Increased expression of miR-221 is associated with shorter overall survival in T-cell acute lymphoid leukemia

Teixeira, Hamilton Luiz Gimenes; Lucena-Araújo, Antonio R.; Santos, Glenda Dias dos; Zanette, Dalila Lucíola; Scheucher, Priscila Santos; Oliveira, Luciana Correa Oliveira de; Dalmazzo, Leandro F.; Silva-Júnior, Wilson A.; Falcão, Roberto Passetto; Rego, Eduardo Magalhães

doi:10.1186/2162-3619-2-10

Cited by 51 publications

(49 citation statements)

References 30 publications

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“…Aberrant expression of miRs has been well described in human GC (Pan et al, 2013). Specifically, miR-221 has been confirmed to be upregulated and may act as an oncogene in many types of human malignancies (Gimenes-Teixeira et al, 2013;Sarkar et al, 2013;Ergun et al, 2014;Sun et al, 2014;Ye et al, 2014a). Liu et al (2012) reported that upregulation of miR-221 in GC correlated with aggressive clinicopathological features and shorter overall survival.…”

Section: Introductionmentioning

confidence: 99%

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

Zt¹,

Hy²,

Fang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Propofol is one of the extensively and commonly used intravenous anesthetic agents. The current study aimed to evaluate the effects of propofol on the behavior of human gastric cancer cells and the molecular mechanisms of this activity. The effects of propofol on SGC7901 and AGS cell proliferation, apoptosis, and invasion were detected by MTT assay, flow cytometric analysis, and matrigel invasion assay. Real-time polymerase chain reaction (PCR) was used to assess microRNA (miR)-221 expression. miR-221 mimics were transfected into SGC7901 and AGS cells to assess the role of miR-221 in propofol-induced anti-tumor activity. Propofol significantly inhibited cell proliferation and invasion and promoted apoptosis of SGC7901 and AGS cells. Propofol also efficiently reduced miR-221 expression. Moreover, transfection of miR-221 mimics reversed the effects of propofol on the biological behavior of gastric cancer cells. Propofol can effectively inhibit proliferation and invasion and induce apoptosis of gastric cancer cells through, at least partly, downregulation of miR-221 expression.

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Section: Introductionmentioning

confidence: 99%

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

Zt¹,

Hy²,

Fang³

et al. 2015

Genet. Mol. Res.

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“…Importantly, miR-221 was identified as the most significantly modulated miRNA in the two PCa GEO datasets. MiR-221 is de-regulated in variety of cancers, primarily as an over-expressed miRNA [55]–[59].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Profiling in Prostate Cancer - The Diagnostic Potential of Urinary miR-205 and miR-214

et al. 2013

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Prostate cancer (PCa) is the most common type of cancer in men in the United States, which disproportionately affects African American descents. While metastasis is the most common cause of death among PCa patients, no specific markers have been assigned to severity and ethnic biasness of the disease. MicroRNAs represent a promising new class of biomarkers owing to their inherent stability and resilience. In the present study, we investigated potential miRNAs that can be used as biomarkers and/or therapeutic targets and can provide insight into the severity and ethnic biasness of PCa. PCR array was performed in FFPE PCa tissues (5 Caucasian American and 5 African American) and selected differentially expressed miRNAs were validated by qRT-PCR, in 40 (15 CA and 25 AA) paired PCa and adjacent normal tissues. Significantly deregulated miRNAs were also analyzed in urine samples to explore their potential as non-invasive biomarker for PCa. Out of 8 miRNAs selected for validation from PCR array data, miR-205 (p<0.0001), mir-214 (p<0.0001), miR-221(p<0.001) and miR-99b (p<0.0001) were significantly downregulated in PCa tissues. ROC curve shows that all four miRNAs successfully discriminated between PCa and adjacent normal tissues. MiR-99b showed significant down regulation (p<0.01) in AA PCa tissues as compared to CA PCa tissues and might be related to the aggressiveness associated with AA population. In urine, miR-205 (p<0.05) and miR-214 (p<0.05) were significantly downregulated in PCa patients and can discriminate PCa patients from healthy individuals with 89% sensitivity and 80% specificity. In conclusion, present study showed that miR-205 and miR-214 are downregulated in PCa and may serve as potential non-invasive molecular biomarker for PCa.

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“…Only a few studies have focused on the prognostic impact of epigenetic changes in pediatric T‐ALL, reporting, for example, that high levels of miR‐16 and miR‐221 are associated with shorter survival. This has, however, not been seen in all studies and, furthermore, these studies were based on quite a low number of patients, which often included both pediatric and adult patients, precluding any firm conclusions as to the prognostic role of miRs in childhood T‐ALL (Kaddar et al, ; Gimenes‐Teixeira et al, ; Xi et al, ). Data on promoters that are differentially methylated in T‐ALL have been applied to define CpG island methylator phenotypes, delineating cases as either hypermethylated or hypomethylated (Borssén et al, ), with hypomethylated cases having a significantly worse event‐free and overall survival in one of the studies (Borssén et al, ).…”

Section: Clinical Genetic and Epigenetic Features And Prognosismentioning

confidence: 99%

Pediatric T‐cell acute lymphoblastic leukemia

Karrman

Johansson

2016

Genes Chromosomes & Cancer

105

111

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The most common pediatric malignancy is acute lymphoblastic leukemia (ALL), of which T‐cell ALL (T‐ALL) comprises 10–15% of cases. T‐ALL arises in the thymus from an immature thymocyte as a consequence of a stepwise accumulation of genetic and epigenetic aberrations. Crucial biological processes, such as differentiation, self‐renewal capacity, proliferation, and apoptosis, are targeted and deranged by several types of neoplasia‐associated genetic alteration, for example, translocations, deletions, and mutations of genes that code for proteins involved in signaling transduction, epigenetic regulation, and transcription. Epigenetically, T‐ALL is characterized by gene expression changes caused by hypermethylation of tumor suppressor genes, histone modifications, and miRNA and lncRNA abnormalities. Although some genetic and gene expression patterns have been associated with certain clinical features, such as immunophenotypic subtype and outcome, none has of yet generally been implemented in clinical routine for treatment decisions. The recent advent of massive parallel sequencing technologies has dramatically increased our knowledge of the genetic blueprint of T‐ALL, revealing numerous fusion genes as well as novel gene mutations. The challenges now are to integrate all genetic and epigenetic data into a coherent understanding of the pathogenesis of T‐ALL and to translate the wealth of information gained in the last few years into clinical use in the form of improved risk stratification and targeted therapies. Here, we provide an overview of pediatric T‐ALL with an emphasis on the acquired genetic alterations that result in this disease. © 2016 Wiley Periodicals, Inc.

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Increased expression of miR-221 is associated with shorter overall survival in T-cell acute lymphoid leukemia

Cited by 51 publications

References 30 publications

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

MicroRNA Profiling in Prostate Cancer - The Diagnostic Potential of Urinary miR-205 and miR-214

Pediatric T‐cell acute lymphoblastic leukemia

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