CHRNA7 inhibits cell invasion and metastasis of LoVo human colorectal cancer cells through PI3K/Akt signaling

Tao, Xiang; Feng, Yu; Fei, Rushan; Qian, Ji; Chen, Wenbin

doi:10.3892/or.2015.4462

Cited by 17 publications

(10 citation statements)

References 41 publications

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“…Liu et al reported that miR-596 could modulate melanoma growth via regulating cell survival and death 34 . Xiang et al found that CHRNA7 inhibited cell invasion and metastasis of LoVo human colorectal cancer cells by PI3K/Akt signaling 35 . Dai et al revealed that miR-424-5p promoted the proliferation and metastasis of colorectal cancer via directly targeting SCN4B 36 .Yuan et al identified a novel splice variant of AC3-33 (C3orf33) in breast cancer 37 .…”

Section: Discussionmentioning

confidence: 99%

Identification of a methylomics-associated nomogram for predicting overall survival of stage I–II lung adenocarcinoma

Wang

Wei

Pan

et al. 2021

Sci Rep

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The aim of this paper was to identify DNA methylation based biomarkers for predicting overall survival (OS) of stage I–II lung adenocarcinoma (LUAD) patients. Methylation profile data of patients with stage I–II LUAD from The Cancer Genome Atlas (TCGA) database was used to determine methylation sites-based hallmark for stage I–II LUAD patients’ OS. The patients were separated into training and validation datasets by using median risk score as cutoff. Univariate Cox, least absolute shrinkage and selection operator (LASSO) and multivariate Cox analyses were employed to develop a DNA methylation signature for OS of patients with stage I–II LUAD. As a result, an 11-DNA methylation signature was determined to be critically associated with the OS of patients with stage I–II LUAD. Analysis of receiver operating characteristics (ROC) suggested a high prognostic effectiveness of the 11-DNA methylation signature in patients with stage I–II LUAD (AUC at 1, 3, 5 years in training set were (0.849, 0.879, 0.831, respectively), validation set (0.742, 0.807, 0.904, respectively), entire TCGA dataset (0.747, 0.818, 0.870, respectively). Kaplan–Meier survival analyses exhibited that survival was significantly longer in the low-risk cohort compared to the high-risk cohort in the training dataset (P = 7e − 07), in the validation dataset (P = 1e − 08), and in the all-cohort dataset (P = 6e − 14). In addition, a nomogram was developed based on molecular factor (methylation risk score) as well as clinical factors (age and cancer status) (AUC at 1, 3, 5 years entire TCGA dataset were 0.770, 0.849, 0.979, respectively). The result verified that our methylomics-associated nomogram had a strong robustness for predicting stage I–II LUAD patients’ OS. Furthermore, the nomogram combined clinical and molecular factors to determine an individualized probability of recurrence for patients with stage I–II LUAD, which stood for a major advance in the field of personalized medicine for pulmonary oncology. Collectively, we successfully identified a DNA methylation biomarker and a DNA methylation-based nomogram to predict the OS of patients with stage I–II LUAD.

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Section: Discussionmentioning

confidence: 99%

Identification of a methylomics-associated nomogram for predicting overall survival of stage I–II lung adenocarcinoma

Wang

Wei

Pan

et al. 2021

Sci Rep

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“…In pathway enrichment analysis for DEGs was performed. Genes such as ALDOB (aldolase, fructose-bisphosphate B) [68], KHK (ketohexokinase) [69], CHRNA7 [70], GSTA3 [71], APOA1 [72], CEBPA (CCAAT enhancer binding protein alpha) [73], PCK1 [74], ATP1A1 [75], CLCA1 [76], EMB (embigin) [77], SLC22A18 [78], FUT5 [79] and ITLN1 [80] were linked with progression of various cancer types, but these genes might be identified with growth of NET. Polymorphic genes such as GSTA1 [81], GSTA2 [82], MGST1 [83], NAT2 [84], SULT1A2 [85], SULT2A1 [86], UGT1A6 [87], UGT2B15 [88], UGT2B17 [89], ABCC2 [90], FUT2 [91] and APOB (apolipoprotein B) [92] were liable for progression of various cancer types, but these polymorphic genes might be diagnosed with growth of NET.…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes and associated pathways in neuroendocrine tumors through bioinformatics analysis and predictions of small drug molecules

