Up-Regulation of Long Noncoding RNA CCAL Predicts Poor Patient Prognosis and Promotes Tumor Metastasis in Osteosarcoma

Zhou, Dakai; Yang, Xiwang; Li, Huining; Yang, Yongbo; Zhu, Zhou; Wu, Na

doi:10.5301/jbm.5000240

Cited by 20 publications

(13 citation statements)

References 15 publications

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“…28 Furthermore, CCAL has been reported to be significantly upregulated in osteosarcoma tissues and facilitate osteosarcoma cell proliferation, migration and invasion. 29 Similar to previous findings, we verified that CCAL was markedly upregulated in osteosarcoma tissues. Higher CCAL expression levels were closely related to shorter overall survival in patients with osteosarcoma.…”

Section: Discussionsupporting

confidence: 91%

LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma

Chen¹,

Yang²,

Chang³

2020

CMAR

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Purpose The objective of this study was to detect the expression of the long noncoding RNA (lncRNA) colorectal cancer-associated lncRNA (CCAL) in osteosarcoma tissues and to investigate its role in angiogenesis and the potential molecular mechanisms associated with this effect in osteosarcoma. Materials and Methods CCAL expression in 40 osteosarcoma tissues and 40 noncancerous tissues was measured by qRT-PCR (quantitative real-time polymerase chain reaction). Tube formation assays were performed to explore the role of CCAL in angiogenesis in osteosarcoma. In addition, the regulatory interaction between CCAL, miR-29b, and ANGPTL4 was investigated via luciferase reporter assay and bioinformatics predictive analysis. Results Compared with noncancerous tissues, the expression of CCAL was markedly upregulated in osteosarcoma tissues. Higher CCAL expression levels were closely related to shorter overall survival in patients with osteosarcoma. Additionally, functional analysis indicated that CCAL could facilitate tumour angiogenesis in vitro and in vivo in osteosarcoma. Mechanistically, CCAL upregulated ANGPTL4 expression in osteosarcoma cells, and ANGPTL4 mediated angiogenic induction by CCAL in osteosarcoma. Moreover, CCAL directly targeted miR-29b in osteosarcoma. More importantly, we demonstrated that CCAL upregulated the expression of ANGPTL4 by sponging miR-29b, which promoted angiogenesis in osteosarcoma. Conclusion Our results show that CCAL promotes angiogenesis by regulating the miR-29b/ANGPTL4 axis in osteosarcoma.

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Section: Discussionsupporting

confidence: 91%

LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma

Chen¹,

Yang²,

Chang³

2020

CMAR

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“…Moreover, CCAL-mediated activation of the WNT pathway increases the expression of the MDR1/P-gp gene, which has been associated with multidrug resistance in colorectal cancer, explaining the negative clinical association between CCAL levels and adjuvant chemotherapy outcome in colon cancer patients [ 107 ]. Recently, CCAL was also associated with metastatic osteosarcomas, but its mode of function in this type of cancer is still under investigation [ 108 ].…”

Section: Crosstalk Mechanisms Of Wnt/β-catenin Signaling and Lncrnasmentioning

confidence: 99%

Crosstalk mechanisms between the WNT signaling pathway and long non-coding RNAs

Zarkou

Galaras

Giakountis

et al. 2018

Non-coding RNA Research

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The WNT/β-catenin signaling pathway controls a plethora of biological processes throughout animal development and adult life. Because of its fundamental role during animal lifespan, the WNT pathway is subject to strict positive and negative multi-layered regulation, while its aberrant activity causes a wide range of pathologies, including cancer. At present, despite the inroads into the molecules involved in WNT-mediated transcriptional responses, the fine-tuning of WNT pathway activity and the totality of its target genes have not been fully elucidated. Over the past few years, long non-coding RNAs (lncRNAs), RNA transcripts longer that 200nt that do not code for proteins, have emerged as significant transcriptional regulators. Recent studies show that lncRNAs can modulate WNT pathway outcome by affecting gene expression through diversified mechanisms, from the transcriptional to post-translational level. In this review, we selectively discuss those lncRNA-mediated mechanisms we believe the most important to WNT pathway modulation.

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“…Therefore, these above lncRNAs are regarded as oncogenes in OS. [23][24][25][26][27][28][29][30][31][32][33] To date, no studies have documented the expression of FLVCR-AS1 in human tumors. In this study, we noticed for the first time that FLVCR-AS1 expression level was remarkably increased in OS patients and high FLVCR-AS1 expression closely related to poor outcome and low 5-year survival rate of OS patients.…”

Section: Discussionmentioning

confidence: 99%

lncRNA FLVCR-AS1 promotes osteosarcoma growth by targeting miR381-3p/CCND1

Yang¹,

He²,

Duan³

et al. 2020

OTT

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Purpose: This article reports on FLVCR-AS1 effects on osteosarcoma (OS) growth. Methods: Tumor tissue and adjacent normal tissue of 48 OS patients were collected. HOS and 143B cells were transfected. Gene expression was examined with qRT-PCR and Western blot. CCK8 assays and cell cloning was performed to measure cell proliferation. Cell cycle and apoptosis were assessed. Luciferase-reporter gene assays and RNA pull-down tests were used to detect targeting relationships between genes. Results: Prominently higher FLVCR-AS1 expression was found in OS tissue and cells, and was associated with poor prognosis (P<0.05, P<0.01, or P<0.001). Compared with the siCtrl group, 143B and HOS cells of the siFLVCR-AS1 group had significantly lower OD 450 values and clone numbers and obviously higher percentages of cells in the G 1 phase and apoptosis (P<0.01 or P<0.001). miR381-3p expression was directly inhibited by FLVCR-AS1, and CCND1 expression was directly suppressed by miR381-3p. Compared with the FLVCR-AS1 group, 143B cells of the FLVCR-AS1 + miR381-3p mimic group and FLVCR-AS1 + siCCND1 group showed remarkably lower OD 450 values and clone numbers obviously higher apoptosis and percentage of cells in the G 1 phase (P<0.05, P<0.01, or P<0.001). Conclusion: FLVCR-AS1 promoted OS growth by upregulating CCND1 expression via downregulation of miR381-3p.

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Up-Regulation of Long Noncoding RNA CCAL Predicts Poor Patient Prognosis and Promotes Tumor Metastasis in Osteosarcoma

Abstract: Our findings suggested that CCAL plays critical roles in OS progression and could act as a therapeutic target in the treatment of OS.

Cited by 20 publications

References 15 publications

<p>LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma</p>

<p>LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma</p>

Crosstalk mechanisms between the WNT signaling pathway and long non-coding RNAs

<p>lncRNA FLVCR-AS1 promotes osteosarcoma growth by targeting miR381-3p/CCND1</p>

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