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Square-shaped single-crystalline SnO(2) nanowires and their sphere-like hierarchical structures were synthesized successfully with a template-free hydrothermal approach. It was found that an intermediate phase-Na(2)Sn(OH)(6)-is first produced because it is slow to dissolve in ethanol/water media. The intermediate phase gradually decomposes and converts into SnO(2) at temperatures higher than 200 °C. The reaction temperature also affects the microstructure of SnO(2) nanomaterials. Uniform square-shaped SnO(2) nanowires, which form sphere-like hierarchical structures in 100% structure yield, can be produced at 285 °C on a large scale. The diameter of the nanowires shows a decrease accompanying the increase of the reaction temperature. The temperature effect could be a result of the faster and oriented growth of SnO(2) nanowires along their [Formula: see text] direction at higher temperature. Chemical sensors constructed with square-shaped SnO(2) nanowires exhibit excellent stability, good sensitivity and selectivity, as well as a quick response and short recovery times under exposure to acetone gas in practical applications.

Metabolic interaction between cancer-associated fibroblasts (CAFs) and colorectal cancer (CRC) cells plays a major role in CRC progression. However, little is known about lipid alternations in CAFs and how these metabolic reprogramming affect CRC cells metastasis. Here, we uncover CAFs conditioned medium (CM) promote the migration of CRC cells compared with normal fibroblasts CM. CAFs undergo a lipidomic reprogramming, and accumulate more fatty acids and phospholipids. CAFs CM after protein deprivation still increase the CRC cells migration, which suggests small molecular metabolites in CAFs CM are responsible for CRC cells migration. Then, we confirm that CRC cells take up the lipids metabolites that are secreted from CAFs. Fatty acids synthase (FASN), a crucial enzyme in fatty acids synthesis, is significantly increased in CAFs. CAF-induced CRC cell migration is abolished by knockdown of FASN by siRNA or reducing the uptake of fatty acids by CRC cells by sulfo-N-succinimidyloleate sodium in vitro and CD36 monoclonal antibody in vivo. To conclude, our results provide a new insight into the mechanism of CRC metastasis and suggest FASN of CAFs or CD36 of CRC cells may be potential targets for anti-metastasis treatment in the future.

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