Six-transmembrane epithelial antigen of prostate-1 (STEAP1) is a relatively newly identified gene target from prostate cancer, breast cancer, and gastric cancer. However, functions of STEAP1 in lung adenocarcinoma (LUAD) are still unknown. In the present study, we explored the molecular and cellular mechanisms of STEAP1 in LUAD. Western blot and Q-PCR were conducted to detect the protein and mRNA expressions respectively. The cell proliferation was tested by CCK8 assay. The effects of STEAP1 on the metastasis and epithelial–mesenchymal transition (EMT) of LUAD were evaluated by EdU assay, wound healing assay, and transwell migratory assay. H1650, H358, HCC827, H1299, H23, A549, H1693 were selected as human LUAD cell lines in the study. Results have shown that STEAP1 expression was up-regulated in LUAD cells compared with normal lung epithelial cells. Knockdowning of STEAP1 suppressed the proliferation, migration, and invasion of LUAD epithelial cells. Importantly, after comparing the proliferation, migration, and invasion of LUAD to the corresponding control groups treated in STAT3 inhibitor ADZ1480, we found that STEAP1 regulates EMT via Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. In conclusion, STEAP1 can serve as a therapeutic target, and it may have important clinical implications for LUAD treatment.
BackgroundThe purpose of this study is to discover potential biomarkers in serum for the detection of small cell lung cancer (SCLC).Methods74 serum samples including 30 from SCLC patients and 44 from healthy controls were analyzed using ClinProt system combined with matrix-assisted laser desorption/ionization time-of-flight masss spectrometry (MALDI-TOF-MS). ClinProt software and genetic algorithm analysis selected a panel of serum markers that most efficiently predicted which patients had SCLC.ResultsThe diagnostic pattern combined with 5 potential biomarkers could differentiate SCLC patients from healthy persons, with a sensitivity of 90%, specificity of 97.73%. Remarkably, 88.89% of stage I/II patients were accurately assigned to SCLC.ConclusionsAnchorchip-time-of-flight spectrometry technology will provide a highly accurate approach for discovering new biomarkers for the detection of SCLC.
The aim of this study is to globally screen and identify the expression protein profiles of lung squamous carcinoma cell (SqCC) using shot-gun proteomics strategy and to further analyze function of individual proteins by bioinformatics, which may likely result in the identification of new biomarkers and provide helpful clues for pathogenesis, early diagnosis, and progression of lung SqCC. The specific tumor cells were isolated and collected from the tissues of six patients with lung SqCC by laser capture microdissection (LCM). Total proteins from the LCM cells were extracted, digested with trypsin. The sequence information of resulting peptides was acquired by high-performance liquid chromatography (HPLC) and tandem mass spectrometry (TMS). The global protein profiles of lung SqCC cell were identified with BioworksTM software in IPI human protein database. Cellular component, molecular function, and biological process of the all proteins were analyzed using gene ontology (GO). About 720,000 tumor cells were satisfactorily collected from tissues of six patients with lung SqCC by LCM and the homogeneities of cell population were estimated to be over 95% as determined by microscopic visualization. The high resolution profiles including HPLC, full mass spectrum, and tandem mass spectrum were successfully obtained. Database searching of the resulting bimolecular sequence information identified 1982 proteins in all samples. The bioinformatics of these proteins, including amino acids sequence, fraction of coverage, molecular weight, isoelectric point, etc., were analyzed in detail. Among them, the function of most proteins was recognized by using GO. Five candidate proteins, Prohibitin (PHB), Mitogen-activated protein kinase (MAPK), Heat shock protein27 (HSP27), Annexin A1(ANXA1), and High mobility group protein B1 (HMGB1), might play an important role in SqCC genesis, progression, recurrence, and metastasis according to relative literatures. We have successfully isolated the interesting cells and effectively solved the heterogeneous problem of lung SqCC using LCM. The globally expressional proteins of lung SqCC cell were identified by shot-gun proteomics strategy. The five proteins might be hopefully used as markers of lung SqCC.
Long non-coding RNAs (lncRNAs) can act as carcinogenic or cancer suppressive factors during the pathogenesis, invasion and metastasis of non-small cell lung cancer (NSCLC). The current study explored the role of long intergenic non-protein coding RNA 00887 (LINC00887) and competing endogenous RNAs (ceRNAs). It was revealed that LINC00887 interacts with several microRNAs (miRs), which regulates downstream genes such as fibronectin 1, MET proto-oncogene, receptor tyrosine kinase and mothers against decapentaplegic homolog 4, which are associated with the spread of lung cancer. The experimental results also suggested that LINC00887 can stimulate miR-613, miR-206 and miR-1-2 to become competing endogenous RNAs, which may regulate the epithelial-mesenchymal transition of NSCLC cells through the transforming growth factor-â signal transduction pathway, and therefore promote the migration of cells and the acquisition of stem cell characteristics. Therefore, it can be concluded that high levels of LINC00887 can accelerate the malignant transformation ability of NSCLC cells.
Lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) are the two major subtypes of non-small-cell lung cancer (NSCLC). This study aimed to compare mRNA and circRNA expression patterns between LUSC and LUAD. Cancer tissues from 8 LUSC patients and 12 LUAD patients were collected to obtain mRNA and circRNA expression profiles. The differentially expressed mRNAs (DEmRNAs) and circRNAs (DE-circRNAs) between LUSC and LUAD were screened. Afterwards, miRNA-DEcircRNA pairs and miRNA-DEmRNA pairs were predicted to construct a competing endogenous RNAs (ceRNAs) network, followed by functional enrichment analysis and survival analysis. In total, 635 DEmRNAs and 245 DEcircRNAs were obtained. The ceRNA analysis revealed that genes, such as EPHA2, EPHA7, NTRK2, CDK6, hsa_circ_027570, hsa_circ_006089, and hsa-circ_035997, had distinct expression patterns between LUSC and LUAD. Also, functional enrichment analysis indicated that DEmRNAs were mainly enriched in ERK1 and ERK2 cascade. Survival analyses suggested that STXBP1 and PMEPA1 were associated the prognosis of with both LUAD and LUSC, whereas EPHA2 and CDK6 might serve as prognostic factors for LUSC and LUAD, respectively. In conclusion, genes such as EPHA2, EPHA7, NTRK2, and CDK6 had different patterns in the two major histological subtypes of NSCLC. Notably, EPHA2 and CDK6 might be considered as potential therapeutic targets for LUSC and LUAD, respectively.
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