Engineered CD8 T cell-derived extracellular vesicles induce enhanced anti-cancer efficacy and targeting to lung cancer cells.

Lung cancer is a common and highly malignant tumor. Although lung cancer treatments continue to advance, conventional therapies are limited and the response rate of patients to immuno-oncology drugs is low. This phenomenon raises an urgent need to develop effective therapeutic strategies for lung cancer.

GDNF family receptor alpha-like antagonist antibody alleviates chemotherapy-induced cachexia in melanoma-bearing mice.

Background: Patients with cancer undergoing chemotherapy experience cachexia with anorexia, body weight loss, and the depletion of skeletal muscles and adipose tissues. Effective treatment strategies for chemotherapy-induced cachexia are scarce. The growth differentiation factor 15 (GDF15)/GDNF family receptor alpha-like (GFRAL)/rearranged during transfection (RET) axis is a critical signalling pathway in chemotherapy-induced cachexia.

Novel antitumor therapeutic strategy using CD4 T cell-derived extracellular vesicles.

Extracellular vesicles (EVs) mediate cell-cell crosstalk by carrying bioactive molecules derived from cells. Recently, immune cell-derived EVs have been reported to regulate key biological functions such as tumor progression. CD4 T cells orchestrate overall immunity; however, the biological role of their EVs is unclear.

Immune cell-derived small extracellular vesicles in cancer treatment.

Small extracellular vesicles (sEVs) secreted by most cells carry bioactive macromolecules including proteins, lipids, and nucleic acids for intercellular communication. Given that some immune cell-derived sEVs exhibit anti-cancer properties, these sEVs have received scientific attention for the development of novel anticancer immunotherapeutic agents. In this paper, we reviewed the latest advances concerning the biological roles of immune cell-derived sEVs for cancer therapy.

Hypothalamic AMPK-induced autophagy increases food intake by regulating NPY and POMC expression.

Hypothalamic AMP-activated protein kinase (AMPK) plays important roles in the regulation of food intake by altering the expression of orexigenic or anorexigenic neuropeptides. However, little is known about the mechanisms of this regulation. Here, we report that hypothalamic AMPK modulates the expression of NPY (neuropeptide Y), an orexigenic neuropeptide, and POMC (pro-opiomelanocortin-α), an anorexigenic neuropeptide, by regulating autophagic activity in vitro and in vivo.

Brain metabolism as a modulator of autophagy in neurodegeneration.

Emerging evidence that autophagy serves as a sweeper for toxic materials in the brain gives us new insight into the pathophysiology of neurodegenerative diseases. Autophagy is important for maintaining cellular homeostasis associated with metabolism. Some neurodegenerative diseases such as Alzheimer׳s and Parkinson׳s diseases are accompanied by altered metabolism and autophagy in the brain.