ArticleClinical and translational medicine2022
Splicing factor arginine/serine-rich 8 promotes multiple myeloma malignancy and bone lesion through alternative splicing of CACYBP and exosome-based cellular communication.
Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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16 citing papers in PubMed, 26 citations in OpenAlex.
- Engineered small extracellular vesicles in hematologic malignancies: mechanisms, therapeutic strategies, and translational challenges.Clinical and experimental medicine · 2026Review
- Effects of exosomes from different origins on osteoclasts.Journal of orthopaedic surgery and research · 2025Review
- RNA Splicing as a Therapeutic Vulnerability in Therapy-Refractory Multiple Myeloma.Blood cancer discovery · 2025Article
- SFRS8 Regulates Memory by Modulating RNA Splicing of Synaptic Genes.Molecular neurobiology · 2025Article
- RNA splicing: Novel star in pulmonary diseases with a treatment perspective.Acta pharmaceutica Sinica. B · 2025Review
- Targeting the RBM39-MEK5 axis synergizes with bortezomib to inhibit the malignant growth of multiple myeloma.Blood advances · 2025Article
- PNPO-Mediated Oxidation of DVL3 Promotes Multiple Myeloma Malignancy and Osteoclastogenesis by Activating the Wnt/β-Catenin Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Alternative Splicing: A Critical Regulator in Human Bone Biology and Tumor Progression.Research (Washington, D.C.) · 2025Review
- Targeting CLK2 and serine/arginine-rich splicing factors inhibits multiple myeloma through downregulating RAE1 by nonsense-mediated mRNA decay mechanism.Cancer science · 2025Article
- Therapeutically Harnessing Tumor Cell-Derived Extracellular Vesicles for Multiple Myeloma: Recent Advances and Future Perspectives.Pharmaceutics · 2024Review
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- Article
- Towards understandings of serine/arginine-rich splicing factors.Acta pharmaceutica Sinica. B · 2023Review
- CD229 interacts with RASAL3 to activate RAS/ERK pathway in multiple myeloma proliferation.Aging · 2022Article
- Splicing factor arginine/serine-rich 8 promotes multiple myeloma malignancy and bone lesion through alternative splicing of CACYBP and exosome-based cellular communication.Clinical and translational medicine · 2022Article
- NAT10 acetylates BCL-XL mRNA to promote the proliferation of multiple myeloma cells through PI3K-AKT pathway.Frontiers in oncology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMultiple myeloma (MM) is a distinctive malignancy of plasma cell within the bone marrow (BM), of which alternative splicing factors play vital roles in the progression. Splicing factor arginine/serine-rich 8 (SFRS8) is the exclusive factor associated with MM prognosis, however its role in MM remains undefined.
methodsThe analyses of 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) assay, immunohistochemistry, flow cytometry and xenograft model were performed to examine cell proliferation, cell cycle and apoptosis in SFRS8 overexpression or knockdown MM cells in vitro and in vivo. The SFRS8-regulated alternative splicing events were identified by RNA immunoprecipitation sequencing (RIP-seq) and validated by RIP-qPCR and Co-IP methods. Exosomes were extracted from the supernatant of myeloma cells by ultracentrifugation. Bone lesion was evaluated by TRAP staining in vitro and SCID/NOD-TIBIA mouse model. A neon electroporation system was utilised to deliver siRNA through exosomes. The effect of siRNA-loaded exosomes in vivo was evaluated by using a patient-derived tumor xenograft (PDX) model and SCID/NOD-TIBIA mouse model.
resultsSFRS8 was significantly upregulated in MM samples and positively associated with poor overall survival (OS) in MM patients. SFRS8 promoted MM cell proliferation in vitro and in vivo. Furthermore, calcyclin binding protein (CACYBP) was identified as the downstream target of SFRS8. Particularly, SFRS8 could reduce CACYBP isoform1 (NM_014412.3) and increase CACYBP isoform2 (NM_001007214.1) by mediating the alternative splicing of CACYBP, thereby altering the ubiquitination degradation of β-catenin to promote MM progression. In addition, SFRS8 promoted osteoclast differentiation through exosomes in vitro and in vivo. More importantly, exosomal siRNA targeting CACYBP isoform2 inhibited tumour growth in PDX and SCID/NOD-TIBIA mouse models.
conclusionOur findings demonstrate that targeting the SFRS8/CACYBP/β-catenin axis may be a promising strategy for MM diagnosis and treatment.
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