Protein-protein interaction inhibitor of SRPKs alters the splicing isoforms of VEGF and inhibits angiogenesis

Li, Qingyun; Zeng, Chuyue; Liu, Haizhen; Yung, Kristen Wing Yu; Chen, Chun; Xie, Qiuling; Wan, Stephanie Winn Chee; Mak, Bertha Sze Wing; Xia, Jiang; Xiong, Sheng; Ngo, Jacky Chi Ki

doi:10.1016/j.isci.2021.102423

Cited by 19 publications

(17 citation statements)

References 62 publications

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“…S5 A ). This could have important implications on the splicing of various gene transcripts and the consequent production of alternative protein isoforms, including, for example, vascular endothelial growth factor ( 67 ). Finally, a third interesting interaction suggested by Mechismo involves R264 of SAM synthase (MAT2A); this modification is located at the interface between the two subunits forming the active dimer of the enzyme, where it contacts E57 of the other MAT2A monomer, ATP, and metal ions serving as cofactors ( supplemental Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The observation that an R-methyl-site is involved in SRSF1–SRPK1 interaction is also intriguing, as Ngo et al. ( 67 ) have recently shown that disrupting this interaction promotes alternative splicing events triggering the translation of a vascular endothelial growth factor isoform that displays antiangiogenic properties. In this study, the authors used a PPI inhibitor to modulate SRSF1–SRPK1 interaction; along this line, based on our result, it will be interesting to assess whether pharmacological modulation of PRMTs can elicit the same functional effect.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

ProMetheusDB: An In-Depth Analysis of the High-Quality Human Methyl-proteome

Massignani

Giambruno

Maniaci

et al. 2022

Molecular & Cellular Proteomics

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

ProMetheusDB: An In-Depth Analysis of the High-Quality Human Methyl-proteome

Massignani

Giambruno

Maniaci

et al. 2022

Molecular & Cellular Proteomics

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“…LIN28 affects angiogenesis by regulating the expression level of let-7d ( 116 ). In breast cancer, SRPK1 can mediate SRSF1 phosphorylation and promote angiogenesis by regulating VEGF premRNA splicing to generate proangiogenic isoforms ( 117 ). Regulation of the mRNA half-life plays an important role in breast cancer.…”

Section: Function Of Rbps In Breast Cancermentioning

confidence: 99%

The function and regulatory mechanism of RNA-binding proteins in breast cancer and their future clinical treatment prospects

Zhong

Liu

et al. 2022

Front. Oncol.

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Breast cancer is the most common female malignancy, but the mechanisms regulating gene expression leading to its development are complex. In recent years, as epigenetic research has intensified, RNA-binding proteins (RBPs) have been identified as a class of posttranscriptional regulators that can participate in regulating gene expression through the regulation of RNA stabilization and degradation, intracellular localization, alternative splicing and alternative polyadenylation, and translational control. RBPs play an important role in the development of normal mammary glands and breast cancer. Functional inactivation or abnormal expression of RBPs may be closely associated with breast cancer development. In this review, we focus on the function and regulatory mechanisms of RBPs in breast cancer, as well as the advantages and challenges of RBPs as potential diagnostic and therapeutic targets in breast cancer, and discuss the potential of RBPs in clinical treatment.

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“…Interestingly, the use of inhibitors of SRPK1, the kinase responsible for SRSF1 activation, has been recently proposed as powerful antiangiogenic strategy to be used for the treatment of various pathological conditions, included cancer. Inhibition of SRPK1, through the blocking of SRSF1 phosphorylation and activity, leads to the induction of VEGF XXX b isoforms and, consequently, significantly reduces the angiogenic potential of targeted cells 16–18 …”

Section: Regulation Of Vegfa Expressionmentioning

confidence: 99%

Non‐coding RNA regulatory networks in post‐transcriptional regulation of VEGFA in cancer

Fontemaggi¹

2022

IUBMB Life

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The switch from the normal quiescent vasculature to angiogenesis in tumors is induced by a variety of growth factors, released from cancer and stromal cells upon oxygen and nutrients deprivation. Vascular endothelial growth factor A (VEGF‐A) is a potent‐secreted mitogen and the only growth factor specific to endothelial cells that is observed almost ubiquitously at sites of angiogenesis. Expression of VEGF‐A in cancer cells is controlled through transcriptional and post‐transcriptional mechanisms. Post‐transcriptional regulation of VEGF‐A occurs at multiple levels, through the control of splicing, mRNA stability and translation rate, enabling a fine‐tuned expression and release of VEGF‐A. Mounting evidence is highlighting the important role played by microRNAs (miRNAs) in the control of VEGF‐A mRNA stability and translation in cancer. Moreover, non‐coding RNAs, as long non‐coding RNAs and circular RNAs, are emerging as crucial modulators of VEGF‐A‐targeting miRNAs, with consequent ability to modulate VEGF‐A expression. This review discusses the recent progress on the ncRNA‐related networks controlling VEGF‐A expression in cancer cells and provides insights into the complexity of VEGF‐A post‐transcriptional regulation.

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Protein-protein interaction inhibitor of SRPKs alters the splicing isoforms of VEGF and inhibits angiogenesis

Cited by 19 publications

References 62 publications

ProMetheusDB: An In-Depth Analysis of the High-Quality Human Methyl-proteome

ProMetheusDB: An In-Depth Analysis of the High-Quality Human Methyl-proteome

The function and regulatory mechanism of RNA-binding proteins in breast cancer and their future clinical treatment prospects

Non‐coding RNA regulatory networks in post‐transcriptional regulation of VEGFA in cancer

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