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Key Clinical Message: Our purpose is to clearly diagnose the tongue and back tuberculosis ulcer through detailed medical history collection combined with examination, so as to provide certain experience for the diagnosis and treatment of oral tuberculosis. [ABSTRACT FROM AUTHOR]

The article focuses on revealing the regulatory potency of CKAP5 in Human Papillomavirus positive Head and Neck Squamous Cell Carcinoma (HPV+ HNSCC) through Competing Endogenous RNA (ceRNA) analysis. It is discussed that Utilizing high-throughput sequencing technology, the study identifies differential gene expression and constructs a ceRNA network, highlighting CKAP5 as a potential therapeutic target in HPV+ HNSCC, emphasizing its significance in disease progression and prognosis.

BRCA2 And CDKN1A Interacting Protein (BCCIP) is initially identified as a tumor suppressor. Some recent studies confirmed its p53 binding capability. In this study, we explored the regulatory effect of BCCIPβ on p53 stability in HPV-positive and HPV-negative HNSCC cells. RNA-seq data from TCGA-HNSC were extracted for transcript isoform analysis in HPV-positive and HPV-negative tumors. HPV16-positive UM-SCC-47 (SCC47) and UM-SCC-104 (SCC104) and HPV-negative SCC-9 (SCC9) and UM-SCC-1 (SCC1) cell lines were used as in vitro cell models. Results showed that BCCIP β was the dominant transcript in both HPV-positive and HPV-negative HNSCC cases. Knockdown of BCCIP β decreased p53 protein concentration in the two HPV-negative cell lines but increased p53 concentration in the two HPV-positive cell lines. BCCIPβ inhibition increased proliferation and G1/S transition of SCC9 and SCC1 cells. In comparison, BCCIPβ inhibition slowed proliferation and increased G1 arrest of SCC104 and SCC47 cells. BCCIPβ inhibition prolonged the half-life of p53 protein and reduced p53 ubiquitination in the two HPV16-positive cell lines. Co-IP assay confirmed interactions among BCCIPβ, HPV E6, and p53 in both SCC104 and SCC47 cells. In comparison, only the interaction between BCCIPα and p53 was confirmed in these two cell lines. Either E6 or BCCIPβ inhibition reduced p53 ubiquitination and increased p53 concentration. However, inhibiting E6 and BCCIPβ at the same did not generate synergistic effects. On the contrary, p53 ubiquitination level was even higher in the combination group, with lower p53 concentration compared to the shE6 group. BCCIPβ overexpression in SCC47 cells with HPV E6 depletion significantly reduced p53 ubiquitination. In conclusion, this study found a novel interaction between HPV E6 and BCCIPβ in HPV16-positive HNSCC cells. The presence of HPV E6 turned BCCIPβ from a p53 stabilizer to a ubiquitination facilitator. This mechanism helps explain why BCCIPβ acted as a tumor suppressor in HPV-negative HNSCC but exerted oncogenic function in HPV16-positive HNSCC. • BCCIP β is the dominant isoform in both HPV-positive/HPV-negative HNSCC. • BCCIPβ has reverse correlations with p53 concertation in HNSCC by HPV status. • BCCIPβ has distinct regulations in proliferation of HNSCC cells by HPV status. • BCCIPβ participates in p53 ubiquitination in HPV-positive HNSCC. • BCCIPβ interacts with E6 and facilitates p53 ubiquitination in HPV-positive HNSCC. [ABSTRACT FROM AUTHOR]

In the present study, RNA interference (RNAi) was used to investigate the effect of vascular cell adhesion molecule 1 (VCAM1) silencing on the proliferation of human oral squamous carcinoma HN12 cells. HN12 cells were divided into three groups: The untreated blank control cell group (CK), the negative control group transfected with non-homologous vector (NC) and the positive group transfected with the target sequence VCAM1 small hairpin RNA (KD). Reverse-transcription polymerase chain reaction and western blot analysis were used to examine the effects of VCAM1-knockdown on the mRNA expression of VCAM1 and subsequent protein expression. Furthermore, the HN12 cell growth inhibition rate was detected using the cell counting kit-8 method. The VCAM1-targeted lentiviral vector RNAi significantly inhibited VCAM1 mRNA, and subsequent protein, expression. Compared with the NC group, the VCAM1 gene knockdown efficiency was ~85%, while the expression level of VCAM1 protein was reduced by ~74% in KD group cells. In addition, cell growth was significantly inhibited in the KD group, with a growth inhibition rate of ~34%. Therefore, this targeted lentiviral vector RNAi effectively inhibited VCAM1 gene, and subsequent protein, expression, as well as the proliferation of oral squamous carcinoma cells. These results may provide an experimental reference for the diagnosis and treatment of oral squamous cell carcinoma. [ABSTRACT FROM AUTHOR]

Abstract: The successful clinical outcome of the implanted tissue-engineered bone is dependent on the establishment of a functional vascular network. A gene-enhanced tissue engineering represents a promising approach for vascularization. Our previous study indicated that hypoxia-inducible factor-1α (HIF-1α) can up-regulate the expression of vascular endothelial growth factor (VEGF) and stromal-derived factor 1 (SDF-1) in bone mesenchymal stem cells (BMSCs). The angiogenesis is a co-ordinated process that requires the participation of multiple angiogenic factors. To further explore the angiogenic effect of HIF-1α mediated stem cells, in this study, we systematically evaluated the function of HIF-1α in enhancing BMSCs angiogenesis in vitro and in vivo. A constitutively active form of HIF-1α (CA5) was inserted into a lentivirus vector and transduced into BMSCs, and its effect on vascularization and vascular remodeling was further evaluated in a rat critical-sized calvarial defects model with a gelatin sponge (GS) scaffold. The expression of the key angiogenic factors including VEGF, SDF-1, basic fibroblast growth factor (bFGF), placental growth factor (PLGF), angiopoietin 1 (ANGPT1), and stem cell factor (SCF) at both mRNAs and proteins levels in BMSCs were significantly enhanced by HIF-1α overexpression compared to the in vitro control group. In addition, HIF-1α-over expressing BMSCs showed dramatically improved blood vessel formation in the tissue-engineered bone as analyzed by photography of specimen, micro-CT, and histology. These data confirm the important role of HIF-1α in angiogenesis in tissue-engineered bone. Improved understanding of the mechanisms of angiogenesis may offer exciting therapeutic opportunities for vascularization, vascular remodeling, and bone defect repair using tissue engineering strategies in the future. [Copyright &y& Elsevier]