<i>Retracted</i>: MicroRNA‐103 confers the resistance to long‐treatment of adriamycin to human leukemia cells by regulation of COP1

Wan, Lin; Tian, Yanlong; Zhang, Rui; Peng, Zhuo; Sun, Jiangli; Zhang, Wanggang

doi:10.1002/jcb.26431

Cited by 22 publications

(11 citation statements)

References 32 publications

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“…WNT/β-catenin, RAS/ERK/ MAPK, JAK/STAT, NOTCH), we believe ncRNA may also play a role in the resistance of PI3K inhibitors [194][195][196][197][198][199]. Not surprisingly, more and more researches have suggested that deviant ncRNA expression is powerfully concerned about tumor drug resistance [200][201][202][203][204][205][206][207][208]. Recent studies have indicated potential mechanism of acquired resistance to dual PI3K/mTOR inhibitors, including elevated glycolysis accompanied with depletion of mitochondrial DNA, and upregulated DNA methyltransferases which Reduce PTEN and PPP2R2B expression [209,210].…”

Section: Resistancesmentioning

confidence: 99%

Targeting PI3K in cancer: mechanisms and advances in clinical trials

et al. 2019

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Phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling is one of the most important intracellular pathways, which can be considered as a master regulator for cancer. Enormous efforts have been dedicated to the development of drugs targeting PI3K signaling, many of which are currently employed in clinical trials evaluation, and it is becoming increasingly clear that PI3K inhibitors are effective in inhibiting tumor progression. PI3K inhibitors are subdivided into dual PI3K/mTOR inhibitors, pan-PI3K inhibitors and isoform-specific inhibitors. In this review, we performed a critical review to summarize the role of the PI3K pathway in tumor development, recent PI3K inhibitors development based on clinical trials, and the mechanisms of resistance to PI3K inhibition.

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Section: Resistancesmentioning

confidence: 99%

Targeting PI3K in cancer: mechanisms and advances in clinical trials

et al. 2019

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“…Secondly, PTEN plays critical roles in regulating not only hematopoietic stem cell activity through a Niche-dependent mechanism, but also hematopoiesis and leukemogenesis [341][342][343]. Furthermore, TAL1, c-Jun, EZH2, TRIM22, ETV6/RUNX1, miR-7, -22, -26b, -103, -125b, -126, -139-5p, -181c, -193a, -628, and -3142, as well as LncRNA HULC, UCA1, linc00239 and LINC00265 control leukemogenesis, proliferation, apoptosis or chemoresistance via PI3K/AKT pathway [344][345][346][347][348][349][350][351][352][353][354][355][356][357][358][359][360][361][362][363]. Hereafter, PI3K/AKT pathway inhibition is regarded as a therapeutic approach [364,365] followed by the preclinical studies in leukemia cells [366,367] in spite of the upregulated expression of P2RY14 in acute leukemia cells resistant to PI3K/ mTOR inhibition [368].…”

Section: (Nct01002248; Nct01476137; Nct00881946) (Tables 2 and 3)mentioning

confidence: 99%

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

et al. 2020

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Given that the PI3K/AKT pathway has manifested its compelling influence on multiple cellular process, we further review the roles of hyperactivation of PI3K/AKT pathway in various human cancers. We state the abnormalities of PI3K/AKT pathway in different cancers, which are closely related with tumorigenesis, proliferation, growth, apoptosis, invasion, metastasis, epithelial-mesenchymal transition, stem-like phenotype, immune microenvironment and drug resistance of cancer cells. In addition, we investigated the current clinical trials of inhibitors against PI3K/AKT pathway in cancers and found that the clinical efficacy of these inhibitors as monotherapy has so far been limited despite of the promising preclinical activity, which means combinations of targeted therapy may achieve better efficacies in cancers. In short, we hope to feature PI3K/ AKT pathway in cancers to the clinic and bring the new promising to patients for targeted therapies.

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“…Upregulation of miR-103 was found by Yefenof et al, to sensitize leukemia cells to glucocorticoids ( 50 ). However, a study by Zhang et al, showed that miR-103 is upregulated in adriamycin-resistant cells ( 51 ). miR-486-3p could act as a tumor-suppressive miRNA in several cancers ( 52 – 54 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of Early Recurrence Factors in Childhood and Adolescent B-Cell Acute Lymphoblastic Leukemia Based on Integrated Bioinformatics Analysis

Huang

Chen

et al. 2020

Front. Oncol.

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Over the past 50 years, great progress has been made in the diagnosis and treatment of acute lymphoblastic leukemia (ALL), especially in pediatric patients. However, early recurrence is still an important threat to the survival of patients. In this study, we used integrated bioinformatics analysis to look for biomarkers of early recurrence of B-cell ALL (B-ALL) in childhood and adolescent patients. Firstly, we obtained gene expression profiles from the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database and the Gene Expression Omnibus (GEO) database. Then, we identified differentially expressed genes (DEGs) based on whether the disease relapsed early. LASSO and Cox regression analysis were applied to identify a subset of four genes: HOXA7, S100A11 , S100A10, and IFI44L. A genetic risk score model was constructed based on these four optimal prognostic genes. Time-dependent receiver operating characteristic (ROC) curves were used to evaluate the predictive value of this prognostic model (3-, 5-, and 10-year AUC values >0.7). The risk model was significantly associated with overall survival (OS) and event-free survival in B-ALL (all p < 0.0001). In addition, a high risk score was an independent poor prognostic risk factor for OS ( p < 0.001; HR = 3.396; 95% CI: 2.387–4.832). Finally, the genetic risk model was successfully tested in B-ALL using an external validation set. The results suggested that this model could be a novel predictive tool for early recurrence and prognosis of B-ALL.

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Retracted: MicroRNA‐103 confers the resistance to long‐treatment of adriamycin to human leukemia cells by regulation of COP1

Cited by 22 publications

References 32 publications

Targeting PI3K in cancer: mechanisms and advances in clinical trials

Targeting PI3K in cancer: mechanisms and advances in clinical trials

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

Identification of Early Recurrence Factors in Childhood and Adolescent B-Cell Acute Lymphoblastic Leukemia Based on Integrated Bioinformatics Analysis

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