (ICC), Overall Concordance Correlation Coefficient (OCCC), and Coefficient Of Variations (COV) were calculated to demonstrate the features' variability and select robust features. ICC and OCCC < 0.5 presented weak reliability, ICC and OCCC between 0.5 and 0.75 illustrated appropriate reliability, values within 0.75 and 0.9 showed satisfying reliability, and values higher than 0.90 indicate exceptional reliability. Besides, features with less than 10% COV have been selected as robust features.

All morphology family (except four features), statistic, and Intensity volume histogram families were not affected by GLD and IA. And the rest of them, 10 and 61 features showed COV ≤ 5% against GLD and IA, respectively. Ten and 80 features showed excellent reliability (ICC values greater than 0.90) against GLD and IA. Eight and 60 features showed OCCC≥0.90 against GLD and IA, respectively. Based on our results Inverse difference normalized and Inverse difference moment normalized from Grey Level Co-occurrence Matrix (GLCM) were the most robust features against GLD and Skewness from intensity histogram family and Inverse difference normalized and Inverse difference moment normalized from GLCM were the most robust features against IA.

Preprocessing can substantially impact the 18F-FDG PET image radiomic features in NSCLC. The impact of gray level discretization on radiomics features is significant and more than Interpolation algorithms.

Reportedly, circular RNAs (circRNAs) exert a crucial regulatory role in cancer. Circ_0001073 is derived from exons 3-5 of ACVR2A gene, which inhibits cancer progression. However, the role and mechanism of circ_0001073 in non-small cell lung cancer (NSCLC) are unclear. This study aimed to explore the role and mechanism of circ_0001073 in the development of NSCLC.

In this experimental study, microarray analysis was employed to filter differential expressed circRNAs in NSCLC tissues. Also, circ_0001073, microRNA-582-3p (miR-582-3p), and repulsive guidance molecule B (RGMB) mRNA expressions were examined by quantitative real-time polymerase chain reaction (qRT-PCR). NSCLC cell multiplication was measured by the cell counting kit-8 (CCK-8) assay. Scratch healing experiment and Transwell experiment were performed to assess cell migration and invasion, respectively. Flow cytometry was applied to analyze the apoptosis of NSCLC cells. Western blot was employed to assess RGMB protein expression. Additionally, dualluciferase reporter gene experiment and RNA immunoprecipitation (RIP) experiment were applied to probe the binding sites between miR-582-3p and circ_0001073 or RGMB.

Circ_0001073 was remarkably under-expressed in NSCLC tissues and cells. Circ_0001073 overexpression impeded the multiplication, migration, and invasion and enhanced the apoptosis of NSCLC cells in vitro. Circ_0001073 directly bound to miR-582-3p and acted as a miRNA sponge to regulate RGMB expression. Besides, miR-582-3p overexpression or knockdown of RGMB remarkably reversed the malignant phenotypes of NSCLC cells induced by the up-regulation of circ_0001073 expression.

Circ_0001073 up-regulates RGMB expression through adsorbing miR-582-3p to inhibit NSCLC progression, suggesting its potential as a novel therapeutic target in NSCLC

There is growing evidence showing that circular RNAs (circRNAs) are crucial regulators in modulating the biological behavior of tumors. This work is aimed to probe the role of circ_0000517 in non-small cell lung cancer (NSCLC) and to elucidate its mechanism of action.

In this experimental study, the differentially expressed circRNAs in NSCLC were screened using the GEO database (GSE158695). Circ_0000517, miR-326, miR-330-5p, and MMP2 expression levels were determined by quantitative real-time polymerase chain reaction (qRT-PCR) analysis and Western blot. The proliferation, apoptosis, migration, and invasion of NSCLC cells were detected by CCK-8, flow cytometry, and transwell assays. RNA immunoprecipitation (RIP), RNA pull-down, and dual-luciferase reporter gene assays were performed to clarify the association between the circ_0000517 and miR-326/miR-330-5p.

Circ_0000517 was shown to be up-regulated in NSCLC tissues and cell lines. The up-regulation of circ_0000517 is closely associated with advanced clinical stage of cancer, lymph node metastasis, and poor prognosis in NSCLC patients. Circ_0000517 knockdown impeded the proliferation, migration, and invasion of NSCLC cells and enhanced their apoptosis. Mechanistically, circ_0000517 was demonstrated to up-regulate MMP2 expression via decoying miR-326 and miR-330-5p to facilitate the malignant biological behaviors of NSCLC cells.

This work reveals that circ_0000517 is implicated in NSCLC cell growth and metastasis through the modulation of miR-326/miR-330-5p/MMP2, providing novel insights into the role of circRNAs in NSCLC progression.

There is growing evidence showing that circular RNAs (circRNAs) are crucial regulators in modulating the biological behavior of tumors. This work is aimed to probe the role of circ_0000517 in non-small cell lung cancer (NSCLC) and to elucidate its mechanism of action.

In this experimental study, the differentially expressed circRNAs in NSCLC were screened using the GEO database (GSE158695). Circ_0000517, miR-326, miR-330-5p, and MMP2 expression levels were determined by quantitative real-time polymerase chain reaction (qRT-PCR) analysis and Western blot. The proliferation, apoptosis, migration, and invasion of NSCLC cells were detected by CCK-8, flow cytometry, and transwell assays. RNA immunoprecipitation (RIP), RNA pull-down, and dual-luciferase reporter gene assays were performed to clarify the association between the circ_0000517 and miR-326/miR-330-5p.

Circ_0000517 was shown to be up-regulated in NSCLC tissues and cell lines. The up-regulation of circ_0000517 is closely associated with advanced clinical stage of cancer, lymph node metastasis, and poor prognosis in NSCLC patients. Circ_0000517 knockdown impeded the proliferation, migration, and invasion of NSCLC cells and enhanced their apoptosis. Mechanistically, circ_0000517 was demonstrated to up-regulate MMP2 expression via decoying miR-326 and miR-330-5p to facilitate the malignant biological behaviors of NSCLC cells.

This work reveals that circ_0000517 is implicated in NSCLC cell growth and metastasis through the modulation of miR-326/miR-330-5p/MMP2, providing novel insights into the role of circRNAs in NSCLC progression.