The PABPC5/HCG15/ZNF331 Feedback Loop Regulates Vasculogenic Mimicry of Glioma via STAU1-Mediated mRNA Decay

Jing, Fangkun; Ruan, Xuelei; Liu, Xiaobai; Yang, Chunqing; Wang, Di; Zheng, Jian; Xue, Yixue; Shen, Shuyuan; Shao, Lianqi; Yang, Yang; Wang, Ping; Ma, Jun; Liu, Yunhui

doi:10.1016/j.omto.2020.03.017

Cited by 22 publications

(24 citation statements)

References 63 publications

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“…This process is called Staufen-mediated mRNA decay (SMD). STAU1 binds to STAU1-binding site (SBS), which was formed when Alu elements in lncRNAs directly bind to the Alu elements in the 3′-untranslated region (3′UTR) of mRNA via basepairing rules, in its target mRNA 3′-untranslated region (3′ UTR) to induce degradation of target mRNA 19 . Alu elements, once were thought of as "junk" DNA, are now proven to function within RNAs to regulate primate gene expression by diverse mechanisms, for example, triggering SMD 20 .…”

Section: Mechanism Of Tincr Regulating the Proliferation And Metastasmentioning

confidence: 99%

The long noncoding RNA TINCR promotes breast cancer cell proliferation and migration by regulating OAS1

Zhuo

et al. 2021

Cell Death Discov.

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Breast cancer is the leading cause of cancer-related death in women around the world. It is urgently needed to identify genes associated with tumorigenesis and prognosis, as well as to elucidate the molecular mechanisms underlying the oncogenic process. Long noncoding RNAs (lncRNAs) are widely involved in the pathological and physiological processes of organisms and play an important role as oncogenes or tumor suppressor genes, affecting the development and progression of tumors. In this study, we focused on terminal differentiation-induced non-coding RNA (TINCR) (GeneID:257000) and explore its role in the pathogenesis of breast cancer. The results showed that TINCR was increased in breast cancer tissue, and high expression level of TINCR was associated with older age, larger tumor size, and advanced TNM stage. High level of TINCR can promote proliferation and metastasis of breast cancer cells, while downregulation of TINCR induces G1-G0 arrest and apoptosis. Mechanismly, TINCR can bind to staufen1 (STAU1) and then guide STAU1 (GeneID:6780) to bind to OAS1 mRNA (NM_016816.4) to mediate its stability. Thus low level of OAS1(GeneID:4938) can lead to cell proliferation and migration. This result elucidates a new mechanism for TINCR in breast cancer development and provides a survival indicator and potential therapeutic target for breast cancer patients.

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Section: Mechanism Of Tincr Regulating the Proliferation And Metastasmentioning

confidence: 99%

The long noncoding RNA TINCR promotes breast cancer cell proliferation and migration by regulating OAS1

Zhuo

et al. 2021

Cell Death Discov.

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“…Many studies have demonstrated that VM is widely existed in various types of malignant tumors such as human gastric cancer, non-small cell lung cancer, melanoma, liver cancer, and glioma 6 - 10 . In glioma, VM has closely correlation with the pathological grade, proliferation, migration and invasion of tumor 11 , 12 .…”

Section: Introductionmentioning

confidence: 92%

SUMOylation of IGF2BP2 promotes vasculogenic mimicry of glioma via regulating OIP5-AS1/miR-495-3p axis

Li¹,

Wang²,

Yi³

et al. 2021

Int. J. Biol. Sci.

