RESUMO
Laryngeal squamous cell carcinoma (LSCC) is an aggressive and lethal malignant neoplasm with extremely poor prognoses. Accumulating evidence has indicated that preferentially expressed antigen in melanoma (PRAME) is correlated with several kinds of cancers. However, there is little direct evidence to substantiate the biological function of PRAME in LSCC. The purpose of the current study is to explore the oncogenic role of PRAME in LSCC. PRAME expression was analyzed in 57 pairs of LSCC tumor tissue samples through quantitative real-time PCR, and the correlation between PRAME and clinicopathological features was analyzed. The result indicated that PRAME was overexpressed in the LSCC patients and correlated with the TNM staging and lymphatic metastasis. The biological functions and molecular mechanism of PRAME in LSCC progression were investigated through in vitro and in vivo assays. Functional studies confirmed that PRAME facilitated the proliferation, invasion, migration, and epithelial-mesenchymal transition of LSCC cells, and PRAME also promoted tumor growth in vivo. HDAC5 was identified as an upstream regulator that can affect the expression of PRAME. Moreover, PRAME played the role at least partially by activating PI3K/AKT/mTOR pathways. The above findings elucidate that PRAME may be a valuable oncogene target, contributing to the diagnosis and therapy of LSCC.
RESUMO
Oral lichen planus (OLP), defined as a potential for malignant transformation, is a chronic inflammatory disease in which abnormal angiogenesis serves a role in the malignant changes of the disease. OLP-associated fibroblasts (OLP-MFs), derived from the stroma of OLP tissues, are characterized by the presence of myofibroblasts and contribute to the secretion of pro-inflammatory cytokines, which may be involved in the molecular pathogenesis of OLP. However, the associated mechanisms of angiogenesis in OLP remain unknown. The present study aimed to verify the expression of intercellular adhesion molecular 1, vascular cell adhesion molecule 1, VEGF and CD34 in OLP, and to investigate whether IL-6 secreted by OLP-MFs promoted OLP angiogenesis and the effect of its corresponding antibody inhibition. The results of the experiments demonstrated that inflammation was present and OLP upregulated the secretion of IL-6 by OLP stromal fibroblasts, thereby enhancing OLP angiogenesis. Anti-IL-6 receptor antibody inhibited OLP-stroma IL-6 signaling and suppressed OLP angiogenesis. The antibody inhibited the inflammatory response by inhibiting the secretion of inflammatory factors, including IL-6, to suppress angiogenesis and reduce disease progression, thus indicating that this could be a potential target to develop a treatment for OLP.
RESUMO
AIM: To prepare bispecific monoclonal antibody (bsmAb) against HIV p24 and human group A erythrocytes, and set up an indirect hemagglutination test for detecting HIV p24. METHODS: Hybridoma cells 2-E(4) secreting anti-HIV p24 mAb and hybridoma cells S(2) secreting anti-human group A erythrocyte mAb were naturalized with 8-Ag and 5-BrdU respectively, making them sensitive to HAT. Then the two hybridoma cells sensitive to HAT were fused by routine method and hybrid-hybridoma cells secreting the bsmAb against HIV p24 and human group A erythrocytes were screened. The bsmAb was used to establish an indirect hemagglutination test for detecting HIV p24. RESULTS: 6 hybrid-hybridoma cell lines were obtained. An indirect hemagglutination test for detecting HIV p24 was set up by using the bsmAb, and its sensitivity reached 400 ng/L. CONCLUSION: The bsmAb against HIV p24 and human group A erythrocytes is prepared and a rapid indirect hemagglutination test for detecting HIV p24 is developed by using the purified bsmAb.
