EFCC1 as a putative prognostic biomarker in lung adenocarcinoma.
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ABSTRACT:
SUBMITTER: Yu S
PROVIDER: S-EPMC7475509 | biostudies-literature | 2020 Aug
REPOSITORIES: biostudies-literature
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EFCC1 as a putative prognostic biomarker in lung adenocarcinoma.
Annals of translational medicine 20200801 16
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Project description:Lung cancer is one of the most common malignancy worldwide and causes estimated 1.6 million deaths each year. Cancer immunosurveillance has been found to play an important role in lung cancer and may be related with its prognosis. KLRK1, encoding NKG2D, is a homodimeric lectin-like receptor. However, there has not been one research of KLRK1 as a biomarker in lung cancer. Data including patients` clinical characteristics and RNAseq information of KLRK1 from TCGA were downloaded. A total of 1019 patients with lung cancer were included in this study, among which 407 patients were female and 611 patients were male. Evaluations of mRNA expression, diagnostic value by ROC (receiver operating characteristic) curves and prognostic value by survival curve, Cox model and subgroup analysis were performed. The level of KLRK1 expression in lung adenocarcinoma cancer tissues and normal lung tissues was detected by qRT-PCR. The CCK-8 assay investigated the proliferation rate and the wound healing assay assessed the migratory ability in vitro. The expression of KLRK1 in tumor was lower than that in normal tissue. KLRK1 expression was associated with gender, histologic grade, stage, T classification and vital status. Patients with high KLRK1 expression presented an improved overall survival (P = 0.0036) and relapse free survival (P = 0.0031). KLRK1 was found to have significant prognostic value in lung adenocarcinoma (P = 0.015), stage I/II (P = 0.03), older patients (P = 0.0052), and male (P = 0.0047) by subgroup overall survival analysis, and in lung adenocarcinoma (P = 0.0094), stage I/II (P = 0.0076), older patients (P = 0.0072), and male (P = 0.0033) by subgroup relapse free survival analysis. Lung adenocarcinoma cancer patients with high KLRK1 expression presented an improved overall survival (P = 0.015) and relapse free survival (P = 0.0094). In vitro studies indicated that KLRK1 inhibited tumor cell proliferation and migration. KLRK1 was an independent prognostic factor and high KLRK1 expression indicated a better overall and relapse free survival. KLRK1 may be a prognostic biomarker for lung adenocarcinoma cancer.
| S-EPMC8821622 | biostudies-literature
Project description:Spondin 2 (SPON2) is a member of the F-spondin superfamily of genes that encode an extracellular matrix protein. SPON2 has been identified by mRNA differential display screening of cancerous and noncancerous lung cell lines in vitro [1], however, its role in pulmonary adenocarcinoma (ADC) patients remains unclear. In our study, we evaluated whether SPON2 can be used as a biomarker for the diagnosis of pulmonary ADC and any association between SPON2 protein levels and clinicopathological characteristics. Firstly, the mRNA levels of SPON2 in pulmonary ADCs and normal adjacent tissue samples were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) (n = 60) assay and the expression of SPON2 protein were detected by tissue microarray immunohistochemistry analysis (TMA-IHC) (n = 280). Overexpression of SPON2 protein in cancerous tissues was associated with the clinical characteristics of ADC patients and their overall survival. Levels of SPON2 mRNA and protein were significantly expressed higher in ADC tissues than in adjacent normal tissues. Finally, through univariate and multivariate regression analysis, we found that overexpression of SPON2 protein levels correlates with differentiation, positive lymph nodes metastasis, higher serum carcinoembryonic antigen (CEA) level and poor overall survival. Overexpression of SPON2 protein is an independent prognostic biomarker in ADC patients. Our data revealed that SPON2 played an oncogene role in ADC development and progression. Inhibiting SPON2 might represent a new strategy for pulmonary ADC.
