Long non-coding RNA LINC00152/miR-613/CD164 axis regulates cell proliferation, apoptosis, migration and invasion in glioma via PI3K/AKT pathway

ZHANG, LINYUN; Wang, Y; Hong, Soon-Kwang

doi:10.4149/neo_2020_190706n598

Cited by 8 publications

(4 citation statements)

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“…Specifically, higher expression of LINC00152 in children with B-ALL was associated with a higher risk of early relapse; conversely, lower expression of LINC01013 was associated with early relapse. The lncRNA LINC00152 is also known as CYTOR (long non-coding RNA cytoskeleton regulator RNA) and has been previously described as an oncogenic lncRNA in many different types of cancer (e.g., [92][93][94][95][96][97]) and may serve as a potential biomarker for cancer detection in both solid tumor tissue and plasma [98,99]. Overall, these reports indicate that lncRNA expression can serve as useful biomarkers in B-ALL.…”

Section: Long Non-coding Rnas In Progenitor B-cell Acute Lymphoblastimentioning

confidence: 99%

Non-Coding RNA Signatures of B-Cell Acute Lymphoblastic Leukemia

Rodriguez

Paculova

Kogut

et al. 2021

IJMS

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Non-coding RNAs (ncRNAs) comprise a diverse class of non-protein coding transcripts that regulate critical cellular processes associated with cancer. Advances in RNA-sequencing (RNA-Seq) have led to the characterization of non-coding RNA expression across different types of human cancers. Through comprehensive RNA-Seq profiling, a growing number of studies demonstrate that ncRNAs, including long non-coding RNA (lncRNAs) and microRNAs (miRNA), play central roles in progenitor B-cell acute lymphoblastic leukemia (B-ALL) pathogenesis. Furthermore, due to their central roles in cellular homeostasis and their potential as biomarkers, the study of ncRNAs continues to provide new insight into the molecular mechanisms of B-ALL. This article reviews the ncRNA signatures reported for all B-ALL subtypes, focusing on technological developments in transcriptome profiling and recently discovered examples of ncRNAs with biologic and therapeutic relevance in B-ALL.

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Section: Long Non-coding Rnas In Progenitor B-cell Acute Lymphoblastimentioning

confidence: 99%

Non-Coding RNA Signatures of B-Cell Acute Lymphoblastic Leukemia

Rodriguez

Paculova

Kogut

et al. 2021

IJMS

View full text Add to dashboard Cite

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“…Furthermore, posttranslational modifications of PARP1, such as mono (ADP-ribosyl)-ation ( 36 , 37 ), phosphorylation, methylation, and acetylation, can modulate its activity. Thus, LINC00152 may influence PARP1 posttranslational modification by binding to the enhancer of zeste homologue 2 (EZH2) ( 38 ) or participate in the phosphatidylinositol 3-kinase/AKT signaling pathway ( 39 ), which may also be important for PARP1 expression and activity.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA LINC00152 Regulates Self-Renewal of Leukemia Stem Cells and Induces Chemo-Resistance in Acute Myeloid Leukemia

et al. 2021

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Relapse of acute myeloid leukemia (AML) has a very poor prognosis and remains a common cause of treatment failure in patients with this disease. AML relapse is partially driven by the chemoresistant nature of leukemia stem cells (LSCs), which remains poorly understood, and our study aimed at elucidating the underlying mechanism. Accumulating evidences show that long noncoding RNAs (lncRNAs) play a crucial role in AML development. Herein, the lncRNA, LINC00152, was identified to be highly expressed in CD34+ LSCs and found to regulate the self-renewal of LSCs derived from AML patients. Importantly, LINC00152 upregulation was correlated with the expression of 16 genes within a 17-gene LSC biomarker panel, which contributed to the accurate prediction of initial therapy resistance in AML. Knockdown of LINC00152 markedly increased the drug sensitivity of leukemia cells. Furthermore, LINC00152 expression was found to be correlated with poly (ADP-ribose) polymerase 1 (PARP1) expression in AML, whereas LINC00152 knockdown significantly decreased the expression of PARP1. Upregulation of LINC00152 or PARP1 was associated with poor prognosis in AML patients. Collectively, these data highlight the importance and contribution of LINC00152 in the regulation of self-renewal and chemoresistance of LSCs in AML.

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“…24,25 Besides, findings by Zhang Y reveal that lncRNA LINC00152 is linked to the expression AKT in lung cancer. 26 Several sources of evidence also report additional lncRNAs associated with cancer via AKT2, including lncRNA H19 in gallbladder cancer cell proliferation and LncRNA Gm15290 in non-Small Cell Lung Cancer progression. 27,28 However, the roles of lncRNA and AKT2 in gastric cancer remain unclear.…”

Section: Discussionmentioning

confidence: 99%