[Retracted] Studying the Role and Molecular Mechanisms of MAP4K3 in Sorafenib Resistance of Hepatocellular Carcinoma

Shi, Yi; Mo, Xiaofei; Hong, Simei; Li, Tianbao; Chen, Baozhen; Chen, Gang

doi:10.1155/2020/4965670

Cited by 5 publications

(4 citation statements)

References 21 publications

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“…E2 binds to its acceptor ER, and proto-oncogene tyrosine-protein kinase Src (c-Src) is phosphorylated by ER, and subsequent c-Src activates Ras. Activated Ras regulates the ERK pathway, in turn triggering kinase activity of proteins Raf, MEK, and ERK [ 47 – 49 ]. E2-stimulated ERK promotes RNA transcription of the Fra1 gene and phosphorylation of Fra1 protein, which in turn inducted ZEB1/2.…”

Section: Molecular Mechanismmentioning

confidence: 99%

A Systematic Review of Lymphangioleiomyomatosis on Diagnosis and Molecular Mechanism

Dong

Jin

Wang³

et al. 2021

BioMed Research International

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Objective. Lymphangioleiomyomatosis (LAM) is a rare low-grade metastatic tumor; however, LAM patients were always found in young age with difficulty for diagnosis. Our study is aimed at observing the clinical characteristics of patients with lymphangiomatosis, including the clinical manifestations, imaging findings, histopathological features, and immunophenotype. Methods. We did a systematic review on LAM/PLAM cases, especially on male cases, and collected the clinical features and molecular mechanisms of PLAM based on previous findings. Results. Diagnosis criteria were summarized by combining CT scans, MRI, immunohistochemistry results, and gene sequencing results for effectively distinguishing between PLAM and similar diseases. Moreover, our study illustrated the molecular mechanism of PLAM as well as the signaling pathway involved in the disease initials. In addition, a male case was reported with differential diagnosis on the clinical manifestations, microscopic features, immunophenotypes, and genotypes. Conclusion. Our review will definitely improve the understanding of diagnosis and treatment in PLAM cases.

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Section: Molecular Mechanismmentioning

confidence: 99%

A Systematic Review of Lymphangioleiomyomatosis on Diagnosis and Molecular Mechanism

Dong

Jin

Wang³

et al. 2021

BioMed Research International

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“…Patients with MGMT promoter methylation were more sensitive to temozolomide (TMZ) chemotherapy and had a better prognosis [ 10 ]. BRAF (v-raf murine viral oncogene homolog B1) mutations were found in pilocytic astrocytomas and have been proved to be a new therapeutic target for inhibition of the mitogen-activated protein kinase (MAPK) cascade, but its prognostic significance is unknown [ 11 ]. Vemurafenib, as a BRAF inhibitor, can have a complete clinical regression of relapsed glioblastoma multiforme [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Potential Drug Prediction of Glioblastoma Based on Drug Perturbation-Induced Gene Expression Signatures

Zhu

Mao

Man

2021

BioMed Research International

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Objectives. Glioblastoma (GBM) is a malignant brain tumor which is the most common and aggressive type of central nervous system cancer, with high morbidity and mortality. Despite lots of systematic studies on the molecular mechanism of glioblastoma, the pathogenesis is still unclear, and effective therapies are relatively rare with surgical resection as the frequently therapeutic intervention. Identification of fundamental molecules and gene networks associated with initiation is critical in glioblastoma drug discovery. In this study, an approach for the prediction of potential drug was developed based on perturbation-induced gene expression signatures. Methods. We first collected RNA-seq data of 12 pairs of glioblastoma samples and adjacent normal samples from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified by DESeq2, and coexpression networks were analyzed with weighted gene correlation network analysis (WGCNA). Furthermore, key driver genes were detected based on the differentially expressed genes and potential chemotherapeutic drugs and targeted drugs were found by correlating the gene expression profiles with drug perturbation database. Finally, RNA-seq data of glioblastoma from The Cancer Genome Atlas (TCGA) dataset was collected as an independent validation dataset to verify our findings. Results. We identified 1771 significantly DEGs with 446 upregulated genes and 1325 downregulated genes. A total of 24 key drivers were found in the upregulated gene set, and 81 key drivers were found in the downregulated gene set. We screened the Crowd Extracted Expression of Differential Signatures (CREEDS) database to identify drug perturbations that could reverse the key factors of glioblastoma, and a total of 354 drugs were obtained with p value < 10-10. Finally, 7 drugs that could turn down the expression of upregulated factors and 3 drugs that could reverse the expression of downregulated key factors were selected as potential glioblastoma drugs. In addition, similar results were obtained through the analysis of TCGA as independent dataset. Conclusions. In this study, we provided a framework of workflow for potential therapeutic drug discovery and predicted 10 potential drugs for glioblastoma therapy.

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“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Manipulated or compromised peer review …”

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confidence: 99%

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confidence: 99%