Integrative Analysis of CD133 mRNA in Human Cancers Based on Data Mining

Wen, Gui-Min; Mou, Fei-Fei; Hou, Wei; Wang, Dan; Pu, Xia

doi:10.1007/s12015-018-9865-2

Cited by 7 publications

(4 citation statements)

References 70 publications

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“…With bioinformatics technology being introduced into medical molecular biology [ 49 ], the scope of basic research can be expanded, and the prediction of important biomarkers can be more convenient and accurate. Furthermore, it's through the bioinformatics methods that comprehensive exploration and analysis of mRNA data sets [ 50 ], miRNA data sets [ 51 ], and lncRNA data sets [ 52 ] in different databases can be conducted, which eventually improves the accuracy of differentially expressed genes determination. This study screened three genes with research values from 919 DEGs.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of Pseudogenes/lncRNA-Hsa-miR-1-3p-PAICS Pathway Promotes the Development of NSCLC

Song

Wang

et al. 2022

Journal of Oncology

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Objective. Non-small cell lung cancer (NSCLC) explains about 80 percent of whole lung cancers, and its 5-year survival rate is impoverished, as when people are first diagnosed, 68% of whom are identified at a dangerous stage. The molecular mechanisms of NSCLC are still being explored. Methods. GSE18842 and GSE19804 were exerted to scan for diversely expressed genes (DEGs) in NSCLC, and then we used GEPIA for the validation of DEGs expression. The prognostic values were determined through Kaplan–Meier analysis. Three target prediction databases indicated potential microRNAs (miRNAs), while miRNet predicted hsa-miR-1-3p′s upstream long non-coding RNAs (lncRNAs) and pseudogenes. UALCAN was utilized to identify the co-expressed genes of PAICS, while enrichment analysis on them was managed with Enrichr. Results. We initially found that the gene expression level of cyclin B1 (CCNB1), cyclin-dependent kinases1 (CDK1), and phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS) had a notable increase in NSCLC. We predicted 6, 10, and 7 microRNAs to target CCNB1, CDK1, and PAICS, respectively. Among miRNA-mRNA (microRNA-messenger RNA) pairs, we deduced that the hsa-miR-1-PAICS axis was the most potential one to inhibit the occurrence of NSCLC. We also noted that the hsa-miR-1-3p-PAICS axis participated in regulating the process of mitosis with mechanical functions. Moreover, we identified 5 pseudogenes and 33 long non-coding RNAs (lncRNAs) that might inhibit the hsa-miR-1-3p-PAICS axis in NSCLC. Conclusions. The pseudogene/lncRNA-hsa-miR-1-3p-PAICS is very important in NSCLC on the basis of this study, thus providing us with effective treatments and promising biomarkers for the diagnosis of NSCLC.

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Section: Discussionmentioning

confidence: 99%

Dysregulation of Pseudogenes/lncRNA-Hsa-miR-1-3p-PAICS Pathway Promotes the Development of NSCLC

Song

Wang

et al. 2022

Journal of Oncology

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“…Our findings also revealed that non-expression of CD133 was associated with a poor degree of histological differentiation, progression to the disease, distant metastasis ( Figure 11 ), and a low OS ( Figure 12 a). Wen and coworkers determined that high CD133 mRNA levels were related to a better survival rate in lung cancer [ 115 ]. Different studies concluded that there was no relationship between CD133 expression and prognosis in NSCLC patients [ 116 , 117 ].…”

Section: Discussionmentioning

confidence: 99%

Polycaprolactone Electrospun Scaffolds Produce an Enrichment of Lung Cancer Stem Cells in Sensitive and Resistant EGFRm Lung Adenocarcinoma

