Ask about this productRelated genes to: RBM10 antibody
- Gene:
- RBM10 NIH gene
- Name:
- RNA binding motif protein 10
- Previous symbol:
- -
- Synonyms:
- DXS8237E, KIAA0122, GPATC9, ZRANB5, GPATCH9, S1-1
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-21
- Date modifiied:
- 2018-10-16
Related products to: RBM10 antibody
Related articles to: RBM10 antibody
- Bladder cancer brain metastasis (BrM) remains a poorly characterized clinical entity in neuro-oncology. The current study combines clinicopathologic and genomic sequencing data to identify prognostic factors in bladder cancer BrM. - Source: PubMed
Publication date: 2026/08/18
Manoranjan BranavanZeller SabrinaPrice HannahReiner Anne SRosenberg Jonathan EIyer GopaMoss Nelson S - Most thyroid cancers are initiated by alterations activating the mitogen-activated protein kinase (MAPK) pathway and progress via additional genomic events. Because papillary thyroid carcinoma (PTC) generally has a favorable prognosis and rarely advances, knowledge about later-acquired genomic alterations and their impact on prognosis is limited. - Source: PubMed
Publication date: 2026/07/10
Toda SojiHiroshima YukihikoIwasaki HiroyukiKadoya MeiSuzuki ChihiroYamazaki HaruhikoOkubo YoichiroSaito AyaMasudo Katsuhiko - SMARCA4-deficient thoracic undifferentiated tumor is a rare and highly aggressive subtype of lung cancer defined in the 2021 World Health Organization classification. Its scarcity and highly undifferentiated histology limit the availability of representative in vitro models and hinder therapeutic development. In this study, we established a novel cell line, TRI-LC21, from the primary tumor of a patient with lung cancer showing pathological features consistent with this entity. TRI-LC21 exhibited stable proliferation, strong colony-forming ability, and robust tumorigenicity in subcutaneous xenograft models. Xenograft tumors recapitulated the histological features and immunophenotype of the original tumor. Cell line authenticity was confirmed by short tandem repeat profiling, and mycoplasma contamination was excluded. Whole-exome sequencing revealed SMARCA4 loss accompanied by co-mutations in TP53, STK11, RBM10, and ARHGAP35. Transcriptome analysis demonstrated decreased expression of epithelial-associated genes and increased expression of stemness- and plasticity-related programs, consistent with an undifferentiated phenotype. Collectively, TRI-LC21 faithfully recapitulates the histological, immunophenotypic, and molecular characteristics of this tumor type and provides a valuable in vitro model for mechanistic investigation and preclinical studies. - Source: PubMed
Publication date: 2026/07/09
Li ShashaLuo HaoWu DongshengKu YinLuo NanzhiGong ZhipengZhou WenjingXie XinyiZhou GuanyuChen YaohuiLiu Lunxu - Although immune checkpoint inhibitors have improved outcomes in lung adenocarcinoma (LUAD), many patients still exhibit inadequate responses. The immunomodulatory functions of RNA-binding motif (RBM) proteins remain poorly understood. Using in vivo and in vitro models of RBM10 deficiency combined with cytokine arrays, CLIP-seq, RIP, and proteomics, we found that RBM10 deficiency promotes an immunosuppressive microenvironment, and targeting key chemokines restored anti-PD-1 efficacy in RBM10-deficient LUAD models. RBM10 deficiency enhanced the polarization and recruitment of M2 tumor-associated macrophages (TAMs), both in vitro and in vivo. Mechanistically, RBM10 loss disrupted STING exon 3 exclusion via alternative splicing and impaired QKI-mediated stabilization of the STING-E3(-) isoform, shifting the splicing balance toward the STING-E3(+) isoform and promoting CCL7 secretion. CCL7 acted through its receptor CCR2 on macrophages, driving M2 polarization and recruitment. This central pathway was further reinforced by a positive feedback loop wherein M2-polarized TAMs transferred mitochondria to tumor cells, potentially contributing to mtDNA-cGAS-STING signaling and sustained CCL7 production. Therapeutically, CCL7/CCR2 blockade synergized with PD-1 inhibition to promote tumor regression in RBM10-deficient tumors. Collectively, RBM10 serves as a key immunoregulator in LUAD by modulating the STING-CCL7-CCR2 axis, and targeting the CCL7-CCR2 axis represents a promising strategy to overcome anti-PD-1 resistance. - Source: PubMed
Publication date: 2026/06/22
Gao WeitongWang RuqiongAn BoQi LishuangJing ZihanRen XingmeiZhou YangXu MingjunLi JiaojiaoLiu JieWang LiyingXu GangLi RouJia DexinYu Yan - To evaluate the efficacy and safety of neoadjuvant sintilimab, a programmed cell death 1 protein (PD-1) blockade combined with chemotherapy in patients with resectable stage II-IIIB epidermal growth factor receptor (EGFR) mutant non-small cell lung cancer (NSCLC). - Source: PubMed
Publication date: 2026/05/28
Zhang ChaoJiang Ben-YuanYan Li-XuPeng Li-ShanLi Jin-HuChen Zhi-YongSun Yu-XuanSu JianLiao Ri-QiangDong SongYan Hong-HongXu Chong-RuiZhou QingYang Xue-NingHu ZhengWu Yi-LongZhong Wen-Zhao