A DHX9-lncRNA-MDM2 interaction regulates cell invasion and angiogenesis of cervical cancer

Ding, Xiangya; Jia, Xuemei; Wang, Cong; Xu, Jingyun; Gao, Shou‐Jiang; Liu, Chun

doi:10.1038/s41418-018-0242-0

Cited by 131 publications

(93 citation statements)

References 51 publications

(55 reference statements)

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“…19 In cervical cancer, lncRNA CCDST enhances the interaction of MDM2 with oncogenic protein DHX9 and facilitates DHX9 degradation, and eventually leading to the inhibition of angiogenesis. 20 Additionally, lncRNAs modulate the expression of specific mRNAs through the ceRNA network, which is also a critical manner to regulate tumor angiogenesis. For example, Sun et al found that LINC00968 reduces angiogenesis by impeding miR-423-5p-mediated PROX1 inhibition in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

<p>Exosomal lncRNA RAMP2-AS1 Derived from Chondrosarcoma Cells Promotes Angiogenesis Through miR-2355-5p/VEGFR2 Axis</p>

Cheng¹,

Zhang²,

Cheng³

et al. 2020

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Objective: Exosomes derived from cancer cells can alter the microenvironment and enhance cancer malignancy through the regulation of peripheral cell functions. The present study focused on the crosstalk between chondrosarcoma cells and human umbilical vein endothelial cells (HUVECs) mediated by exosomes derived from chondrosarcoma cells and aimed to explore the potential molecular mechanism. Materials and Methods: Chondrosarcoma cell-derived exosomes were isolated and characterized. Cell proliferation assay, tube formation assay and transwell migration assay were performed to characterize the effects of exosomes on HUVECs. The lncRNA microarray was used to select differentially expressed lncRNAs in HUVECs treated with or without exosomes. Serum samples of patients with chondrosarcoma were collected to analyze the correlation between the RAMP2-AS1 level and the clinicopathological features. Online databases were used to predict the target microRNA of RAMP2-AS1. Dual luciferase reporter assay, Western blotting and qRT-PCR assays were performed to verify the interactions among RAMP2-AS1, miR-2355-5p and VEGFR2. Rescue experiments were conducted to validate the existence of the RAMP2-AS1/miR-2355-5p/VEGFR2 axis. Results: The exosomes secreted by chondrosarcoma cells could enhance HUVECs proliferation, migration and tube formation. LncRNA microarray analysis revealed that exosomes carried lncRNA RAMP2-AS1, and further verification showed that the level of RAMP2-AS1 was increased in the serum of chondrosarcoma patients and was closely related to local invasiveness, distant metastasis and poor prognosis. Subsequent experiments demonstrated that RAMP2-AS1 knockdown could partly abrogate the promoting effects on angiogenesis induced by exosomes derived from chondrosarcoma cells. Moreover, dual luciferase reporter assay and rescue experiments suggested that the RAMP2-AS1/miR-2355-5p/VEGFR2 axis was responsible for exosome-induced angiogenesis of HUVECs. Conclusion: Chondrosarcoma cell-derived exosomes carry lncRNA RAMP2-AS1, which acts as a ceRNA of miR-2355-5p to regulate VEGFR2 expression, thereby positively regulating the angiogenic ability of HUVECs. Thus, exosomal RAMP2-AS1 has the potential as a novel biomarker and therapeutic target for chondrosarcoma.

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Section: Discussionmentioning

confidence: 99%

<p>Exosomal lncRNA RAMP2-AS1 Derived from Chondrosarcoma Cells Promotes Angiogenesis Through miR-2355-5p/VEGFR2 Axis</p>

Cheng¹,

Zhang²,

Cheng³

et al. 2020

OTT

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“…It has been reported that the E3 ubiquitin ligase MDM2 can interact with DHX9 and mediate the degradation of DHX9 through the UPS pathway (Ding et al, 2018). Thus, we tested whether HBx could hinder the MDM2-mediated degradation of DHX9 through ubiquitination.…”

Section: Hbx Inhibits the Ubiquitination Of Dhx9 Proteinmentioning

confidence: 99%

Hepatitis B virus X protein modulates upregulation of DHX9 to promote viral DNA replication

Shen

Chen

et al. 2019

Cellular Microbiology

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Hepatitis B virus (HBV) infection is a major cause of acute and chronic liver diseases.During the HBV life cycle, HBV hijacks various host factors to assist viral replication.In this research, we find that the HBV regulatory protein X (HBx) can induce the upregulation of DExH-box RNA helicase 9 (DHX9) expression by repressing proteasome-dependent degradation mediated by MDM2. Furthermore, we demonstrate that DHX9 contributes to viral DNA replication in dependence on its helicase activity and nuclear localization. In addition, the promotion of viral DNA replication by DHX9 is dependent on its interaction with Nup98. Our findings reveal that HBxmediated DHX9 upregulation is essential for HBV DNA replication. K E Y W O R D S hepatitis B Virus, HBx protein, DHX9, ubiquitylation, Nup98

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“…Long noncoding RNA (lncRNAs) and circular RNAs (cir-cRNAs) are important factors in human cancer pathogenesis [15,20,21]. Both lncRNAs and circRNAs lack the ability to encode proteins and circRNAs are characterized by the covalent conjunction and lacking of the 3′ and 5′ end.…”

Section: Discussionmentioning

confidence: 99%

A novel circular RNA circENTPD7 contributes to glioblastoma progression by targeting ROS1

et al. 2020

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Background: Circular RNAs (circRNAs) are identified to play an important role in many human cancers, such as glioblastoma. However, the potential mechanisms underlying the relationship between circRNAs and glioblastoma pathogenesis are still elusive. This study is designed to investigate the role of circRNAs in glioblastoma progression. Methods:The present study is designed to investigate the mechanism by which circRNAs involves in glioblastoma pathogenesis. By using circRNAs microarray, we detected the dysregulated circRNAs and identified an up-regulated circRNA, circENTPD7 in glioblastoma tissues. Cell proliferation was measured using a CCK-8 assay. Cell clone formation ability was assessed with a clone formation test. We used the bioinformatics website to predict circRNA-miRNA and miRNA-mRNA interactions. CircRNA-miRNA interaction was confirmed by dual-luciferase reporter assays and RNA-RNA pulldown assay.Results: circENTPD7 (hsa_circ_0019421) was upregulated in glioblastoma tissues. Kaplan-Meier survival analysis indicated that glioblastoma patients had a poor overall survival when circENTPD7 expression levels were high. Knockdown of circENTPD7 inhibited the motility and proliferation of glioblastoma cells. Moreover, we demonstrated that circENTPD7 acted as a sponge of miR-101-3p to regulate the expression of ROS1 further promoted the proliferation and motility of glioblastoma cells. Conclusions:Taken together, these findings indicate that circRNA circENTPD7 promotes glioblastoma cell proliferation and motility by regulating miR-101-3p/ROS1.

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A DHX9-lncRNA-MDM2 interaction regulates cell invasion and angiogenesis of cervical cancer

Cited by 131 publications

References 51 publications

<p>Exosomal lncRNA RAMP2-AS1 Derived from Chondrosarcoma Cells Promotes Angiogenesis Through miR-2355-5p/VEGFR2 Axis</p>

<p>Exosomal lncRNA RAMP2-AS1 Derived from Chondrosarcoma Cells Promotes Angiogenesis Through miR-2355-5p/VEGFR2 Axis</p>

Hepatitis B virus X protein modulates upregulation of DHX9 to promote viral DNA replication

A novel circular RNA circENTPD7 contributes to glioblastoma progression by targeting ROS1

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