bims-migras 2026-10-25 papers

Issue of 2026–10–25
two papers selected by
Cliff Dominy

Extracell Vesicles Circ Nucl Acids. 2026 ;7(3): 1472-1495

Migrasomes in cancers: from the biogenesis mechanism to therapeutic implications.

Luomeng Qian, Shoujun Wang, Paulina Kucharzewska, Jiachang Li, Sihe Zhang.

Migrasomes are a newly identified class of extracellular vesicles (EVs) with a distinctive pomegranate-like morphology that are generated specifically from migrating cells. They are increasingly recognized as critically important mediators of intercellular communication involved in diverse physiological and pathological processes. However, their roles in cancers remain incompletely defined, and a consensus on migrasome-mediated malignant phenotypes is still lacking. In this review, we first summarize the current knowledge of migrasome biogenesis, distribution, and isolation methodologies. We then systematically discuss the multifaceted roles of migrasomes within the tumor microenvironment (TME), with particular emphasis on their contribution to cancer metastasis, progression and drug resistance. Furthermore, we explore the potential clinical applications of migrasomes in cancer diagnosis and therapy, and outline the key challenges and controversies that hinder their translation into clinical practice. Overall, this review provides an updated perspective on the roles of migrasomes in cancer biology and highlights the emerging opportunities for migrasome-informed targeted therapeutics.

Keywords: Migrasome; cancer; diagnosis; drug resistance; therapy

DOI: https://doi.org/10.20517/evcna.2026.70

Hlife. 2026 Feb;4(2): 92-106

Migrasome-driven mitocytosis relieves mitochondrial damage induced by chikungunya virus TF and 6K.

Shengnan Wang, Dan Zhang, Leiliang Zhang.

Chikungunya virus (CHIKV) infection induces the formation of migrasomes, yet their specific role in CHIKV pathogenesis remains unclear. This study explores the mechanisms underlying mitochondrial damage induced by CHIKV 181 clone 25 (CHIKV 181/25) and the role of migrasomes in mitigating this damage. Using cultured cell lines, we assessed the impact of CHIKV infection on mitochondrial integrity and function, with particular emphasis on the viroporin proteins transframe (TF) and 6K. We utilized fluorescence microscopy and transmission electron microscopy to visualize the interplay between migrasome formation and damaged mitochondria. Additionally, calcium imaging assays were conducted to evaluate intracellular calcium levels, and RNA sequencing was performed to examine gene expression. Our results demonstrated that CHIKV infection leads to mitochondrial damage, mediated by the action of TF and 6K. Notably, migrasomes induced by nonstructural protein 1 (nsP1) effectively clearing impaired mitochondria through mitocytosis. Furthermore, we identified the arginine residue R37 within the viroporin proteins of CHIKV as crucial for inducing mitochondrial damage through elevated intracellular calcium levels. Importantly, R37 within TF from other alphaviruses is also critical for mitochondrial damage. In conclusion, our findings elucidate the complex interplay between CHIKV and mitochondrial dysfunction, positioning migrasomes as potential mediators in alleviating CHIKV-induced mitochondrial damage.

Keywords: 6K; chikungunya virus; migrasome; mitochondrial damage; transframe (TF)

DOI: https://doi.org/10.1016/j.hlife.2025.12.002