Background Stratum corneum is located in the outermost layer of the skin and is the most important part of the skin barrier. Stratum corneum mainly contains keratinocytes, lipids, and desmosomes. Their normal metabolic process is closely related to the function of skin barrier. Aims This paper reviews the structure and function of stratum corneum, influencing factors, skin diseases, and common solutions. Methods An extensive literature search was conducted on the structure and function of stratum corneum, influencing factors, skin diseases, and common solutions. Results This paper reviews the structure and function of stratum corneum and the influence of various factors on stratum corneum metabolism. At the same time, the existing skin problems, skin diseases, and common solutions are summarized. Conclusions This information will help to understand the function, molecular mechanism, and influencing factors of stratum corneum metabolism, and provide new ideas for stratum corneum health management and cosmetic research and development.

In recent decades, the incidence of thyroid cancer (TC) has rapidly increased, leading us to explore the complex underlying mechanisms. We identified the gene Phospholipase C Delta 3 (PLCD3) as a potential oncogene in TC by conducting the whole transcriptome sequencing. Our study is to understand the oncogenic role of PLCD3 in TC. We verified the overexpression of PLCD3 in TC from The Cancer Genome Atlas, Gene Expression Omnibus databases, and a locally validated cohort. Clinical correlation analysis showed that PLCD3 expression was related to histological type, T stage, lymph node metastasis (LNM), and disease stage. The high expression of PLCD3 could be a distinguishing factor for TC and its LNM. The biological function was examined using small interfering RNA-transfected TC cell lines. Silenced PLCD3 could inhibit colony formation, migration, and invasion ability and promote apoptosis of TC cell lines. PLCD3 silencing reversed the epithelial-mesenchymal transition but induced the apoptotic progress. Further exploration revealed that PLCD3 might be associated with critical genes of the Hippo pathway. The expressions of RHOA, YAP1/TAZ, and their downstream targets were decreased significantly when PLCD3 was down-regulated. YAP1 overexpression rescued the tumor-suppressive effect caused by PLCD3 silencing. This study demonstrates that PLCD3 is an oncogene that supports tumorigenesis and progression in TC, and PLCD3 may be a potential target gene for TC treatment.

B and T lymphocyte attenuator (BTLA) is a newly identified immune checkpoint molecular belonging to the CD28 immunoglobulin superfamily. However, the expression and clinical value of BTLA in skin cutaneous melanoma (SKCM) has not been widely characterized. We found that BTLA levels were upregulated in metastatic melanoma compared to normal skin tissues and primary melanoma. Higher BTLA was also correlated with improved prognosis in SKCM based on several datasets. The multivariate Cox regression model revealed that BTLA was an independent survival indicator in metastatic melanoma. Tumor microenvironment analysis indicated BTLA was positively associated with the infiltrating levels of different immune cells and the activity of the anti-cancer immunity cycle. Importantly, BTLA accurately predicted the outcome of melanoma patients treated with MAGE-A3 blocker or first-line anti-PD-1. The present findings disclose that BTLA is a reliable biomarker for prognosis and immunotherapeutic response and might contribute to developing novel SKCM immunological treatment strategies.

Background. Thyroid carcinoma (TC) is an increasingly common malignancy of endocrine organs, and its most frequently encountered histotype is papillary thyroid cancer (PTC). Identifying new potential gene alterations is important for completely elucidating the mechanism of PTC initiation and progression. Thus, we performed whole transcriptome sequence analysis (RNA-seq) on 79 PTC tissue samples and paired adjacent nontumor tissue samples to study the molecular mechanism of TC tumorigenesis and progression further. The results of RNA-seq analysis showed that spectrin beta, nonerythrocytic 2 (SPTBN2), was markedly overexpressed in PTC tissues relative to that in the paired nontumor tissues. Additionally, the analysis results for 502 PTC samples and 58 nontumor thyroid samples from The Cancer Genome Atlas dataset were consistent with our RNA-seq results. However, the molecular mechanisms and function of SPTBN2 in TC progression remain unknown. Methods. We examined SPTBN2 gene expression in 48 papillary thyroid tumor tissues and paired adjacent normal thyroid tissues by using qRT-PCR. SPTBN2 expression in the TC cell lines was silenced by small interfering RNA. Then, the transfected TC cells were used to investigate the in vitro function of SPTBN2. Result. The expression of SPTBN2 was significantly upregulated in our RNA-seq cohort, our local validated cohort, and TCGA RNA-seq cohort. The results of the in vitro experiment revealed that in TC cell lines, SPTBN2 downregulation considerably suppressed tumor cell proliferation, the cell cycle, migration, colony formation, and invasion and induced cell apoptosis. Furthermore, the protein levels of CCNE2, CDK2, CDK4, and Bcl-2 were downregulated, and those of P21, Bax, cleaved caspase-8, and cleaved caspase-3 had increased in transfected TC cells relative to in control TC cells. Conclusion. The downregulation of SPTBN2 caused apoptosis and retarded G1/S cell cycle transition in TC cells. Thus, SPTBN2 may be a good candidate gene for TC diagnosis and therapy.

Purpose The incidence rate of breast cancer (BC) has increased annually. Downstream neighbor of son (DONSON) critically affects cell cycle progression and maintains stable genomic properties; however, its relevant effects on BC growth and progression require in-depth investigation. Methods DONSON upregulation was validated in public databases. DONSON expression in matched BC and adjacent tissues and cell lines (MDA-MB-231, BT-549, and HS-578T) was determined using quantitative reverse transcription polymerase chain reaction. In vitro apoptosis, invasion, migration, and proliferation tests were performed to ascertain the functions of DONSON in BC cell lines. Then, using western blot analysis, the levels of DONSON downstream proteins were determined. Results Compared to the control, DONSON was expressed at higher levels in BC tissues and cell lines. DONSON knockdown facilitated apoptosis and limited proliferation, migration, invasion, and S/G2 transition of BC cells in vitro . Furthermore, DONSON overexpression promoted BC cell proliferation and inhibited apoptosis in vitro . Moreover, DONSON knockdown reduced cyclin A1 and cyclin-dependent kinase 2 levels. Moreover, DONSON knockdown limited the progression of epithelial-mesenchymal transition. Conclusion DONSON critically affects BC growth and serves as a possible target and marker for the efficacy of subsequent therapies.