A novel lncRNA, loc107985872, promotes lung adenocarcinoma progression via the notch1 signaling pathway with exposure to traffic-originated PM2.5 organic extract

Guo, Huaqi; Feng, Yuanming; Yu, Hengyi; Xie, Yichun; Luo, Fei; Wang, Yan

doi:10.1016/j.envpol.2020.115307

Cited by 21 publications

(15 citation statements)

References 55 publications

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“…Besides, PSEN1/γ-secretase complex is conducive to the processing of P-cadherin, N-cadherin, and E-cadherin, thus modulating cell movement and invasion (Li et al, 2016). The result that PSEN1 fosters cancer cell EMT was also confirmed in gastric cancer and lung adenocarcinoma (Guo et al, 2020;Pan et al, 2021). Hence, we speculated that PSEN1 could modulate SNSCC cell EMT and verified the promotion effect by assessing expression of EMT-related proteins in multiple cotransfection groups, whereas miR-654-3p could modulate PSEN1 to hamper SNSCC cell EMT, which was in accord with earlier studies.…”

Section: Discussionmentioning

confidence: 83%

MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis

2022

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Background: MiR-654-3p can repress malignant progression of cancer cells, whereas no relative reports were about its modulatory mechanism in sinonasal squamous cell carcinoma (SNSCC). This research committed to approaching modulatory effect of miR-654-3p on SNSCC cells.Methods: Bioinformatics methods were utilized for analyzing interaction of miR-654-3p/cAMP-responsive element binding protein 1 (CREB1)/presenilin-1 (PSEN1). Expression levels of miR-654-3p, CREB1, and PSEN1 mRNA were assessed by quantitative real-time polymerase chain reaction. Western blot was completed for level assessment of CREB1, PSEN1, and epithelial–mesenchymal transition–related proteins. The targeted relationship between miR-654-3p and CREB1, or CREB1 and PSEN1 was authenticated via dual-luciferase assay and ChIP assay. A trail of experiments in vitro was used for detection of the effects of miR-654-3p/CREB1/PSEN1 axis on malignant progression of SNSCC cells.Results: CREB1 as the downstream target mRNA of miR-654-3p could activate transcription of its downstream target gene PSEN1. Besides, miR-654-3p could target CREB1 to repress PSEN1 expression, thus restraining proliferation, migration, invasion, epithelial–mesenchymal transition, and hastening apoptosis of SNSCC cells.Conclusion: MiR-654-3p as an antitumor gene targeted CREB1 to hamper malignant progression of SNSCC through miR-654-3p/CREB1/PSEN1 axis.

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Section: Discussionmentioning

confidence: 83%

MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis

2022

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“…The sampling lter membranes were taken out from the sampler after collecting PM 2.5 for 5 to 7 days, balanced in the dryer for 24 hours, wrapped in tin foil and stored at -20℃. The extraction method of Po has been demonstrated in our previous articles (Guo et al 2020, Wei et al 2016). Finally, the Po extract was dissolved in dimethyl sulfoxide in 400 µg/ml and stored at -20°C.…”

Section: Methodsmentioning

confidence: 92%

The Role of Estrogen Receptor β in PM2.5 Organic Extract-Induced Pulmonary Inflammation in Female and Male Mice

Guo

Feng

et al. 2022

Preprint

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Automobile exhaust is one of the main sources of PM2.5 in urban areas, and traffic-originated PM2.5 organic extract (Po) can promote inflammation in different organs, especially in the lung. In addition, sex differences were reported in many inflammatory diseases, but the triggering factors of sex differences in inflammatory responses are still unclear. In this study, we investigated the effects of Po exposure on pulmonary inflammatory responses and evaluated the role of sex in this process. Mice were exposed to 100 µg/m3 Po for 12 weeks by an inhalation exposure system in a polycarbonate chamber. In Po-exposed mice, the lung histopathological analysis shown obvious inflammation, the cell numbers in bronchoalveolar lavage fluid (BALF) were significantly increased, and most inflammatory cytokines in BALF were upregulated. Factorial analysis of variance was carried out to investigate the interaction between sex and Po exposure in these effects. The results shown that the increase of inflammatory cell numbers and the fluctuation of cytokine levels (TNF-α, IL-5, and GRO/KC) in BALF induced by Po were significantly different between female and male mice. Notably, these differences were diminished while Po-exposed mice were injected with PHTPP, an ERβ antagonist (1 mg/kg, i.p.). We hypothesized that Po-induced inflammatory responses were different between female and male mice, and ERβ was involved in these processes. To our knowledge, this is the first investigation about the role of sex in Po-induced adverse effects. This study provided a theoretical basis for understanding the sex differences in the adverse effects of environmental pollutants.

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“…PSEN1 is a recognized gene associated with Alzheimer's disease, which can induce the intramembrane division of Notch receptors and then activate Notch signaling pathways. A study shows that its abnormal expression may activate downstream Notch1 signaling pathways and be related to the development of lung cancer [22][23][24] .…”

Section: Discussionmentioning

confidence: 99%

Identification and Validation of a Novel Prognostic Model of Inflammation-related Gene Signature of Lung Adenocarcinoma

Luo

Wang

et al. 2022

Preprint

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Previous literatures have suggested the importance of inflammatory response during lung adenocarcinoma (LUAD) development. This study aimed at exploring the inflammation-related genes and developing a prognostic signature for predicting the prognosis of LUAD. Survival‑associated inflammation-related genes were identified by univariate Cox regression analysis in the dataset of The Cancer Genome Atlas (TCGA). The least absolute shrinkage and selection operator (LASSO) penalized COX regression model was used to derive a risk signature and divide samples into high-, medium- and low- risk group. Univariate and multivariate analyses suggested that the level of risk group was an independent prognostic factor of survival. Time-dependent receiver operating characteristic (ROC) curve indicated the AUC of 1-, 3- and 5- years of the risk signature was 0.715, 0.719, 0.699 respectively. A prognostic nomogram was constructed by integrating risk group and clinical features. The independent dataset GSE30129 of Gene Expression Omnibus (GEO) was used for verification. Furthermore, we performed Gene set enrichment analysis(GSEA) and discussed the differences in tumor mutation, tumor microenvironment among risk groups. Single Sample Gene Set Enrichment Analysis (ssGSEA) and CIBERSORT results suggested the status of immune cell infiltration was highly associated with risk groups. In a cohort of LUAD from The Cancer Immunome Atlas(TCIA) that predicted immune responses to CTLA-4 and PD-1/PD-L1 inhibitors, immunotherapy performed better in the low-risk group. Partial targeted drugs and chemotherapy drugs for lung cancer had higher drug sensitivity in the high-risk group. The level of risk group can provide some reference significance for the selection of immunotherapy and drug regimen for LUAD patients.

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A novel lncRNA, loc107985872, promotes lung adenocarcinoma progression via the notch1 signaling pathway with exposure to traffic-originated PM2.5 organic extract

Cited by 21 publications

References 55 publications

MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis

MiR-654-3p Constrains Proliferation, Invasion, and Migration of Sinonasal Squamous Cell Carcinoma via CREB1/PSEN1 Regulatory Axis

The Role of Estrogen Receptor β in PM2.5 Organic Extract-Induced Pulmonary Inflammation in Female and Male Mice

Identification and Validation of a Novel Prognostic Model of Inflammation-related Gene Signature of Lung Adenocarcinoma

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