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An azo-type thermosensitive crosslinking agent was prepared from azobisisobutyramidine hydrochloride (V-50) and maleic anhydride. It is then copolymerized with acrylamide (AM) and acrylic acid (AA) to prepare thermosensitive self-degradation microgel. The microgel particles are uniformly dispersed in the aqueous solution in the form of particles. Water absorption and swelling experiments of microgel showed that the water absorptivity of microgel decreased with the increase of salinity. And the microgel have the best water absorptivity under a neutral environment. The results of microgel degradation experiments showed that the higher the temperature, the shorter the degradation time, and the degradation is complete within 5 h at 100 °C. The solid residue measured by the degradation liquid is almost 0, indicating that the microgel can be thoroughly degraded at high temperature. The polymer solution after degradation can be measured by gel chromatograph and the average molecular weight is Mn=1.9 × 105g/mol. And the swelling and degradation mechanism were summarized. [ABSTRACT FROM AUTHOR]

Metastasis is the most prevalent cause of cancer deaths, and immunological components of the tumor microenvironment, especially tumor‐associated macrophages (TAMs), play a vital role in cancer metastasis. However, the underlying mechanisms of TAMs on non‐small‐cell lung cancer (NSCLC) metastasis remain largely unexplored. Herein, we demonstrated that M2‐like TAMs facilitate the migration and invasion of cancer cells in vitro and in vivo through intercellular delivery of M2‐like macrophage‐derived exosomes (M2‐exos). Importantly, we found that M2‐exos had considerably higher levels of integrin (ITG) αV and β3. The impact of M2‐like macrophage‐mediated invasion and migration of NSCLC cells was clearly decreased when ITG αVβ3 was blocked. Mechanistically, exosomal ITG αVβ3 produced from M2‐like macrophages successfully triggered the focal adhesion kinase signaling pathway in recipient cells, boosting the migratory and invasive abilities of NSCLC cells. Clinically, we found that metastatic NSCLC patients had greater ITG αV and β3 expression, which was associated with a worse prognosis. This study reveals a novel mechanism by which M2‐exos significantly increased NSCLC cell migration and invasion by delivering integrin αVβ3. Exosomal ITG αVβ3 can be used as a potential prognostic marker, and blocking ITG αVβ3 could be a viable treatment option for preventing tumor metastasis. [ABSTRACT FROM AUTHOR]