bims-migras 2026-06-14 papers

Issue of 2026–06–14
two papers selected by
Cliff Dominy

J Natl Cancer Cent. 2026 Jun;6(3): 219-233

Migrasomes program tissue microenvironment: from physiology to oncology, future perspectives in clinical advances.

Shaosen Zhang, Jiaoting Chen, Yancheng Lai, Caihong Wang.

Cancer remains a critical global health challenge, necessitating an in-depth investigation into spatiotemporal dimensions. Migrasomes, a class of migration-dependent organelles that sequester spatiotemporal and biochemical cues, offer a previously overlooked pathway for microenvironmental programming during tumor evolution. At the cellular level, migrasomes mediate extensive intercellular communication and material transfer, while facilitating cellular quality control via the extrusion of damaged organelles. Within tissue microenvironments, these organelles exert context-dependent, bidirectional effects, modulating homeostasis in processes such as wound healing, senescence, inflammation, and microbial infection, while being exploited in cancer to drive proliferation, angiogenesis, immunomodulation, and metastasis. This review elucidates the intricate role of migrasomes within tumor microenvironments and other tissue settings, discusses their potential involvement in the transition from tissue homeostasis to malignancy, and evaluates their potential implications for clinical therapeutic strategies, as well as diagnostic and prognostic biomarkers.

Keywords: Aging; Chronic inflammation; Microbiome; Migracytosis; Migrasome; Tumor microenvironment; Wound healing

DOI: https://doi.org/10.1016/j.jncc.2026.03.009

Int J Mol Sci. 2026 May 24. pii: 4724. [Epub ahead of print]27(11):

Metformin Alleviates Stress-Induced Premature Senescence of Vascular Endothelial Cells by Regulating Mitocytosis.

Hui Lu, Qing Mu, Boqun Wang, Yan Chen, Binghui Zeng, Lisha Gu, Wei Zhao.

Stress-induced premature senescence (SIPS) of endothelial cells can cause endothelial dysfunction. As a first-line antidiabetic agent, the specific role of metformin in SIPS has not yet been clarified. In this study, an in vitro SIPS model was induced by exposing human umbilical vein endothelial cells (HUVECs) to hydrogen peroxide (H2O2), and the effects of metformin on cell senescence, proliferation, migration, tube formation, and mitochondrial function were evaluated. Gene expressions altered by metformin were profiled via transcriptome sequencing. Specifically, the potential involvement of migrasome-mediated mitocytosis in metformin-driven effects was examined using confocal microscopy and siRNA-mediated silencing. The results showed that metformin significantly reduced SA-β-gal activity and restored the migration and tube-forming capacities of H2O2-induced senescent HUVECs. Moreover, metformin regulated mitochondrial dynamics, restored mitochondrial membrane potential, and attenuated intracellular oxidative stress. Notably, transcriptomic and functional analyses suggested that metformin enhanced migrasome formation and migrasome-mediated mitocytosis. Inhibition of migrasome formation by siTSPAN4 abolished the protective effect of metformin against SIPS. Collectively, these findings demonstrate that metformin alleviates early SIPS-associated changes in HUVECs and suggest that migrasome-mediated mitocytosis contributes to this protection by ameliorating mitochondrial dysfunction. This provides novel mechanistic insight into the vascular protective effects of metformin.

Keywords: metformin; mitocytosis; stress-induced premature senescence; vascular endothelial cells

DOI: https://doi.org/10.3390/ijms27114724