Ask about this productRelated genes to: SPOPL Blocking Peptide
- Gene:
- SPOPL NIH gene
- Name:
- speckle type BTB/POZ protein like
- Previous symbol:
- -
- Synonyms:
- BTBD33
- Chromosome:
- 2q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2007-10-25
- Date modifiied:
- 2016-02-10
Related products to: SPOPL Blocking Peptide
Related articles to: SPOPL Blocking Peptide
- DNA methylation plays a critical role in myelodysplastic syndrome (MDS). Here, we aimed to observe the effects of polydatin (PD) on DNA methylation in MDS cells on a genome-wide scale and explore the underlying mechanisms, providing new evidence for PD as a novel hypermethylation agent. We used the Gene Expression Omnibus (GEO) online database to evaluate the DNA methylation characteristics of MDS patients. A Human Methylation 850 K BeadChip was used to evaluate the effects of PD on DNA methylation in SKM-1 cells. Western blotting (WB) was used to observe changes in the expression of related proteins. Cytoscape was used to determine the key genes that were hypermethylated by PD. The therapeutic effects were evaluated using flow cytometry experiment and a cell counting kit-8 (CCK-8) assay in vitro. Data from the GEO online database revealed that aberrant gene hypomethylation plays an important role in MDS. In MDS cells, 448 genes (71.91%) were hypermethylated following PD treatment. These hypermethylated genes are related to cancer-related signaling pathways. Moreover, key hypermethylated genes, including PIK3CA, ITPR3 and SPOPL, were identified, and these three genes are all oncogenes. Most importantly, PD decreased the protein expression of the above three oncogenes. Finally, we found that PD could inhibit the proliferation of MDS cells, arrest them in the S phase and induce their apoptosis. Our findings demonstrated that PD has therapeutic effects on MDS by inhibiting the protein expression of oncogenes via hypermethylation in vitro, indicating that PD may be a novel hypermethylation agent. - Source: PubMed
Publication date: 2025/05/29
Zhou QingbingLiang YuanbinChen RuofanWang HongzhiGuo QiuyueLiu LiZhu XiaoboXu Fengqin - Recent studies have increasingly shown that glioma stem cells (GSCs) are extremely important for developing and treating glioblastoma multiforme (GBM). The Broad-complex, Tram-track, and Bric-a-brac protein family is functionally related to a variety of tumor stem cells, and the role of SPOPL as a member of this family in GSCs deserves to be investigated. - Source: PubMed
Publication date: 2023/07/31
Hu TianyuXuan RuohengHan ErqiaoCai LingshanXia Zhibo - First-line treatment for osteosarcoma includes chemotherapy and surgery. However, the five-year survival rate of refractory osteosarcoma remains unsatisfactory. Osteosarcoma cancer stem cells, possessing stemness and chemoresistance, are one of the critical causes of poor response to chemotherapy. Elucidating regulatory signaling pathways of osteosarcoma cancer stem cells may provide a rationale for improving regimens against chemoresistant osteosarcoma. Methotrexate (MTX)-resistant osteosarcoma cells were established. microRNA expression profiles were used for detecting differentially expressed microRNA in resistant clones and the parental cells. microRNA target databases were employed to predict potential microRNA and mRNA interactions. Flow cytometry was performed to measure stem cell marker Prominin-1 (CD133)-positive cells. Immunofluorescence staining was applied to detect CD133 expression. miR-197-3p mimic or anti-miR-197-3p stably transfected cells were used to generate xenograft models. In the study, we found that miR-197-3p was increased in MTX-resistant cell lines. Overexpression of miR-197-3p enhanced the expression of cancer stem cell markers CD133, Octamer-binding protein 4 (), Transcription factor SOX-2 (), and Homeobox protein NANOG (), as well as chemoresistance-associated genes ATP-dependent translocase ABCB1 () and Broad substrate specificity ATP-binding cassette transporter ABCG2 (), whereas miR-197-3p knockdown inhibited stemness and recovered sensitivity to MTX. We also classified the tumor suppressor Speckle-type POZ protein-like () as a target of miR-197-3p. The miR-197-3p mutation that could not combine promoter regions was unable to sustain stemness or chemoresistance. Collectively, we discovered miR-197-3p conferred osteosarcoma stemness and chemotherapy resistance by targeting , prompting promising therapeutic candidates for refractory osteosarcoma treatment. - Source: PubMed
Publication date: 2023/02/01
Zhang JingyongWang ShubaoBai YangAli Aasi MohammadDeng JiewenChen YushiFu YonghuiHe Ming - High-risk localized prostate cancer (HRLPC) is associated with a substantial risk of recurrence and disease mortality. Recent clinical trials have shown that intensifying anti-androgen therapies administered before prostatectomy can induce pathologic complete responses or minimal residual disease, called exceptional response, although the molecular determinants of these clinical outcomes are largely unknown. Here, we perform whole-exome and transcriptome sequencing on pre-treatment multi-regional tumor biopsies from exceptional responders (ERs) and non-responders (NRs, pathologic T3 or lymph node-positive disease) to intensive neoadjuvant anti-androgen therapies. Clonal SPOP mutation and SPOPL copy-number loss are exclusively observed in ERs, while clonal TP53 mutation and PTEN copy-number loss are exclusively observed in NRs. Transcriptional programs involving androgen signaling and TGF-β signaling are enriched in ERs and NRs, respectively. These findings may guide prospective validation studies of these molecular features in large HRLPC clinical cohorts treated with neoadjuvant anti-androgens to improve patient stratification. - Source: PubMed
Tewari Alok KCheung Alexander T MCrowdis JettConway Jake RCamp Sabrina YWankowicz Stephanie ALivitz Dimitri GPark JihyeLis Rosina TBosma-Moody AliceHe Meng XiaoAlDubayan Saud HZhang ZhenweiMcKay Rana RLeshchiner IgnatyBrown MylesBalk Steven PGetz GadTaplin Mary-EllenVan Allen Eliezer M - Advances in prostate cancer lag behind other tumor types partly due to the paucity of models reflecting key milestones in prostate cancer progression. Therefore, we develop clinically relevant prostate cancer models. - Source: PubMed
Publication date: 2020/06/23
Palanisamy NallasivamYang JunShepherd Peter D ALi-Ning-Tapia Elsa MLabanca EstefaniaManyam Ganiraju CRavoori Murali KKundra VikasAraujo John CEfstathiou EleniPisters Louis LWan XinhaiWang XuemeiVazquez Elba SAparicio Ana MCarskadon Shannon LTomlins Scott AKunju Lakshmi PChinnaiyan Arul MBroom Bradley MLogothetis Christopher JTroncoso PatriciaNavone Nora M