Polonio‐Alcalá

Rabionet

Ruiz‐Martínez

et al. 2021

Cancers

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The establishment of a three-dimensional (3D) cell culture model for lung cancer stem cells (LCSCs) is needed because the study of these stem cells is unable to be done using flat surfaces. The study of LCSCs is fundamental due to their key role in drug resistance, tumor recurrence, and metastasis. Hence, the purpose of this work is the evaluation of polycaprolactone electrospun (PCL-ES) scaffolds for culturing LCSCs in sensitive and resistant EGFR-mutated (EGFRm) lung adenocarcinoma cell models. We performed a thermal, physical, and biological characterization of 10% and 15%-PCL-ES structures. Several genes and proteins associated with LCSC features were analyzed by RT-qPCR and Western blot. Vimentin and CD133 tumor expression were evaluated in samples from 36 patients with EGFRm non-small cell lung cancer through immunohistochemistry. Our findings revealed that PC9 and PC9-GR3 models cultured on PCL-ES scaffolds showed higher resistance to osimertinib, upregulation of ABCB1, Vimentin, Snail, Twist, Sox2, Oct-4, and CD166, downregulation of E-cadherin and CD133, and the activation of Hedgehog pathway. Additionally, we determined that the non-expression of CD133 was significantly associated with a low degree of histological differentiation, disease progression, and distant metastasis. To sum up, we confirmed PCL-ES scaffolds as a suitable 3D cell culture model for the study of the LCSC niche.

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“…As we know, CSCs are responsible for tumor initiation and propagation, which also plays a vital role in predicting prognosis in cancer patients, high levels of CSCs lead to poor prognosis and targetting CSCs results in prolonged survival [6,38,39]. Tumor sphere culture in low-adherent plate is one of the enrich methods for CSCs, while CD133+ cells are defined as pancreatic CSCs [40]. Thus, in our study, the data showed that QYHJ significantly reduced the tumor sphere forming and decreased the number of CD133+ cells, which also promoted the inhibition effect of GEM.…”

Section: Discussionmentioning

confidence: 99%

Qingyihuaji formula reverses gemcitabine resistant human pancreatic cancer through regulate lncRNA AB209630/miR-373/EphB2-NANOG signals

Chen

Wang

2019

Bioscience Reports

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To investigate the possible mechanism of Qingyihuaji formula (QYHJ) for reversing gemcitabine (GEM) resistant human pancreatic cancer. Cell proliferation, apoptosis, migration and invasion were detected in CFPAC-1 cells. Xenograft mice established with CFPAC-1 through subcutaneous on 33 immunodeficient nude mice and randomly divided into four groups: vehicle, GEM (35 mg/kg), QYHJ (40 g/kg), and GEM + QYHJ (35 mg/kg + 40 g/kg) groups for 28-day treatment. Tumor growth and the mRNA expression of lncRNA AB209630, miR373, EphB2, and NANOG evaluated in dissected tumor tissue by real-time PCR, the CD133+ cancer stem cells were isolated by flow cytometer, and the changes of the tumor sphere forming were measured. QYHJ, especially the combination of GEM and QYHJ, was significantly inhibited the cell proliferation and migration of CFPAC-1 in vitro in the indicated times. The combination of GEM and QYHJ also remarkably promoted the cell apoptosis of CFPAC-1. QYHJ treatment effectively blocked the tumor growth in nude mice. QYHJ, especially GEM + QYHJ treatment, was significantly increased the mRNA expression of lncRNA AB209630, significantly decreased the mRNA levels of miR373, EphB2 and NANOG, and markedly reduced the tumor sphere formation and the numbers of CD133+ stem cells. In addition, GEM alone treatment had no significant effect in the above biomarker changes. QYHJ could effectivly enhance the antihuman pancreatic tumor activity of GEM, which may be through inhibiting pancreatic cancer stem cell differentiation by lncRNA AB209630/miR-373/EphB2-NANOG signaling pathway.

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Integrative Analysis of CD133 mRNA in Human Cancers Based on Data Mining

Cited by 7 publications

References 70 publications

Dysregulation of Pseudogenes/lncRNA-Hsa-miR-1-3p-PAICS Pathway Promotes the Development of NSCLC

Dysregulation of Pseudogenes/lncRNA-Hsa-miR-1-3p-PAICS Pathway Promotes the Development of NSCLC

Polycaprolactone Electrospun Scaffolds Produce an Enrichment of Lung Cancer Stem Cells in Sensitive and Resistant EGFRm Lung Adenocarcinoma

Qingyihuaji formula reverses gemcitabine resistant human pancreatic cancer through regulate lncRNA AB209630/miR-373/EphB2-NANOG signals

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