| S-EPMC5601735 | biostudies-literature
Project description:BackgroundLung cancer is the leading cause of cancer-related death, and adenocarcinoma is the most common type of lung cancer. Although emerging evidence implicates the role of several aldehyde dehydrogenases in cancer progression, the expression and clinical significance of aldehyde dehydrogenase 3B1 in lung adenocarcinoma has never been studied.MaterialsIn our study, the expression of aldehyde dehydrogenase 3B1 in 250 cases of lung adenocarcinoma was detected with immunohistochemistry, and the patients were further divided into subgroups with different aldehyde dehydrogenase 3B1 expression. Using real-time polymerase chain reaction, we investigated the aldehyde dehydrogenase 3B1 messenger RNA in 20 lung adenocarcinoma and paired normal lung tissues. With the χ2 test, we evaluated the clinical significance of aldehyde dehydrogenase 3B1 by analyzing its correlation with the clinicopathological factors. Propensity score matching was performed to balance the baseline of cohort. With univariate and multivariate analyses, we screened the prognostic factors of lung adenocarcinoma and identified the independent prognostic factors before and after the propensity score matching.ResultsAldehyde dehydrogenase 3B1 expression was significantly associated with the sex and age of patients, tumor size, and histological grade. High expression of aldehyde dehydrogenase 3B1 predicted the poor prognosis (P = .003). Moreover, male patients (P = .020), large tumor size (P = .009), advanced T stage (P = .001), positive lymphatic invasion (P < .001), and advanced tumor-node-metastasis stage (P < .001) were all the prognostic factors for unfavorable outcome. Aldehyde dehydrogenase 3B1 was an independent prognostic biomarker of lung adenocarcinoma, indicating the poor prognosis. In addition, after balancing the baseline characteristics by propensity score matching, we also demonstrated that aldehyde dehydrogenase 3B1 was an independent prognostic biomarker of lung adenocarcinoma (P = .007).ConclusionsAldehyde dehydrogenase 3B1 was an independent prognostic biomarker of lung adenocarcinoma, indicating the unfavorable prognosis. Postoperative detection of aldehyde dehydrogenase 3B1 would help stratify the high-risk patients with lung adenocarcinoma and guide individual treatment.
| S-EPMC7412899 | biostudies-literature
Project description:BackgroundLung adenocarcinoma (LUAD) is a highly prevalent and deadly form of lung cancer and is a significant health concern worldwide. Although the expression of serine protease 3 (PRSS3) is elevated in certain cancers, its function in LUAD is yet unclear. The aim of this study was to investigate the mechanism of PRSS3 in lung adenocarcinoma, and validate PRSS3 as a reliable prognostic biomarker in lung adenocarcinoma.MethodsThe Cancer Genome Atlas (TCGA) provides RNA expression data and patient medical information for LUAD patients. To determine which genes are expressed differently in LUAD and normal lung tissues, we carefully examined these data. We then used Cox regression analysis to examine the expression and survival data to pinpoint the genes that are strongly associated with patient survival. The PRSS3 gene affects patient prognosis. Afterward, we divided LUAD patients into low- and high-expression groups on the basis of the median PRSS3 expression to examine the relationship between immune cells and PRSS3. The results of the CIBERSORT and CIBERSORTx studies revealed correlations between PRSS3 and the degree of infiltration of several immune cell types. After the groups with low and high PRSS3 expressions were compared, PRSS3-related genes were identified, and functional enrichment analysis was performed. Furthermore, a model was developed to predict patient prognosis according to clinical characteristics and PRSS3 expression. After the bioinformatics analyses were completed, we validated the differential expression of PRSS3 in samples obtained from our center via Western blotting and immunohistochemistry (IHC).ResultsWe found that PRSS3 expression is highly upregulated in LUAD and that high PRSS3 expression is associated with a poorer prognosis in the TCGA database. Single-sample gene enrichment analysis revealed a strong correlation between PRSS3 and the immunological microenvironment. The clinical model developed on the basis of the PRSS3 showed great accuracy and can be used as a significant diagnostic indicator for LUAD. Western blotting and IHC confirmed a substantial increase in PRSS3 expression in LUAD. Herein, we analyzed an available dataset for a clinical cohort and revealed that elevated levels of PRSS3 are indicative of unfavorable outcomes in patients diagnosed with LUAD.ConclusionsPRSS3 is significantly upregulated in LUAD and can be used as a marker for LUAD diagnosis and prognosis assessment. Further study of PRSS3 could provide valuable insight into the mechanisms underlying the occurrence and progression of LUAD.
