Surface plasmon in nanoscaled materials has recently attracted a great deal of attention due to its possibility in a wide range of application. From a practical standpoint, it is desirable for the devices having a tunability of surface plasmon frequency. To achieve this goal, in this study, a composite consisting of two-dimensional gold nanoparticles array embedded in elastic polydimethylsiloxane (PDMS) membrane has been synthesized. Because the elastic PDMS membrane has a high malleability, with an external stress, it is very easy to regulate the interparticle distance in the gold nanoparticle array. The change in the distance between each nanoparticle will alter the surface plasmon interaction, and hence surface plasmon frequency can be manipulated. It is found that when the interparticle distance increases, the enhanced surface plasma mutual coupling will cause the blueshift of surface plasmon resonance frequency. The observed result satisfies the forecast based on electromagnetic theory.

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The authors would like to thank the members of their research team for their valuable suggestions and contributions to this work.

Long noncoding RNAs play a key role in the progression of colorectal cancer (CRC). However, the role and mechanism of LOC550643 in CRC cell growth and metastasis remain largely unknown. In this study, we assessed the clinical impacts of LOC550643 on CRC through the analysis of The Cancer Genome Atlas database, which revealed the significant upregulation of LOC550643 in CRC. Moreover, the high expression of LOC550643 was associated with poor survival in patients with CRC (p = 0.001). Multivariate Cox regression analysis indicated that LOC550643 overexpression was an independent prognostic factor for shorter overall survival in patients with CRC (adjusted hazard ratio, 1.90; 95% confidence interval, 1.21–3.00; p = 0.006). A biological function analysis revealed that LOC550643 knockdown reduced colon cancer cell growth by hindering cell cycle progression. In addition, LOC550643 knockdown significantly induced cell apoptosis through the inhibition of signaling activity in phosphoinositide 3-kinases. Moreover, LOC550643 knockdown contributed to the inhibition of migration and invasion ability in colon cancer cells. Furthermore, miR-29b-2-5p interacted with the LOC550643 sequence. Ectopic miR-29b-2-5p significantly suppressed colon cancer cell growth and motility and induced cell apoptosis. Our findings suggest that, LOC550643–miR-29b-2-5p axis was determined to participate in the growth and metastasis of colon cancer cells; this could serve as a useful molecular biomarker for cancer diagnosis and as a potential therapeutic target for CRC.