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Rationale: Glioma is the most common primary malignant tumor of human central nervous system, and its rich vascular characteristics make anti-angiogenic therapy become a therapeutic hotspot. However, the existence of glioma VM makes the anti-angiogenic therapy ineffective. SUMOylation is a post-translational modification that affects cell tumorigenicity by regulating the expression and activity of substrate proteins. Methods: The binding and modification of IGF2BP2 and SUMO1 were identified using Ni 2+ -NTA agarose bead pull-down assays, CO-IP and western blot; and in vitro SUMOylation assays combined with immunoprecipitation and immunofluorescence staining were performed to explore the detail affects and regulations of the SUMOylation on IGF2BP2. RT-PCR and western blot were used to detect the expression levels of IGF2BP2, OIP5-AS1, and miR-495-3p in glioma tissues and cell lines. CCK-8 assays, cell transwell assays, and three-dimensional cell culture methods were used for evaluating the function of IGF2BP2, OIP5-AS1, miR-495-3p, HIF1A and MMP14 in biological behaviors of glioma cells. Meantime, RIP and luciferase reporter assays were used for inquiring into the interactions among IGF2BP2, OIP5-AS1, miR-495-3p, HIF1A and MMP14. Eventually, the tumor xenografts in nude mice further as certained the effects of IGF2BP2 SUMOylation on glioma cells. Results: This study proved that IGF2BP2 mainly binds to SUMO1 and was SUMOylated at the lysine residues K497, K505 and K509 sites, which can be reduced by SENP1. SUMOylation increased IGF2BP2 protein expression and blocked its degradation through ubiquitin-proteasome pathway, thereby increasing its stability. The expressions of IGF2BP2 and OIP5-AS1 were up-regulated and the expression of miR-495-3p was down-regulated in both glioma tissues and cells. IGF2BP2 enhances the stability of OIP5-AS1, thereby increasing the binding of OIP5-AS1 to miR-495-3p, weakening the binding of miR-495-3p to the 3'UTR of HIF1A and MMP14 mRNA, and ultimately promoting the formation of VM in glioma. Conclusions: This study first revealed that SUMOylation of IGF2BP2 regulated OIP5-AS1/miR-495-3p axis to promote VM formation in glioma cells and xenografts growth in nude mice, providing a new idea for molecular targeted therapy of glioma.

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“…STAU1-mediated mRNA decay has been shown to also play a significant role in the control of cancer cell proliferation [ 75 , 76 ]. A recent study in glioblastoma indicated that SMD of the transcription factor retina and anterior neural fold homobox2 (RAX2) transcript is required for inhibition of tumor growth and metastasis.…”

Section: Role Of Stau1 In the Regulation Of Cell Functions And Its Associated Impact On Cancermentioning

confidence: 99%

The multifunctional RNA-binding protein Staufen1: an emerging regulator of oncogenesis through its various roles in key cellular events

Almasi

Jasmin

2021

Cell. Mol. Life Sci.

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The double-stranded multifunctional RNA-binding protein (dsRBP) Staufen was initially discovered in insects as a regulator of mRNA localization. Later, its mammalian orthologs have been described in different organisms, including humans. Two human orthologues of Staufen, named Staufen1 (STAU1) and Staufen2 (STAU2), share some structural and functional similarities. However, given their different spatio-temporal expression patterns, each of these orthologues plays distinct roles in cells. In the current review, we focus on the role of STAU1 in cell functions and cancer development. Since its discovery, STAU1 has mostly been studied for its involvement in various aspects of RNA metabolism. Given the pivotal role of RNA metabolism within cells, recent studies have explored the mechanistic impact of STAU1 in a wide variety of cell functions ranging from cell growth to cell death, as well as in various disease states. In particular, there has been increasing attention on the role of STAU1 in neuromuscular disorders, neurodegeneration, and cancer. Here, we provide an overview of the current knowledge on the role of STAU1 in RNA metabolism and cell functions. We also highlight the link between STAU1-mediated control of cellular functions and cancer development, progression, and treatment. Hence, our review emphasizes the potential of STAU1 as a novel biomarker and therapeutic target for cancer diagnosis and treatment, respectively.

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The PABPC5/HCG15/ZNF331 Feedback Loop Regulates Vasculogenic Mimicry of Glioma via STAU1-Mediated mRNA Decay

Cited by 22 publications

References 63 publications

The long noncoding RNA TINCR promotes breast cancer cell proliferation and migration by regulating OAS1

The long noncoding RNA TINCR promotes breast cancer cell proliferation and migration by regulating OAS1

SUMOylation of IGF2BP2 promotes vasculogenic mimicry of glioma via regulating OIP5-AS1/miR-495-3p axis

The multifunctional RNA-binding protein Staufen1: an emerging regulator of oncogenesis through its various roles in key cellular events

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