In 2021, scientists at the Max Planck Institute for Marine Microbiology in Bremen, Germany, reported an astonishing new form of symbiosis: They found a unique bacterium that lives inside a ciliate—a unicellular eukaryote—and provides it with energy. The symbiont’s role is thus strongly reminiscent of mitochondria, with the key difference that the endosymbiont derives energy from the respiration of nitrate, not oxygen.

Now the researchers from Bremen set out to learn more about the environmental distribution and diversity of these peculiar symbionts. “After our initial discovery of this symbiont in a freshwater lake, we wondered how common these organisms are in nature,” says Jana Milucka from the Max Planck Institute for Marine Microbiology. “Are they extremely rare and therefore eluded detection so long? Or do they exist elsewhere and if so, what are their metabolic capacities?”

📝 — Kono, et al.

In this paper, the authors attempted to load liposomes on the surface of MSCs by using the magnetic anionic liposome/atelocollagen complexes that we previously developed and assessed the characters of liposome-loaded MSCs as drug carriers.

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Mesenchymal stem cells (MSCs) have a tumor-homing capacity; therefore, MSCs are a promising drug delivery carrier for cancer therapy. To maintain the viability and activity of MSCs, anti-cancer drugs are preferably loaded on the surface of MSCs, rather than directly introduced into MSCs. In this study, we attempted to load liposomes on the surface of MSCs by using the magnetic anionic liposome/atelocollagen complexes that we previously developed and assessed the characters of liposome-loaded MSCs as drug carriers. We observed that large-sized magnetic anionic liposome/atelocollagen complexes were abundantly associated with MSCs via electrostatic interactions under a magnetic field, and its cellular internalization was lower than that of the small-sized complexes.

Cancer cells have evolved sophisticated strategies to evade the immune system, prolonging their survival and growth. They have also developed survival tactics to resist immune checkpoint inhibition (ICI) treatments. Yet, our understanding of how cancer cells escape the immune response or immune activities perpetuated by anti-cancer immunotherapies remains incomplete. A recent study published in Cancer Discovery has shed light on one such mechanism, revealing how tumors develop ICI resistance and enhancing our understanding of cancer immunotherapy.

The researchers screened 208 metastatic castration-resistant prostate cancer (mCRPC) biopsies searching for genes commonly observed in tumors. Once they identified candidate genes, the investigators compared their expression to that of signatures related to cytotoxic T cells (CTLs), the immune cell subset responsible for identifying and killing cancer cells. The analysis identified an enzyme, ubiquitin-like modifier activating enzyme 1 (UBA1), which the researchers found particularly interesting. Tumors with high expression of UBA1 had low expression of CTL genes.

Further investigation revealed that elevated UBA1 expression predicted which tumors would develop resistance to ICI and which patients would experience the shortest survival outcomes.