LncRNA GAS5 Represses Osteosarcoma Cells Growth and Metastasis via Sponging MiR-203a

Wang, Yang; Kong, Daliang

doi:10.1159/000487178

Cited by 58 publications

(46 citation statements)

References 27 publications

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“…In addition to activating PI3K pathway, some ncRNAs have been reported to inhibit the activity of PI3K signaling. lncRNA GAS5 expression is lower in tumor cells compared to normal cells; its over-expression inhibits tumor cell proliferation and migration while treatment with PI3K activator reduces the inhibitory effects [66][67][68][69][70][71][72]. Table 1 shows the examples of lncRNA that interact with PI3K signaling in different types of cancer.…”

Section: Non-coding Rna and Other Factors In Regulation Of Pi3k Pathwaymentioning

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: Non-coding Rna and Other Factors In Regulation Of Pi3k Pathwaymentioning

confidence: 99%

Targeting PI3K in cancer: mechanisms and advances in clinical trials

et al. 2019

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“…However, lncRNAs can also play tumorigenic roles. GAS5 inhibited osteosarcoma cell growth and metastasis by targeting miR-203a [29]. And MRPL39 hindered the progression of gastric cancer via the direct interaction with miR-130 [30].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA NEAT1/miR-338-3p axis impedes the progression of acute myeloid leukemia via regulating CREBRF

et al. 2020

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Background: Acute myeloid leukemia (AML) is a heterogeneous hematological disease. Our purpose of the research was to investigate the regulatory influence of long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1)/microRNA-338-3p (miR-338-3p)/CREB3 regulatory factor (CREBRF) in AML progression. Methods: The associated RNA and protein levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. Cell growth was assessed through colony formation assay and 3-(4,5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Flow cytometry was exploited to determine the apoptosis rate. Cell migration and invasion were detected by transwell assay. The combination of miR-338-3p and NEAT1 or CREBRF was analyzed via the dual-luciferase reporter assay. Results: NEAT1 and CREBRF were down-regulated in AML tissues and cells. NEAT1 up-regulation suppressed cell growth, migration and invasion but enhanced apoptosis of AML cells. Inhibition of CREBRF reverted the NEAT1induced effects on AML cells. Moreover, NEAT1 directly targeted miR-338-3p and miR-338-3p targeted CREBRF. NEAT1/ miR-338-3p could affect cellular behaviors of AML cells via the modulation of CREBRF. Conclusion: NEAT1/miR-338-3p axis repressed the AML progression through regulating CREBRF, which might afford a favorable perspective for the AML treatment molecularly.

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“…Previous studies have revealed that cytoplasmic lncRNAs generally function as ceRNAs to regulate mRNA expression via sponging versatile miRNAs, thereby playing a pivotal role in cancer metastasis (Lian et al , ; Shan et al , ; Sun et al , ; Wang and Kong, ; Yan et al , ). In fact, lncRNAs exert their functions in several biological processes via interaction with DNA, proteins, and RNAs, which is dependent on the subcellular localization of the lncRNAs within the cells to a large extent (Chen et al , ).…”

Section: Discussionmentioning

confidence: 99%

SMAD3/SP1 complex‐mediated constitutive active loop between lncRNA PCAT7 and TGF‐β signaling promotes prostate cancer bone metastasis

Lang

Dai

et al. 2020

Molecular Oncology

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Bone metastasis is associated with cancer‐related death in patients with prostate cancer (PCa). Long noncoding RNAs (lncRNAs) play critical roles in tumor progression of PCa. Nevertheless, the biological function of lncRNAs in PCa bone metastasis remains unclear. PCAT7 was identified as a bone metastasis‐related lncRNA via analyzing TCGA dataset. Meanwhile, PCAT7 was found to be elevated in primary PCa tissues with bone metastasis and associated with bone metastasis status and poor prognosis of patients with PCa. Functionally, our results reveal that PCAT7 overexpression promotes PCa bone metastasis in vivo, as well as migration, invasion, and EMT of PCa cells in vitro; on the contrary, PCAT7 knockdown has an inverse effect. Mechanistically, PCAT7 activates TGF‐β/SMAD signaling by upregulating TGFBR1 expression via sponging miR‐324‐5p. In turn, TGF‐β signaling forms a positive feedback loop with PCAT7 via SMAD3/SP1 complex‐induced PCAT7 upregulation. Finally, the clinical positive correlation between PCAT7 and TGFBR1 and TGF‐β signaling activity, and the negative association with miR‐324‐5p are further demonstrated in PCa tissues and clinical primary PCa cells. This study reveals a novel mechanism that is responsible for the constitutive activation of TGF‐β signaling in PCa bone metastasis, implying that PCAT7 can act as a potential therapeutic target against bone metastasis of PCa via disrupting the constitutive active loop between PCAT7 and TGF‐β signaling.

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LncRNA GAS5 Represses Osteosarcoma Cells Growth and Metastasis via Sponging MiR-203a

Cited by 58 publications

References 27 publications

Targeting PI3K in cancer: mechanisms and advances in clinical trials

Targeting PI3K in cancer: mechanisms and advances in clinical trials

Long non-coding RNA NEAT1/miR-338-3p axis impedes the progression of acute myeloid leukemia via regulating CREBRF

SMAD3/SP1 complex‐mediated constitutive active loop between lncRNA PCAT7 and TGF‐β signaling promotes prostate cancer bone metastasis

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