| S-EPMC11912035 | biostudies-literature
Project description:As a lncRNA, AL365181.3 is aberrantly expressed in multiple cancer types, including lung adenocarcinoma (LUAD). However, the biological process underlying the ability of AL365181.3 to promote the progression of LUAD is unclear. Here, the pancancer expression level of AL365181.3 was analyzed via the TCGA and GTEx databases, as well as its clinical characteristics and prognostic value. We investigated the biological functions of AL365181.3 in LUAD using various in vitro and in vivo assays. We found that AL365181.3 was significantly more highly expressed in many types of cancer tissues, including LUAD tissues, than in adjacent normal tissues. LUAD patients with high AL365181.3 expression had poor prognoses. Functional enrichment analyses indicated that AL365181.3 is involved in the regulation of metabolism, MAPK signaling and other tumor regulatory signaling pathways. Finally, we found that AL365181.3 knockdown reduced the proliferation, migration and invasion capacity of LUAD cells, and AL365181.3 knockdown resulted in a reduced in vivo tumorigenic capacity of LUAD cells. These findings provide a comprehensive understanding of the role of AL365181.3 in LUAD.
| S-EPMC11836369 | biostudies-literature
Project description:E2F transcription factors (E2Fs) are a family of transcription factors critical regulators of the cell cycle, apoptosis, and differentiation, thus influencing tumorigenesis. However, the specific roles of E2Fs in lung adenocarcinoma (LUAD) remain unclear. Data from The Cancer Genome Atlas (TCGA) were used. R version. 4.0.3 and multiple databases (TIMER, cBioportal, gene expression profile interaction analysis [GEPIA], LinkedOmics, and CancerSEA) were utilized to investigate mRNA expression, mutational analysis, prognosis, clinical correlations, co-expressed gene, pathway and network, and single-cell analyses. Immunohistochemistry (IHC) confirmed that E2F transcription factor 7 (E2F7) correlated with LUAD. Among the E2Fs, E2F7 was identified by constructing a prognostic model most significantly associated with overall survival (OS) in LUAD patients. The univariate and multivariate Cox regression analyses showed that E2F7, p-T stage, and p-TNM stage were closely related to OS and progression-free survival (PFS) (P < .05) in LUAD. E2F 7/8 were also identified as significantly associated with tumor stage in the GEPIA database. Compared with paracancerous tissues, E2F7 was up-regulated in LUAD by IHC, and E2F7 might be positively correlated with larger tumors and higher TNM stages. E2F7 may primarily regulate DNA repair, damage, and cell cycle processes and thus affect LUAD tumorigenesis, invasion, and metastasis by LinkedOmics and CancerSEA. E2F7 serves as a potential prognostic biomarker for LUAD.
| S-EPMC10798722 | biostudies-literature
Project description:BackgroundAlthough it has a poor prognosis, patients with lung adenocarcinoma (LUAD) have a relatively higher 5-year survival period. Thus, it is necessary to identify effective prognostic markers to evaluate the effect of early treatment. RS1 gene encodes retinoschisin, a key protein in congenital retinoschisis, while few studies have been reported on the association between RS1 and cancer prognosis.MethodsWe performed bioinformatic analyses based on the data obtained from The Cancer Genome Atlas and Gene Expression Omnibus databases to demonstrate the expression level of RS1 was related to the LUAD prognosis and our findings were verified in-vitro and clinical samples. Then, we explored the potential mechanism of how RS1 expression influenced the prognosis of LUAD.ResultsCompared with normal tissues, the RS1 expression was significantly lower in tumor tissues. The Multivariate Cox regression model showed that RS1 could be used as an independent prognostic indicator. Furthermore, we found significant differences in immune cell infiltration between RS1 high and low expression groups, and the proteasome pathway was found enriched in RS1 low expression samples.ConclusionIn conclusion, our study suggests that RS1 is a novel prognostic biomarker for LUAD. Differences in immune cell infiltration and signaling pathways may contribute to the poor prognosis of LUAD caused by low RS1 expression.
| S-EPMC9200886 | biostudies-literature
Project description:Currently, there is no reliable biomarker to clinically predict the prognosis of lung adenocarcinoma (ADC). The receptor-tyrosine-kinase like orphan receptor 1 (ROR1) is reported to be overexpressed and associated with poor prognosis in several tumors. This study aimed to examine the expression of ROR1 and evaluate its prognostic significance in human lung ADC patients. In this present study, Western blot analysis and immunohistochemistry were performed to characterize expression of ROR1 protein in lung ADC patients. The results revealed that ROR1 protein expression was significantly higher in lung ADC tissues than that in their adjacent non-tumor tissues. Patients at advanced stages and those with positive lymph node metastasis expressed higher level of ROR1 (P < 0.001). Moreover, Chi-square test showed that ROR1 expression was correlated to gender (P = 0.028), the 7th edition of the American Joint Committee on Cancer tumor-node-metastasis (AJCC TNM) staging system and lymph node metastasis (P < 0.001). Kaplan-Meier survival analysis indicated an association of high ROR1 expression with worse overall survival (OS) in lung ADC patients (P < 0.001). Multivariate COX regression analysis further confirmed that ROR1 is an independent prognostic predictor (P < 0.001, HR = 4.114, 95% CI: 2.513-6.375) for OS. Therefore, ROR1 expression significantly correlates with malignant attributes of lung ADC and it may serve as a novel prognostic marker in lung ADC patients.
