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Aguilar Garner posted an update 6 months, 1 week ago
On the whole, the findings of the present study demonstrated that JMJD2C promotes the malignancy of MM via the activation of the β‑catenin pathway. These results suggested that JMJD2C may be a potential target for MM treatment.CD155/T cell immunoreceptor with Ig and ITIM domains (TIGIT) is a novel type of immune checkpoint. CD155 is an adhesion molecule that is upregulated during tumor progression and promotes the proliferative and migratory abilities of tumor cells via various pathways. TIGIT, an inhibitory receptor, is mainly expressed on natural killer (NK), CD8+ T, CD4+ T and T regulatory (Treg) cells. CD155 transmits immune signals via interacting with the inhibitory checkpoint receptor TIGIT, thereby inhibiting the function of T and NK cells. Several preclinical studies have supported the use of TIGIT blockade as a monotherapy or combined with other immune checkpoint inhibitors for the treatment of advanced solid malignant tumors. The present review summarized the current knowledge on CD155/TIGIT and the lymphocyte‑mediated inhibitory mechanism of CD155/TIGIT. Daporinad price An in‑depth understanding of the role of CD155/TIGIT in tumors may aid to improve the application of immune checkpoint inhibitors in tumor therapy.The biological functions of circular RNAs in liver tumorigenesis have been well demonstrated by a number of studies. Nevertheless, to the best of our knowledge, the role and mechanism of action of hsa_circ_0008537 (circ_0008537) in liver cancer pathogenesis remain undetermined. In the present study, circ_0008537 expression was associated with the GLI3 gene and was markedly increased in liver cancer tissue specimens and cells. High expression levels of circ_0008537 exhibited a poor prognosis. In addition, circ_0008537 overexpression resulted in an increased proliferation, migration and invasion of liver cancer cells, whereas circ_0008537 knockdown exhibited opposite effects. circ_0008537 acted as a sponge of microRNA‑153‑3p (miR‑153‑3p), and a negative correlation was observed between circ_0008537 and miR‑153‑3p expression in liver cancer. Transfection with miR‑153‑3p further abolished the effects of circ_0008537 on the malignant behavior of liver cancer cells. Furthermore, circ_0008537 indirectly affected the expression levels of pro‑survival protein myeloid cell leukemia 1 (MCL1) and snail family zinc finger 1 (Snail1) via miR‑153‑3p in liver cancer cells. In conclusion, the data indicated that circ_0008537 facilitated liver carcinogenesis by indirectly regulating miR‑153‑3p and leading to the release of MCL1 and Snail1.Dysregulation of Rab proteins has been observed in various types of cancer. Ectopic expression of Rab31, a member of the Rab protein family, is involved in cancer development and progression. However, the specific role and potential molecular mechanism underlying the functions of Rab31 remain largely unknown. Therefore, the current study aimed to investigate the functions of Rab31 in the development of cancer. Human oral squamous cell carcinoma (OSCC) samples were examined to determine the expression profile of Rab31 and its association with the clinicopathological characteristics of patients with OSCC. Knockdown of Rab31 expression with short hairpin RNA was performed to analyze the functions of Rab31 in vitro and in vivo. The expression of Rab31 was significantly elevated in human OSCC samples compared with that in normal oral mucosal epithelial tissues, and high expression levels were associated with high pathological grades. Furthermore, positive expression of Rab31 was associated with a poor prognosis ination of a new therapeutic target for the treatment of OSCC.Human bone marrow‑derived mesenchymal stem cells secreting tumor necrosis factor‑related apoptosis‑inducing ligand (MSCs‑TRAIL) have demonstrated effective anti‑tumor activity against various tumors including lung, pancreatic and prostate tumors, although several tumor types are not responsive. In such case, other reagents may decrease tumor growth via TRAIL‑mediated cell death. The present study aimed to examine the effectiveness of valproic acid (VPA) in enhancing the efficacy of TRAIL, which was delivered using MSCs. Moreover, the present study examined the induced tumor tropism of MSCs via cell viability and migration assays. Combination treatment with VPA and MSCs‑TRAIL enhanced the glioma therapeutic effect by increasing death receptor 5 and caspase activation. Migration assays identified increased MSC migration in VPA and MSCs‑TRAIL‑treated glioma cells and in the tumor site in glioma‑bearing mice compared with VPA or MSC‑TRAIL treatment alone. In vivo experiments demonstrated that MSC‑based TRAIL gene delivery to VPA‑treated tumors had greater therapeutic efficacy compared with treatment with each agent alone. These findings suggested that VPA treatment increased the therapeutic efficacy of MSC‑TRAIL via TRAIL‑induced apoptosis and enhanced tropism of MSCs, which may offer a useful strategy for tumor gene therapy.Helicobacter pylori (H. pylori) infection is a major risk factor for the development of gastric cancer. The authors previously demonstrated that in mice deficient in myeloid differentiation primary response 88 (Myd88‑/‑), infection with Helicobacter felis (H. felis) a close relative of H. pylori, subsequently rapidly progressed to neoplasia. The present study examined circulating tumor cells (CTCs) by measuring the expression of cytokeratins, epithelial‑to‑mesenchymal transition (EMT)‑related markers and cancer stem cell (CSC) markers in bone marrow and peripheral blood from Myd88‑/‑ and wild‑type (WT) mice. Cytokeratins CK8/18 were detected as early as 4 months post‑infection in Myd88‑/‑ mice. By contrast, cytokeratins were not detected in WT mice even after 7 months post‑infection. The expression of Mucin‑1 (MUC1) was observed in both bone marrow and peripheral blood at different time points, suggesting its role in gastric cancer metastasis. Snail, Twist and ZEB were expressed at different levels in bone marrow and peripheral blood. The expression of these EMT‑related markers suggests the manifestation of cancer metastasis in the early stages of disease development. LGR5, CD44 and CD133 were the most prominent CSC markers detected. The detection of CSC and EMT markers along with cytokeratins does reinforce their use as biomarkers for gastric cancer metastasis. This early detection of markers suggests that CTCs leave primary site even before cancer is well established. Thus, cytokeratins, EMT, and CSCs could be used as biomarkers to detect aggressive forms of gastric cancers. This information may prove to be of significance in stratifying patients for treatment prior to the onset of severe disease‑related characteristics.