Head and neck squamous cell carcinomas (HNSCCs) are one of the most frequently detected cancers in the world; not all mechanisms related to the expression of keratin in this type of cancer are known. The aim of this study was to evaluate type II cytokeratins (KRT): KRT6A, KRT6B, and KRT6C protein concentrations in 54 tumor and margin samples of head and neck squamous cell carcinoma (HNSCC). Moreover, we examined a possible association between protein concentration and the clinical and demographic variables. Protein concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Significantly higher KRT6A protein concentration was found in HNSCC samples compared to surgical margins. An inverse relationship was observed for KRT6B and KRT6C proteins. We showed an association between the KRT6C protein level and clinical parameters T and N in tumor and margin samples. When analyzing the effect of smoking and drinking on KRT6A, KRT6B, and KRT6C levels, we demonstrated a statistically significant difference between regular or occasional tobacco and alcohol habits and patients who do not have any tobacco and alcohol habits in tumor and margin samples. Moreover, we found an association between KRT6B and KRT6C concentration and proliferative index Ki-67 and HPV status in tumor samples. Our results showed that concentrations of KRT6s were different in the tumor and the margin samples and varied in relation to clinical and demographic parameters. We add information to the current knowledge about the role of KRT6s isoforms in HNSCC. We speculate that variations in the studied isoforms of the KRT6 protein could be due to the presence and development of the tumor and its microenvironment. It is important to note that the analyses were performed in tumor and surgical margins and can provide more accurate information on the function in normal and cancer cells and regulation in response to various factors.

Tumour-derived exosomes have recently been shown to participate in the formation and progression of different cancer processes, including tumour microenvironment remodelling, angiogenesis, invasion, metastasis, and drug resistance. However, the function and mechanism of exosome-encapsulated nucleic acids and proteins in bladder cancer remain unclear. This study aimed to investigate the effects of tumour-derived exosomes on the tumorigenesis and development of bladder cancer.
In this study, gene expression profiles and clinical information were collected from The Cancer Genome Atlas (TCGA) database and two independent Gene Expression Omnibus (GEO) datasets. The nucleic acids and proteins encapsulated in bladder cancer-derived exosomes were obtained from the ExoCarta database. Based on these databases, the expression patterns of exosomal mRNAs and proteins and the matched clinicopathological characteristics were analysed. Furthermore, we carried out a series of experiments to verify the relevant findings.
A total of 7280 differentially expressed mRNAs were found in TCGA data, of which 52 mRNAs were shown to be encapsulated in bladder cancer-derived exosomes. Survival analysis based on the UALCAN database showed that among the top 10 upregulated and the top 10 downregulated exosomal genes, only the expression of KRT6B had a statistically significant effect on the survival of bladder cancer patients. Additionally, clinical correlation analysis showed that the elevated level of KRT6B was highly associated with bladder cancer stage, grade, and metastasis status. GSEA revealed that KRT6B was involved not only in epithelial-mesenchymal transition-related pathways but also in the immune response in bladder cancer. Ultimately, our experimental results were also consistent with the bioinformatic analysis.
KRT6B, which can be detected in bladder cancer-derived exosomes, plays an important role in the epithelial-mesenchymal transition and immune responses in bladder cancer. Further research will enable its potentially prognostic marker and therapeutic target for bladder cancer.

The study was performed to investigate the relationship between KRT6B and Notch1 in the development and progress of hepatocellular carcinoma. The cell viability was detected by CCK8 assay. The cell apoptosis was assessed by annexin V-PI double-labeling staining on a flow cytometry. Expression of genes and proteins were analyzed by real-time PCR and Western blotting, respectively. KRT6B gene was overexpressed using a lentiviral expression vector in a human hepatoma cell line in vitro, in order to explore the mechanism by which the KRT6B promoted cell growth. The results of CCK8 and immunohistochemistry showed that honokiol induced cell death in a concentration- dependent manner, and suppressed human hepatoma cells\' proliferation. The mRNA and protein expression of Notch1 was significantly lower in human hepatoma cells with honokiol treatment than that in the untreatment group. Activation of Notch-1 by exogenous transfection of Notch1 intracellular domain increased KRT6B expression in human hepatoma cells. Furthermore, cells were transfected with the wild type pLenti-KRT6B vector, the protein expression of KRT6B and NOTCH1 was significantly upregulated in human hepatoma cells with honokiol treatment. Overexpression of KRT6B promoted hepatoma cells\' proliferation and showed anti-apoptosis effect. This study demonstrated that honokiol could induce human hepatoma cells\' apoptosis. KRT6B, a key mediator of Notch signaling, was downregulated in honokiol-induced hepatocellular carcinoma apoptosis, suggesting that KRT6B might be a novel therapeutic target for the treatment of hepatocellular carcinoma.