Molecular profiles of non-small cell lung cancers in cigarette smoking and never-smoking patients

Szymanowska-Narloch, Amelia; Jassem, Ewa; Skrzypski, Marcin; Muley, Thomas; Meister, Michael; Dienemann, Hendrik; Tarón, Miquel; Rosell, Rafael; Rzepko, Robert; Jarząb, Michał; Marjański, Tomasz; Pawłowski, Ryszard; Rzyman, Witold; Jassem, Jacek

doi:10.2478/ams-2013-0025

Cited by 24 publications

(19 citation statements)

References 49 publications

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“…Moreover, DLG1 deficiency results in incorrect spindle polarity and a delay in cells transiting orientation [78], which disrupts cellular structure and distribution [82]. Interestingly, DLG1 protein levels are significantly lower in NSCLC and hepatocellular carcinoma (HCC) than in the corresponding normal tissues [83,84], but are nearly undetectable in poorly differentiated stages of colon adenocarcinoma [85], in contrast to our findings and the existing literature. One possible reason is that DLG1 dysregulation in advanced tumor progression or in more malignant forms depends on its spatial/temporal distribution.…”

Section: Discussioncontrasting

confidence: 88%

Downregulation of hsa-microRNA-204-5p and identification of its potential regulatory network in non-small cell lung cancer: RT-qPCR, bioinformatic- and meta-analyses

Liang

Gan

et al. 2020

Respir Res

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Background: Pulmonary malignant neoplasms have a high worldwide morbidity and mortality, so the study of these malignancies using microRNAs (miRNAs) has attracted great interest and enthusiasm. The aim of this study was to determine the clinical effect of hsa-microRNA-204-5p (miR-204-5p) and its underlying molecular mechanisms in non-small cell lung cancer (NSCLC). Methods: Expression of miR-204-5p was investigated by real-time quantitative PCR (RT-qPCR). After data mining from public online repositories, several integrative assessment methods, including receiver operating characteristic (ROC) curves, hazard ratios (HR) with 95% confidence intervals (95% CI), and comprehensive meta-analyses, were conducted to explore the expression and clinical utility of miR-204-5p. The potential objects regulated and controlled by miR-204-5p in the course of NSCLC were identified by estimated target prediction and analysis. The regulatory network of miR-204-5p, with its target genes and transcription factors (TFs), was structured from database evidence and literature references. Results: The expression of miR-204-5p was downregulated in NSCLC, and the downtrend was related to gender, histological type, vascular invasion, tumor size, clinicopathologic grade and lymph node metastasis (P<0.05). MiR-204-5p was useful in prognosis, but was deemed unsuitable at present as an auxiliary diagnostic or prognostic risk factor for NSCLC due to the lack of statistical significance in meta-analyses and absence of large-scale investigations. Gene enrichment and annotation analyses identified miR-204-5p candidate targets that took part in various genetic activities and biological functions. The predicted TFs, like MAX, MYC, and RUNX1, interfered in regulatory networks involving miR-204-5p and its predicted hub genes, though a modulatory loop or axis of the miRNA-TF-gene that was out of range with shortage in database prediction, experimental proof and literature confirmation. Conclusions: The frequently observed decrease in miR-204-5p was helpful for NSCLC diagnosis. The estimated target genes and TFs contributed to the anti-oncogene effects of miR-204-5p.

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Section: Discussioncontrasting

confidence: 88%

Downregulation of hsa-microRNA-204-5p and identification of its potential regulatory network in non-small cell lung cancer: RT-qPCR, bioinformatic- and meta-analyses

Liang

Gan

et al. 2020

Respir Res

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“…DLG1 expression was also analyzed in lung, larynx, breast and, more recently, in hepatocellular cancers. In all cases, a clear downregulation of its levels was found in late stages of malignancy (Fuja et al, 2004;Byeon et al, 2011;Szymanowska-Narloch et al, 2013;Wu et al, 2016). Moreover, in some of these reports, DLG1 upregulation and loss from cell borders were also observed, as well as mislocalization in intermediate lesions.…”

Section: Epithelial Cancer Progressionmentioning

confidence: 79%

Differential expression of DLG1 as a common trait in different human diseases: an encouraging issue in molecular pathology

