Carcinoembryonic antigen (CEA) is highly expressed in embryo and colorectal cancer (CRC) and has been widely used as a marker for CRC. Emerging evidence has demonstrated that elevated CEA levels promote CRC progression. However, the mechanism of the increased CEA expression in patients with primary and recurrent CRC is still an open question. In this study, we showed that c‐KIT, ELK1, and CEA were hyperexpressed in patients with CRC, especially patients with recurrent disease. From bioinformatics analysis, we picked ELK1 as a candidate transcription factor (TF) for CEA; the binding site of ELK1 within the CEA promoter was confirmed by chromatin immunoprecipitation and dual luciferase reporter assays. Overexpression of ELK1 increased CEA expression in vitro, while knockdown of ELK1 decreased CEA. Upregulated ELK1 promoted the adhesion, migration, and invasion of CRC cells, however knockdown of CEA blocked the activities of ELK1‐overexpressed CRC cells. Furthermore, we explored the role of c‐KIT‐ERK1/2 signaling in activation of ELK1. Blocking c‐KIT signaling using Imatinib or ISCK03 reduced p‐ELK1 expression and consequently decreased CEA levels in CRC cells, as did blocking the ERK1/2 pathway by U0126. Compared with wild type littermates, the c‐kit loss‐of‐functional Wadsm/m mice showed lowered c‐KIT, ELK1, and CEA expression. In conclusion, our study revealed that ELK1, which was activated by c‐KIT‐ERK1/2 signaling, was a key TF for CEA expression. Blocking ELK1 or its upstream signaling could be an alternative way to decelerate CRC progression. Besides being a biomarker for CRC, CEA could be used for guiding targeted therapy.

In this study, polymer (polyethylene glycol [PEG] and Chitosan)‐coated silver oxide nanoparticles (NPs) have been prepared by hydrothermal method. The polymer‐encapsulated NPs are characterized by materials‐related characterization techniques such as X‐Ray diffraction (XRD), scanning electron microscope (SEM), Ultraviolet–visible (UV–Vis), photoluminescence (PL), and Fourier‐transform infrared (FTIR) spectroscopy. The crystallite size of silver oxide NPs is 43.39 nm and reduces to 34.56 nm and 30.43 nm for PEG and Chitosan functionalized NPs, respectively. SEM micrographs show the spherical morphology of the synthesized nanomaterials with the grain size of pristine, PEG, and Chitosan functionalized silver oxide NPs as 60.9 ± 14.1, 70.9 ± 10.3, and 57.2 ± 7.8 nm, respectively. The band gap of silver oxide NPs increases upon polymer functionalization. PEGlyation of silver oxide NPs has enhanced its anticancer potential significantly against liver cancer cell line (HuH‐7), shows least cell viability, and IC50 value is as low as 0.106 μg/mL and in the case of Chitosan coating 4.505 μg/mL. The antibacterial properties and biofilm inhibition are investigated against bacterial extracts of Escherichia coli and Staphylococcus aureus. The polymer‐coated silver oxide NPs have shown enhanced antibacterial potential against both S. aureus and E. coli. CAM assay is used to evaluate the wound‐healing ability of nanomaterials. Alginate gels incorporated with NPs have promoted wound healing. Our results revealed that the surface modification by PEG and Chitosan improved the therapeutic potential of silver oxide NPs.

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