Devarbhavi

Vastrad²,

Tengli

et al. 2020

Preprint

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Neuroendocrine tumor (NET) is one of malignant cancer and is identified with high morbidity and mortality rates around the world. With indigent clinical outcomes, potential biomarkers for diagnosis, prognosis and drug target are crucial to explore. The aim of this study is to examine the gene expression module of NET and to identify potential diagnostic and prognostic biomarkers as well as to find out new drug target. The differentially expressed genes (DEGs) identified from GSE65286 dataset was used for pathway enrichment analyses and gene ontology (GO) enrichment analyses and protein - protein interaction (PPI) analysis and module analysis. Moreover, miRNAs and transcription factors (TFs) that regulated the up and down regulated genes were predicted. Furthermore, validation of hub genes was performed. Finally, molecular docking studies were performed. DEGs were identified, including 453 down regulated and 459 up regulated genes. Pathway and GO enrichment analysis revealed that DEGs were enriched in sucrose degradation, creatine biosynthesis, anion transport and modulation of chemical synaptic transmission. Important hub genes and target genes were identified through PPI network, modules, target gene - miRNA network and target gene - TF network. Finally, survival analyses, receiver operating characteristic (ROC) curve and RT-PCR validated the significant difference of ATP1A1, LGALS3, LDHA, SYK, VDR, OBSL1, KRT40, WWOX, NINL and PPP2R2B between metastatic NET and normal controls. In conclusion, the DEGs and hub genes with their regulatory elements identified in this study will help us understand the molecular mechanisms underlying NET and provide candidate targets for future research.

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“…Activation of nAChRs in non-neuronal cells elicits the non-ionic signaling events that regulate protein phosphorylation and dephosphorylation, which is a novel function of nAChR subunit proteins in non-excitable cells. Activation of α7nAChR can activate p38 MAPK, AKT, RAS/RAF/MEK/ERK and JAK2 ( 49 , 50 ). In the present study, we determined the expression of phosphorylated STAT3, NF-κB p65 and PI3K p85 in THP-derived macrophages with or without α7nAChR knockdown (TMa7 −/− and TM).…”

Section: Discussionmentioning

confidence: 99%

α7 nicotinic acetylcholine receptor in tumor-associated macrophages inhibits colorectal cancer metastasis through the JAK2/STAT3 signaling pathway

et al. 2017

Self Cite

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Considerable evidence has implied that α7 nicotinic receptor subtypes play an important role in chronic inflammatory and neuropathic pain signaling. The aim of the present study was to determine the role of endogenous α7nAChR signaling in tumor-associated macrophages (TAMs) in human colorectal cancer (CRC) metastasis and prognosis. α7nAChR expression in primary tumor cells and adjacent stroma cells especially in TAMs in 51 CRC patients was observed. Using a human monocyte THP-derived macrophages (TMs) with α7nAChR-siRNA knockdown (TMα7−/−) and a CRC cell Transwell co-culture model, the migration and invasion of two CRC cells, LoVo and SW620, were determined. Western blotting was carried out to investigate the expression of multiple molecules involved in the NF-κB, STAT3, PI3K signaling pathways in mimic TAMs, i.e., TMs exposed to in-direct LoVo cell stimulation. A nicotinic α7 receptor antagonist [α-bungarotoxin (α-Btx)] and three pharmaceutical inhibitors: AG490 (JAK2/STAT3 inhibitor), LY294002 (PI3K inhibitor) and Bay 11–7082 (NF-κB inhibitor) were applied to evaluate whether these signaling pathways were associated with the enhanced migration of CRC cells when co-cultured with α7nAChR knockdown TMs. The results revealed that the expression of α7nAChR in TAMs differed in patients. However, CRC patients who had a high incidence of hepatic metastasis showed no or low expression of α7nAChR in TAMs. TMs with α7nAChR-siRNA knockdown (TMα7−/−) significantly enhanced the migration and invasion of the two CRC cell lines LoVo and SW620. α7nAChR knockdown in TMs significantly downregulated phosphorylation of STAT3, PI3K p85 and NF-κB p65 after co-culturing with LoVo cells. Inhibition of JAK2/STAT3 prevented the TMα7−/−-enhanced migration of LoVo cells. α7nAChR expressed in TAMs in human CRC patients plays an important role in preventing metastasis and could be a prognostic marker in CRCs, which may be regulated by the JAK2/STAT3 signaling pathway.

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CHRNA7 inhibits cell invasion and metastasis of LoVo human colorectal cancer cells through PI3K/Akt signaling

Cited by 17 publications

References 41 publications

Identification of a methylomics-associated nomogram for predicting overall survival of stage I–II lung adenocarcinoma

Identification of a methylomics-associated nomogram for predicting overall survival of stage I–II lung adenocarcinoma

Identification of key genes and associated pathways in neuroendocrine tumors through bioinformatics analysis and predictions of small drug molecules

α7 nicotinic acetylcholine receptor in tumor-associated macrophages inhibits colorectal cancer metastasis through the JAK2/STAT3 signaling pathway

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