Marziali

Dizanzo

Cavatorta

et al. 2019

Biological Chemistry

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Human disc large (DLG1) is a scaffolding protein that through the interaction with diverse cell partners participates in the control of key cellular processes such as polarity, proliferation and migration. Experimental data have mainly identified DLG1 as a tumor suppressor. An outstanding point for DLG1 protein is that altered DLG1 expression andDLG1gene mutations were observed in different pathologies, including cancer and neurological and immunological disorders. Evident changes in DLG1 abundance and/or cell localization were identified in a number of studies suggesting its participation in molecular mechanisms responsible for the development of such illnesses. In this review, we focus on some of the latest findings regarding DLG1 alterations in different diseases as well as its potential use as a biomarker for pathological progression. We further address the current knowledge on the molecular mechanisms regulating DLG1 expression and the posttranslational modifications that may affect DLG1 cell localization and functions. Despite the advances in this field, there are still open questions about the precise molecular link between alterations in DLG1 expression and the development of each specific pathology. The complete understanding of this concern will give us new scenarios for the design of promising diagnosis and therapeutic tools.

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“…Aldo-keto reductase family 1, member B10 (AKR1B10), is primarily expressed in human colon and small intestine but overexpressed in breast cancer, hepatocellular carcinoma, non-small cell lung carcinoma, cervical and endometrial cancers [2–9]. Our previous studies have shown that AKR1B10 is secreted through a lysosome-mediated non-classical pathway, which leads to the increase of AKR1B10 in the serum of breast cancer patients.…”

Section: Introductionmentioning

confidence: 99%

AKR1B10 promotes breast cancer cell migration and invasion via activation of ERK signaling

Guo

Duan

et al. 2017

Oncotarget

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BackgroundAldo-keto reductase family 1, member B10 (AKR1B10), is known to be significantly induced in the cells of various cancers such as breast cancer. However, the mechanisms of AKR1B10 promoting tumorigenesis in breast cancer remain unclear. In the present study, we demonstrated the potential role and mechanism of AKR1B10 in the invasion and migration of breast cancer cells.MethodsThe expression level of AKR1B10 in breast carcinoma, para-carcinoma and cancer tissues were detected by immunohistochemical evaluation and real-time polymerase chain reaction (RT-PCR), and the correlationships between AKR1B10 expression and clinicopathological features in breast cancer patients (n=131) were investigated. AKR1B10 was ectopically expressed in MCF-7 cells or silenced in BT-20 cells. The roles of AKR1B10 expression in the migration and invasion of MCF-7 cells and BT-20 cells were explored by wound healing assay, transwell migration assay and transwell matrigel invasion assay, and finally the activation level of extracellular signal-regulated kinase 1/2 (EKR1/2) activation and the expression level of matrix metalloproteinase-2 (MMP2) and vimentin in MCF-7 and BT-20 cells were measured by western blot.ResultsWe found that AKR1B10 expression was increased in malignant tissues, which was correlated positively with tumor size, lymph node metastasis (p<0.05). MCF-7/AKR1B10 cells displayed a higher ability of migration (43.57±1.04%) compared with MCF-7/vector cells (29.12±1.34%) in wound healing assay, and the migrated cell number of MCF-7/AKR1B10 was more (418.43±9.62) than that of MCF-7/vector (222.43±17.75) in transwell migration assay without matrigel. We furtherly confirmed MCF-7/AKR1B10 cells invaded faster compared with MCF-7/vector cells by transwell matrigel invasion assay. Finally, we found AKR1B10 induced the migration and invasion of MCF-7 and BT-20 cells by activating EKR signaling, which promoted the expressions of MMP2 and vimentin. PD98059, a specific inhibitor of the activation of MEK, blocked the migration and invasion by inhibiting the expression of MMP2 and vimentin.ConclusionsAKR1B10 is overexpressed in breast cancer, and promotes the migration and invasion of MCF-7 and BT-20 cells by activating ERK signaling pathway.

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Molecular profiles of non-small cell lung cancers in cigarette smoking and never-smoking patients

Cited by 24 publications

References 49 publications

Downregulation of hsa-microRNA-204-5p and identification of its potential regulatory network in non-small cell lung cancer: RT-qPCR, bioinformatic- and meta-analyses

Downregulation of hsa-microRNA-204-5p and identification of its potential regulatory network in non-small cell lung cancer: RT-qPCR, bioinformatic- and meta-analyses

Differential expression of DLG1 as a common trait in different human diseases: an encouraging issue in molecular pathology

AKR1B10 promotes breast cancer cell migration and invasion via activation of ERK signaling

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