bims-migras Biomed News
on Migrasomes
Issue of 2026–05–10
two papers selected by
Cliff Dominy
  1. PinX1 inhibits migrasomes-mediated mitochondrial transfer to confer cisplatin sensitivity in nasopharyngeal carcinoma.
  2. Identification of a migrasome-related lncRNA signature and its prognostic and immunological role in bladder cancer.
  1. Oncogene. 2026 May 05.
    PinX1 inhibits migrasomes-mediated mitochondrial transfer to confer cisplatin sensitivity in nasopharyngeal carcinoma.
    Juan Zhang, Junqi Wang, Tingfeng Liang, Fang Chen, Zhenchao Zhu, Yong He, Xueyong Hu, Jing Li, Shuaijun Chen, Chaosheng Yu.
      Chemotherapy resistance is a major factor contributing to the failure of nasopharyngeal carcinoma (NPC) treatment. Migrasomes can export damaged mitochondria out of the cell, and the timely removal of damaged mitochondria is key to cancer cell resistance. However, whether migrasomes regulate tumor resistance remains unknown. Here, we elucidated the role and mechanism of migrasomes in chemoresistance of NPC. We found that the formation of migrasomes was increased in cisplatin-resistant NPC cells, and inhibiting migrasome formation reduced cisplatin resistance. PinX1 was lowly expressed in tumor tissues of patients with high migrasome scores. Upstream mechanism analyses showed that TP53 was effectively bound to the promoter of PinX1, thereby enhancing its transcriptional activity. Knockdown of PinX1 facilitated migrasome formation via its telomerase inhibitory domain 252-328aa region binding to Rab11a, which relied on serine residues at the N-terminal 25aa site for promoting migrasome formation. Mechanistically, PinX1 recruited RanBP2 to induce the SUMOylation of Rab11a, leading to the degradation of Rab11a at the K207 site. Furthermore, PinX1 reduced cancer cell energy metabolism by inhibiting the export of damaged mitochondria via migrasomes. Collectively, TP53-activated PinX1 recruits RanBP2 to Rab11a, triggering Rab11a K207 SUMOylation and degradation, leading to impaired migrasome formation and mitochondrial transfer, and ultimately suppresses cisplatin resistance in NPC. Our study provides a new target for clinical reversal of chemotherapy resistance in patients with NPC.
    DOI:  https://doi.org/10.1038/s41388-026-03741-9
  2. Front Immunol. 2026 ;17 1763443
    Identification of a migrasome-related lncRNA signature and its prognostic and immunological role in bladder cancer.
    Junlin Shen, Chun Wang, Tian'en Li, Heyang Guan, Mingpeng Zhang, Ruitao Li, Yaqun Zhang, Liwei Liu, Jing Tian, Zhiqun Shang.
       Background: Bladder cancer (BLCA) is a highly heterogeneous malignancy with considerable variability in clinical outcomes. Reliable biomarkers for prognosis and treatment guidance remain urgently needed. Migrasomes, recently identified cellular organelles involved in intercellular communication, have been implicated in cancer progression, yet their associated long non-coding RNAs (lncRNAs) and prognostic relevance in BLCA remain unclear.
    Methods: We integrated transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) to identify migrasome-related lncRNAs through co-expression analysis. A prognostic signature was constructed using univariate Cox, LASSO, and multivariate regression analyses. Patients were stratified into high- and low-risk groups across training, validation, and entire cohorts. Kaplan-Meier survival, ROC curves, PCA, and Cox analyses were used for validation. Functional annotation was conducted via GO, KEGG, and GSEA. Immune infiltration and tumor microenvironment features were evaluated using ESTIMATE and CIBERSORT, while tumor mutation burden (TMB), immune escape potential, and drug sensitivity were also analyzed. Single-cell RNA sequencing (scRNA-seq) analysis delineated cellular heterogeneity and intercellular communication patterns related to the risk signature in the BLCA microenvironment. Finally, experimental validation of SEC24B-AS1, a key lncRNA within the model, was performed through qRT-PCR, CCK-8, colony formation, and migration assays to confirm its biological relevance.
    Results: A robust prognostic signature comprising migrasome-related lncRNAs was established, effectively distinguishing patients into high- and low-risk groups with significantly different survival outcomes. The signature remained an independent prognostic factor after multivariate adjustment. Functional enrichment analyses revealed marked biological distinctions between the two groups. Immune profiling showed higher immune and stromal scores in high-risk patients, together with distinct immune cell composition and function. High-risk tumors also exhibited elevated TMB and increased immune evasion potential. Drug sensitivity analysis identified compounds with differential responses between risk subgroups. Single-cell transcriptomic analysis indicated that the signature reflects cellular heterogeneity and intercellular communication patterns within the BLCA microenvironment. Experimental validation of SEC24B-AS1, a key lncRNA in the model, demonstrated its impact on tumor cell proliferation and migration, supporting the biological relevance of the prognostic signature in BLCA.
    Conclusion: This study presents a novel migrasome-related lncRNA signature that independently predicts survival in bladder cancer and reflects the tumor immune landscape.
    Keywords:  bladder cancer; genomic mutation burden; migrasome-related lncRNAs; prognostic biomarker signature; single-cell transcriptomic profiling; therapeutic sensitivity; tumor immune landscape
    DOI:  https://doi.org/10.3389/fimmu.2026.1763443
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