RBM35A Blocking Peptide
- Known as:
- RBM35A Blocking Peptide
- Catalog number:
- 33r-6542
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- RBM35A Blocking Peptide
Related genes to: RBM35A Blocking Peptide
- Gene:
- ESRP1 NIH gene
- Name:
- epithelial splicing regulatory protein 1
- Previous symbol:
- RBM35A
- Synonyms:
- FLJ20171
- Chromosome:
- 8q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-22
- Date modifiied:
- 2019-02-20
Related products to: RBM35A Blocking Peptide
Related articles to: RBM35A Blocking Peptide
- Epithelial-mesenchymal transition (EMT) drives phenotypic plasticity in bladder cancer and contributes to tumor progression, therapeutic resistance, and recurrence. While epithelial splicing regulatory proteins (ESRPs) are established modulators of EMT-associated splicing programs, the downstream mechanisms through which they influence tumor cell state remain incompletely understood. Here, we identify CD44 isoform switching as a functionally relevant component of ESRP2-dependent control of epithelial plasticity. Using epithelial (RT4) and mesenchymal (UM-UC-3) bladder cancer models, we show that distinct cellular states are characterized by different CD44 isoform landscapes, with epithelial cells enriched in CD44 variant isoforms and mesenchymal cells dominated by the standard isoform CD44s. Functional perturbation studies revealed that ESRP2 exerts a stronger effect than ESRP1 on CD44 isoform composition, promoting epithelial-associated CD44 variant isoforms while suppressing CD44s. Induction of EMT in RT4 cells was accompanied by downregulation of ESRP1/2 and a shift toward CD44s enrichment. Conversely, depletion of CD44s attenuated EMT-associated transcriptional and morphological changes and partially reversed the effects of ESRP2 loss on EMT marker expression. In mesenchymal UM-UC-3 cells, CD44s depletion reduced migratory capacity and impaired spheroid growth, further supporting a functional contribution of CD44 isoform balance to mesenchymal behavior. Collectively, our findings indicate that ESRP2-dependent regulation of CD44 isoform composition is closely linked to epithelial-mesenchymal plasticity in bladder cancer. These findings provide insight into splicing-associated regulation of tumor cell state and underscore the importance of isoform-resolved analyses for understanding cancer progression. - Source: PubMed
Publication date: 2026/08/28
Bajdak-Rusinek KWierzbinka MSundararajan VSieroń LStępień K LDiak NJankowska KSalamon MWójtowicz WDziedzic-Kowalska ADutczak RHałacińska KMachnik G - Recent evidence suggests that cardiovascular diseases and cancer are linked through circulating factors, mainly proteins with oncogenic properties found in heart failure (HF) patients. However, the role of long non-coding RNAs (lncRNAs) as potential factors in cancer progression associated with HF remains unknown. This study aims to determine the role of HF-related lncRNAs in cancer progression. Using public RNA-sequencing datasets from the left ventricle and whole blood of HF patients, as well as colon cancer tumors, we identified HF-related lncRNAs with predicted competing endogenous RNA (ceRNA) interactions. These were integrated with co-expression analysis and upregulated colon cancer protein-coding genes to construct an HF-related regulatory network associated with colon cancer and epithelial-mesenchymal transition (EMT)-associated genes. LINC00670-overexpressing DLD-1 colon cancer cells showed increased migration and expression of Vimentin, along with N-cadherin, ZEB1, ESRP1, and E-cadherin transcript levels. Long-read nanopore sequencing of LINC00670-overexpressing DLD-1 cells revealed positively correlated genes, including type I interferon signaling pathway genes (STAT1 and SLC7A11) and epithelial-mesenchymal transition (EMT)-associated migratory genes (DDIT4 and PABPC1), as genes associated with the response to HF-related LINC00670 overexpression. Our findings reveal LINC00670 as an HF-related lncRNA that promotes partial EMT-transcriptional changes associated with type I interferon-associated genes, suggesting that LINC00670 plays a key role in inducing mesenchymal traits in the cardio-oncological context. - Source: PubMed
Publication date: 2026/07/29
Jimenez-Gallegos DanicaCorrales Wladimir APeñaloza-Otarola AllanNorambuena-Soto IgnacioUrquiza-Zurich SebastianMarchese DomenicaSigcho FranciscoArias-Carrasco RaulTorres Vicente AQuest Andrew F GMunita RobertoMaracaja-Coutinho ViniciusLavandero Sergio - Bladder cancer (BCa) is a highly prevalent urological malignancy and one of the most frequently occurring cancers worldwide, necessitating the development of diagnostic and therapeutic biomarkers. This study aimed to explore candidate genes that may be involved in the carcinogenesis of BCa. - Source: PubMed
Publication date: 2026/07/18
Sajjadi SanaRamezani AminAlavimanesh SajadAlipoor HojatTakhshid Mohammad Ali - Epithelial splicing regulatory protein 1 (ESRP1) is a key regulator of epithelial-mesenchymal transition (EMT) and cancer progression, including in pancreatic ductal adenocarcinoma (PDAC). We show that ESRP1-mediated isoform switching of DNA methyltransferase 3B (DNMT3B) correlates with the metastatic potential of pancreatic cancer cells. The expression of DNMT3B splicing variants was closely linked to ESRP1 level. Ectopic expression of mesenchymal DNMT3B isoforms 3 and 7, lacking part of the methyltransferase catalytic domain, significantly enhanced lung metastasis and tumor growth, while epithelial DNMT3B isoforms 1 and 2, with an intact catalytic domain, suppressed these effects in mouse models. Differential expression of DNMT3B isoforms also correlated with overall survival in PDAC patients. Deletion of exons 21-22, differentially spliced region between epithelial and mesenchymal isoforms, increased cell proliferation and migration, similar to mesenchymal DNMT3B. RNA sequencing revealed that mesenchymal DNMT3B isoforms 3 and 7 were associated with aggressive tumor phenotypes. Among differentially expressed target genes of DNMT3B isoforms, Fibulin 1 (FBLN1), a key regulator of the tumor microenvironment, regulates cancer cell migration and EMT. Taken together, our results highlight the central role of ESRP1-mediated DNMT3B isoform switching in pancreatic cancer progression and metastasis and suggest that DNMT3B isoforms may serve as potential biomarkers for this disease. - Source: PubMed
Publication date: 2026/07/10
Hong EunjiPark HyeyeonKim JunilKang Jin MukPark SujinMin TaehongPark JinahPang KyoungwhaKim PyunggangSon MinjungOoshima AkiraKim DaeunIm JeongeunKwon WooilTakeshima HideyukiKu Ja-LokKim HongbeomUshijima ToshikazuJang Jin-YoungKwon Yong JungPark DaechanPark Seok HeeKim Seong-Jin - Breast cancer remains one of the most prevalent malignancies among women, with doxorubicin resistance posing a significant challenge that undermines treatment success and survival outcomes. Aberrant alternative splicing (AS), driven by dysregulation or mutations in splicing factors (SFs), is implicated in cancer initiation, progression, and drug resistance. This study aims to investigate the association of the epithelial cell-specific splicing factor ESRP1 with doxorubicin resistance in breast cancer, focusing on how ESRP1 deficiency correlates with AS changes that promote chemoresistance. - Source: PubMed
Publication date: 2026/06/21
Zhang JingChen LibinSong QinglingXu LiLi YinghuaLi WenWang Jie