Zhen Zhang

Abstract Research on tumour cell‐derived small extracellular vesicles (sEVs) that regulate tumour microenvironment (TME) has provided strategies for targeted therapy of head and neck squamous cell carcinoma (HNSCC). Herein, we demonstrated that sEVs derived from HNSCC cancer cells carried CD73 (sEVs CD73 ), which promoted malignant progression and mediated immune evasion. The sEVs CD73 phagocytosed by tumour‐associated macrophages (TAMs) in the TME induced immunosuppression. Higher CD73 high TAMs infiltration levels in the HNSCC microenvironment were correlated with poorer prognosis, while sEVs CD73 activated the NF‐κB pathway in TAMs, thereby inhibiting immune function by increasing cytokines secretion such as IL‐6, IL‐10, TNF‐α, and TGF‐β1. The absence of sEVs CD73 enhanced the sensitivity of anti‐PD‐1 therapy through reversed immunosuppression. Moreover, circulating sEVs CD73 increased the risk of lymph node metastasis and worse prognosis. Taken together, our study suggests that sEVs CD73 derived from tumour cells contributes to immunosuppression and is a potential predictor of anti‐PD‐1 responses for immune checkpoint therapy in HNSCC.

Abstract Tumour cells under hypoxia tend to modulate the number and contents of extracellular vesicles (EVs) to regulate the tumour microenvironment (TME) and thus promote tumour progression. However, the mechanism of how hypoxia influences the secretion of EVs remains to be elucidated. Here, we confirm the increased production of EVs in head and neck squamous cell carcinoma (HNSCC) cells under hypoxia, where endosome‐derived EVs are the main subtype affected by insufficient O 2 . The accumulation of hypoxia‐inducible factor‐1α (HIF‐1α) under hypoxia directly downregulates the expression of ATP6V1A, which is pivotal to maintain the homeostasis of lysosomes. Subsequently, impaired lysosomal degradation contributes to the reduced fusion of multivesicular bodies (MVBs) with lysosomes and enables the secretion of intraluminal vesicles (ILVs) as EVs. These findings establish a HIF‐1α‐regulated lysosomal dysfunction‐EV release axis and provide an exquisite framework to better understand EV biogenesis.

BACKGROUND: No studies have compared fractional microplasma radio frequency (RF) technology with the carbon dioxide fractional laser system (CO2 FS) in the treatment of atrophic acne scars in the same patient. OBJECTIVE: To compare the efficacy and safety of fractional microplasma RF with CO2 FS in the treatment of atrophic acne scars. METHODS AND MATERIALS: Thirty-three Asian patients received three sessions of a randomized split-face treatment of fractional microplasma RF or CO2 FS. RESULTS: Both modalities had a roughly equivalent effect. Échelle d'Évaluation Clinique Des Cicatrices d'Acné scores were significantly lower after fractional microplasma RF (from 51.1 ± 14.2 to 22.3 ± 8.6, 56.4% improvement) and CO2 FS (from 48.8 ± 15.1 to 19.9 ± 7.9, 59.2% improvement) treatments. There was no statistically significant difference between the two therapies. Twelve subjects (36.4%) experienced postinflammatory hyperpigmentation (PIH) after 30 of 99 treatment sessions (30.3%) on the CO2 FS side and no PIH was observed on the fractional microplasma RF sides. CONCLUSION: Both modalities have good effects on treating atrophic scars. PIH was not seen with the fractional microplasma RF, which might make it a better choice for patients with darker skin.