| S-EPMC5103212 | biostudies-literature
Project description:ObjectiveTo explore the potential clinical and prognostic significance of Homo sapiens solute carrier family 35 member F2 (SLC35F2) in the context of lung adenocarcinoma (LUAD).MethodsThe expression pattern of SLC35F2 in LUAD tissues and normal tissues was analyzed in The Cancer Genome Atlas (TCGA) datasets and validated in 12 pairs of fresh clinical LUAD tissues and their corresponding adjacent normal tissues using quantitative real-time PCR (qRT-PCR) and western blotting. Immunohistochemistry (IHC) was used to assess the protein expression of SLC35F2 in 60 paraffin-embedded LUAD tissues, and its associations with clinicopathological parameters were further examined. The prognostic significance of SLC35F2 mRNA expression was also evaluated using the Kaplan-Meier method, and Cox regression models in LUAD patients from the TCGA database. The potential utility of SLC35F2 as an indicator of recurrence or metastasis was explored through the follow-up of selected clinical LUAD cases. Lastly, gene set enrichment analysis (GSEA) was conducted to investigate the underlying biological mechanisms and signaling pathways.ResultsBioinformatics analysis utilizing the TCGA database indicated that SLC35F2 mRNA exhibited heightened expression in LUAD tissues when compared to normal tissues. These findings were further substantiated through the examination of 12 pairs of clinical LUAD tissues and their corresponding adjacent normal tissues, employing qRT-PCR and western blotting techniques. IHC results from a cohort of 60 LUAD patients demonstrated an up-regulation of SLC35F2 in 38 out of 60 individuals (63.3 %), which exhibited a significant correlation with tumor size, lymph node metastasis, and clinical stage (all P < 0.05). Both the Kaplan-Meier curve and the Cox proportional hazard analyses indicated a strong association between the up-regulation of SLC35F2 mRNA expression and unfavorable overall survival (OS) in patients with LUAD, as observed in the TCGA datasets (P < 0.05). The follow-up findings from select clinical LUAD cases provided evidence that the expression of SLC35F2 could serve as a dependable biomarker for monitoring the recurrence or metastasis. Additionally, the GSEA highlighted the enrichment of apoptosis, adhesion, small cell lung cancer (SCLC), and p53 signaling pathways in the subgroup of LUAD patients with elevated SLC35F2 expression.ConclusionSLC35F2 exhibited an up-regulated in both mRNA and protein expression, rendering it a valuable independent prognostic indicator for patients diagnosed with LUAD.
| S-EPMC10767229 | biostudies-literature
Project description:MAFB is a basic leucine zipper (bZIP) transcription factor specifically expressed in macrophages. We have previously identified MAFB as a candidate marker for tumor-associated macrophages (TAMs) in human and mouse models. Here, we analyzed single-cell sequencing data of patients with lung adenocarcinoma obtained from the GEO database (GSE131907). Analyzed data showed that general macrophage marker CD68 and macrophage scavenger receptor 1 (CD204) were expressed in TAM and lung tissue macrophage clusters, while transcription factor MAFB was expressed specifically in TAM clusters. Clinical records of 120 patients with lung adenocarcinoma stage I (n = 57), II (n = 21), and III (n = 42) were retrieved from Tsukuba Human Tissue Biobank Center (THB) in the University of Tsukuba Hospital, Japan. Tumor tissues from these patients were extracted and stained with anti-human MAFB antibody, and then MAFB-positive cells relative to the tissue area (MAFB+ cells/tissue area) were morphometrically quantified. Our results indicated that higher numbers of MAFB+ cells significantly correlated to increased local lymph node metastasis (nodal involvement), high recurrence rate, poor pathological stage, increased lymphatic permeation, higher vascular invasion, and pleural infiltration. Moreover, increased amounts of MAFB+ cells were related to poor overall survival and disease-free survival, especially in smokers. These data indicate that MAFB may be a suitable prognostic biomarker for smoker lung cancer patients.
| S-EPMC9456510 | biostudies-literature