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Medicine

Targeting mitocytosis potentiates mitochondria drug delivery for antimetastasis therapy

A new approach to cancer treatment harnesses the body's natural mechanism to eliminate damaged mitochondria, thereby preventing tumor spread.

Illustration: Blue Dot News

1 min read

In the intricate dance of cancer cells, a delicate balance is struck between survival and death. When mitochondria, the powerhouses within these cells, become damaged, a compensatory pathway called mitocytosis kicks in to preserve them. This process allows the cell to expel the damaged mitochondria through structures called migrasomes, maintaining the mitochondrial homeostasis and cellular viability.

However, this balancing act can be disrupted by cancer therapies aimed at targeting the tumor's mitochondria. Researchers have been searching for ways to harness this phenomenon to their advantage. In a breakthrough study, scientists discovered that by inhibiting mitocytosis, they could effectively target and damage the tumor's mitochondria. But what if they could also leverage this process to their advantage? That's where the clever idea of using nanotechnology comes in.

By developing a targeted delivery system that could simultaneously inhibit mitocytosis and block its activation, researchers were able to create a potent strategy for cancer therapy. This approach allowed them to significantly enhance the efficacy of antimetastatic treatments, paving the way for new possibilities in cancer treatment. The discovery of this effective approach matters because it offers hope for more targeted and efficient therapies, potentially leading to improved outcomes for patients with metastatic cancer.

The people behind the work

  • Deng Y et al.

    Author

    Published in Science advances

Source: Science advances

Sources & Verification

Every statement in this story is drawn from the facts below. Each is linked to a primary or reputable source — follow any citation to check it for yourself.

  1. Mitocytosis is a compensatory pathway responding to mitochondria stress in migratory cells, which expels damaged mitochondria through migrasomes, preserving mitochondrial homeostasis and cellular viability. Science advances
  2. We found distinct responses to mitochondria-targeted therapy across breast tumor models distinguished by migrasome expression (4T1 > E0771 > EMT6). Science advances
  3. The antimetastatic efficacy of mitochondrial damage was notably compromised in the migrasome-high 4T1 tumor model due to robust mitocytosis activation, which is merely explored and lacks effective strategy. Science advances
  4. Here, we developed a mitochondria-targeted nanoplatform (RH-NPs) with the functions of mitocytosis inhibition and mitochondrial damage. Science advances
  5. Mitochondria-targeted triphenylphosphonium-modified lonidamine (TPP-LND) and integrin inhibitor cilengitide (CGT) were separately loaded into a nanodelivery system (TL/RH-NPs and CGT/RH-NPs, respectively). Science advances
  6. TL/RH-NPs effectively targeted and damaged tumor mitochondria. Science advances
  7. Simultaneously, upon mitocytosis activation, CGT/RH-NPs hitchhiked with damaged mitochondria into migrasomes to block mitocytosis via integrin inhibition. Science advances
  8. This strategy significantly potentiated antimetastatic efficacy in 4T1 tumor models, which established an effective approach for mitocytosis modulation and optimization of mitochondria-targeted therapies. Science advances

Part of the Blue Dot News 2026 retrospective — an archive reconstructed automatically from the published scientific record. The science is real and cited above; this is not original daily reporting, and it is deliberately kept out of the live news feed.

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