A peptide–nanowire interface that can effectively capture cancer-derived exosomes and release captured intact exosomes was constructed.

Understanding the metastatic cascade is critical for the treatment and prevention of cancer-related death. Within a tumor, immune cells have the capacity to fuse with tumor cells to generate tumor-immune hybrid cells (THCs). THCs are hypothesized to be a subset of cancer cells with the capacity to enter circulation as circulating hybrid cells (CHC) and seed metastases. To understand the mechanism of THC metastasis, we investigated CHCs in peripheral blood from patients with stage IV colorectal cancer (CRC), as well as THCs in tissues of primary colorectal cancers and their liver metastasis sites using immunofluorescence, spatial proteomic, spatial transcriptomic, molecular classification, and molecular pathway analyses. Our findings indicated a high prevalence of CHCs and THCs in patients with stage IV CRC. THCs expressed CTLA4 in primary CRC lesions and correlated with upregulation of CD68, CD4, and HLA-DR in metastatic liver lesions, which is found in the consensus molecular subtype (CMS) 1 of primary CRC tissue. Pathway analysis of these genes suggested that THCs are associated with neutrophils due to upregulation of neutrophil extracellular trap signaling (NET) and neutrophil degranulation pathways. These data provide molecular pathways for the formation of THCs suggesting fusion with neutrophils, which may facilitate extravasation and metastatic seeding.

A CD9-binding peptide (RSHRLRLH), screened from EWI-2, was characterized, and its inhibition effect on cancer-cell migration and invasion was demonstrated.

Colorectal cancers (CRC) with KRAS mutations (KRAS^mut) are frequently included in consensus molecular subtype 3 (CMS3) with profound metabolic deregulation. We explored the transcriptomic impact of KRAS^mut, focusing on the tumor microenvironment (TME) and pathways beyond metabolic deregulation. The status of KRAS^mut in patients with CRC was investigated and overall survival (OS) was compared with wild-type KRAS (KRAS^wt). Next, we identified CMS, and further investigated differentially expressed genes (DEG) of KRAS^mut and distinctive pathways. Lastly, we used spatially resolved gene expression profiling to define the effect of KRAS^mut in the TME regions of CMS3-classified CRC tissues. CRC patients with KRAS^mut were mainly enriched in CMS3. Their specific enrichments of immune gene signatures in immunosuppressive TME were associated with worse OS. Activation of TGFβ signaling by KRAS^mut was related to reduced pro-inflammatory and cytokine gene signatures, leading to suppression of immune infiltration. Digital spatial profiling in TME regions of KRAS^mut CMS3-classified tissues suggested up-regulated genes, CD40, CTLA4, ARG1, STAT3, IDO, and CD274, that could be characteristic of immune suppression in TME. This study may help to depict the complex transcriptomic profile of KRAS^mut in immunosuppressive TME. Future studies and clinical trials in CRC patients with KRAS^mut should consider these transcriptional landscapes.

Silver nanoparticles (AgNPs) were synthesized in skim natural rubber latex, the by-product from concentrated latex production. The role of ammonia was investigated by varying the concentration to be 0.217, 0.362, 0.377, 0.392, and 0.406 wt%. The emergence of AgNPs was detected by UV-visible spectrophotometer and electrical conductivity meter. Upon increasing ammonia concentration, the ABS peak increased to a maximum and slightly shifted to a higher wavelength and then it decreased afterward and slightly shifted to a lower wavelength. The shift of the ABS peak was consistent with the conductivity result. The kinetic model was proposed to explain the competition between the reducing effect and size-controlling effect of ammonia. The reducing effect seemed to dominate in the low range of concentration while the size-controlling effect via the formation of AgNH32+ complex ion was important in the higher range. The TEM figures evidently confirmed the effects.