LncRNA CCAT2 promotes angiogenesis in glioma through activation of VEGFA signalling by sponging miR-424

Sun, Song; Shu, Yu-Gao; Tao, Mei-Yi

doi:10.1007/s11010-020-03712-y

Cited by 34 publications

(28 citation statements)

References 40 publications

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“…2 LncRNA CCAT2 contributes to glioma progression by activating VEGFA pathway. 15 LncRNA LINC00467 upregulation promotes glioma development through repressing P53 level. 16 Previous study showed that LINC00173 downregulation promotes non-small cell lung cancer cell growth and survival.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma</p>

Du¹,

Liu²,

Tian³

et al. 2020

CMAR

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Background: Glioma is one of the leading causes of cancer-related deaths. This study aimed to investigate the function and mechanism of long noncoding RNA (lncRNA) LINC00173 in the regulation of glioma progression. Methods: LINC00173 expression was measured using qRT-PCR. Survival rate was analyzed through Kaplan-Meier method. CCK8, colony formation and EdU assays were performed to measure cell proliferation while transwell was used to determine cell migration and invasion. Luciferase reporter assay was conducted to test RNA interaction. Results: LINC00173 expression was elevated in glioma tissues and cells. LINC00173 high expression predicted poor prognosis. Loss of LINC00173 inhibited proliferation, migration and invasion. LINC00173 interacted with miR-765 to enhance NUTF2 expression. MiR-765 expression was negatively correlated with LINC00173 and NUTF2 in glioma tissues. NUTF2 level was increased in glioma tissues. NUTF2 overexpression rescued the potential of proliferation, migration and invasion in LINC00173-silenced cells. Conclusion: Our research demonstrated that LINC00173 promotes glioma progression through targeting miR-765/NUTF2 axis.

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Section: Discussionmentioning

confidence: 99%

<p>Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma</p>

Du¹,

Liu²,

Tian³

et al. 2020

CMAR

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“…Primary tumor cells and host cells secrete various factors that support CSC survival and dissemination, creating a pre-metastatic microenvironment (Kaplan et al, 2005;Chin and Wang, 2016;Sivan et al, 2019). Further, CSCs can modulate angiogenesis by producing proangiogenic factors such as VEGFA (Chand et al, 2016) to induce unregulated tumor angiogenesis and metastasis (Carmeliet and Jain, 2011;Treps et al, 2017;Sun et al, 2020; Figure 3 and Table 1). Here, malignant alterations of the BM niche in hematologic tumors, primary bone tumors and bone metastasis are highlighted.…”

Section: Dysregulation Of Bone Vasculature In Bone Malignanciesmentioning

confidence: 99%

Bone Angiogenesis and Vascular Niche Remodeling in Stress, Aging, and Diseases

Stucker

Chen

Watt

et al. 2020

Front. Cell Dev. Biol.

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The bone marrow (BM) vascular niche microenvironments harbor stem and progenitor cells of various lineages. Bone angiogenesis is distinct and involves tissue-specific signals. The nurturing vascular niches in the BM are complex and heterogenous consisting of distinct vascular and perivascular cell types that provide crucial signals for the maintenance of stem and progenitor cells. Growing evidence suggests that the BM niche is highly sensitive to stress. Aging, inflammation and other stress factors induce changes in BM niche cells and their crosstalk with tissue cells leading to perturbed hematopoiesis, bone angiogenesis and bone formation. Defining vascular niche remodeling under stress conditions will improve our understanding of the BM vascular niche and its role in homeostasis and disease. Therefore, this review provides an overview of the current understanding of the BM vascular niches for hematopoietic stem cells and their malfunction during aging, bone loss diseases, arthritis and metastasis.

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“…Long non-coding RNAs (lncRNAs) have emerged as an important factor in multiple pathophysiological processes of central nervous system (CNS) diseases, such as angiogenesis, neurogenesis, and apoptosis (Chandran et al, 2017). For instance, the lncRNA CCAT2 promotes angiogenesis in glioma through the activation of VEGFA signaling by sponging miR-424 (Sun et al, 2020). The lncRNA MALAT-1 has been shown to have neuroprotective effects on spinal cord ischemic/reperfusion injury by regulating miR-204 (Qiao et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

Cheng

et al. 2020

Front. Cell Dev. Biol.

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Endogenous repair after chronic compressive spinal cord injury (CCSCI) is of great clinical interest. Ischemia-hypoxia-induced angiogenesis has been proposed to play an important role during this repair process. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are involved in the pathophysiological processes of various diseases. Here, we identified a lncRNA (Xist; X-inactive specific transcript) with upregulated expression in cervical spine lesions during endogenous neurological repair in CCSCI rats. Therapeutically, the introduction of Xist to rats increased neurological function in vivo as assayed using the Basso, Beattie, and Bresnahan (BBB) score and inclined plane test (IPT). We found that the introduction of Xist enhanced endogenous neurological repair by promoting angiogenesis and microvessel density after CCSCI, while depletion of Xist inhibited angiogenesis and cell sprouting and migration. Mechanistically, Xist promoted angiogenesis by sponging miR-32-5p and modulating Notch-1 expression both in vitro and in vivo. These findings suggest a role of the Xist/miR-32-5p/Notch-1 axis in endogenous repair and provide a potential molecular target for the treatment of ischemia-related central nervous system (CNS) diseases.

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LncRNA CCAT2 promotes angiogenesis in glioma through activation of VEGFA signalling by sponging miR-424

Cited by 34 publications

References 40 publications

<p>Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma</p>

<p>Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma</p>

Bone Angiogenesis and Vascular Niche Remodeling in Stress, Aging, and Diseases

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

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