Here, we have developed a localized catalytic hairpin assembly (LCHA) strategy for intracellular miR-21 imaging by using DNA nanowires confining both hairpin probes in a compact space.

No abstract

It is of great value to detect biological molecules in live cells.However,probes for imaging low-abundance targets in live cells are limited by the one-to-one signal-triggered model. Here,weintroduce the concept of the amplified FRET nanoflare,which employs high-abundance endogenous mRNA as fuel strands to amplify the detection of lowa bundance intracellular miRNA. As far as we know,this is the first report of an endogenous mRNA-powered nanomachine for intracellular molecular detection. We experimentally prove the mechanism of the nanomachine and demonstrate its specificity and sensitivity.T he proposed amplified FRET nanoflare can act as an excellent intracellular molecular detection strategy that is promising for biological and medical applications.

We have designed dual-microRNA-controlled cascaded logic DNA circuits for cancer cell subtype identification. The basic idea is to improve sensitivity by cascading DNAzyme and hybridization chain reaction (HCR), and improve accuracy by simultaneous detection of miR-122 and miR-21.

Obesity is involved in tumor progression. However, the corresponding mechanisms remain largely unknown. Here, we report that adipocytes increase the invasive ability of tumor cells by producing exosomes with a high level of MMP3. Compared with 3T3-L1 cells, 3T3-L1 adipocytes are enriched in MMP3 protein and can transfer MMP3 to 3LL lung cancer cells. Then, MMP3 activates MMP9 activity in 3LL cells and promotes invasion in vitro and in vivo via MMP9. Furthermore, MMP3 protein levels in lung tumor tissues from obese patients are increased compared with those of non-obese patients. In addition, MMP3 protein levels are positively correlated with MMP9 activity in tumor tissues. Therefore, our results reveal a novel mechanism in the adipocyte-derived exosome-mediated promotion of lung tumor metastasis, which extends our knowledge regarding obesity and tumor progression.

The incidence of lung cancer increases annually. However, the effects of the present methods for the treatment of lung cancer are extremely poor. It has been reported that exosomes from heat‑stressed 3LL Lewis lung tumor cells effectively elicit systemic antitumor immunity. CD40 signaling is critical in the activation of dendritic cells (DCs), which are important in the induction of antitumor immunity. In the present study, exosomes from CD40 ligand gene‑modified 3LL tumor cells (CD40L‑EXO) were identified to be more immunogenic compared with control‑EXO and lac Z-EXO. CD40L‑EXO induced a more mature phenotype of the DCs and promoted them to secrete high levels of interleukin‑12. CD40L‑EXO‑treated DCs induced a greater proliferation of allogeneic T cells in the mixed lymphocyte reaction. Moreover, CD40L‑EXO induced robust tumor antigen‑specific CD4+ T cell proliferation ex vivo. CD40L‑EXO were also extremely effective in the protective and therapeutic antitumor tests in vivo. These results indicate that CD40L‑EXO may be used as an efficient vaccine for lung cancer immunotherapy.

No abstract

SummaryAutophagy can mediate antiviral immunity. However, it remains unknown whether autophagy regulates the immune response of dendritic cells (DCs) to influenza A (H1N1) pdm09 infection. In this study, we found that infection with the H1N1 virus induced DC autophagy in an endocytosis-dependent manner. Compared with autophagy-deficient Beclin-1 +/À mice, we found that bone-marrow-derived DCs from wild-type mice (WT BMDCs) presented a more mature phenotype on H1N1 infection. Wildtype BMDCs secreted higher levels of interleukin-6 (IL-6), tumour necrosis factor-a ( Our data indicate that autophagy is important in the regulation of the DC immune response to H1N1 infection, thereby extending our understanding of host immune responses to the virus.