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Valentine Stiles posted an update 6 months ago
e five mRNAs, including SFRP1, EDNRB, NR4A3, FHL2, NKX3‑1, IL6ST and FOXO1, may be involved in hepatocellular carcinoma tumorigenesis.Radiotherapy can induce the infiltration of immune suppressive cells which are involved in promoting tumor progression and recurrence. A number of natural products with immunomodulating abilities have been gaining attention as complementary cancer treatments. This attention is partly due to therapeutic strategies which have proven to be ineffective as a result of tumor‑induced immunosuppressive cells found in the tumor microenvironment. The present study investigated whether HS‑1793, a resveratrol analogue, can enhance the antitumor effects by inhibiting lymphocyte damage and immune suppression by regulatory T cells (Tregs) and tumor‑associated macrophages (TAMs), during radiation therapy. FM3A cells were used to determine the role of HS‑1793 in the radiation‑induced tumor immunity of murine breast cancer. HS‑1793 treatment with radiation significantly increased lymphocyte proliferation with concanavalin A (Con A) stimulation and reduced the DNA damage of lymphocytes in irradiated tumor‑bearing mice. The administration of HS‑1793 also decreased the number of Tregs, and reduced interleukin (IL)‑10 and transforming growth factor (TGF)‑β secretion in irradiated tumor‑bearing mice. In addition, HS‑1793 treatment inhibited CD206+ TAM infiltration in tumor tissue when compared to the controls or irradiation alone. Mechanistically, HS‑1793 suppressed tumor growth via the activation of effector T cells in irradiated mice. On the whole, the findings of the present study reveal that HS‑1793 treatment improves the outcome of radiation therapy by enhancing antitumor immunity. selleck Indeed, HS‑1793 appears to be a good therapeutic candidate for use in combination with radiotherapy in breast cancer.Dual specificity tyrosine‑phosphorylation‑regulated kinase 2 (DYRK2) is a protein kinase that functions as a novel tumor suppressor. Previous studies have reported that DYRK2 expression is decreased in colorectal cancer compared with adjacent non‑tumor tissues. However, the regulatory mechanisms by which the expression of DYRK2 is diminished remain unknown. The aim of the present study was to determine the regulatory mechanisms of DYRK2 expression. The present study identified the promoter regions of the DYRK2 gene and demonstrated that they contained CpG islands in human cancer cells. In addition, the DYRK2 promoter region exhibited a higher level of methylation in colorectal cancer tissues compared with healthy tissues from clinical samples. DYRK2 expression was increased at the mRNA and protein level in colorectal cancer cell lines by treatment with 5‑Azacytidine, a demethylating agent. The results further demonstrated that knockdown of DNA methyltransferase (DNMT) 1 elevated DYRK2 expression in colorectal cancer cell lines. A colitis‑related mouse carcinogenesis model also exhibited a lower DYRK2 level in colorectal cancer tissues compared with adjacent non‑tumor tissues. In this model, nuclear staining of DNMT1 was detected in colorectal cancer cells, whereas a cytoplastic distribution pattern of DNMT1 staining was exhibited in healthy tissue. Overall, these findings suggested that DYRK2 expression was downregulated via transcriptional regulation by DNMT1 to elevate the proliferation of colorectal cancer cells.Tongue cancer is one of the most common types of cancer, but its molecular etiology and pathogenesis remain unclear. The aim of the present study was to elucidate the pathogenesis of tongue cancer and investigate novel potential diagnostic and therapeutic targets. Four matched pairs of tongue cancer and paracancerous tissues were collected for RNA sequencing (RNA‑Seq), and the differentially expressed genes were analyzed. The RNA‑Seq data of tongue cancer tissues were further analyzed using bioinformatics and reverse transcription‑quantitative PCR analysis. The sequenced reads were quantified and qualified in accordance with the analysis demands. The transcriptomes of the tongue cancer tissues and paired paracancerous tissues were analyzed, and 1,700 upregulated and 2,249 downregulated genes were identified. Gene Ontology analysis uncovered a significant enrichment in the terms associated with extracellular matrix (ECM) organization, cell adhesion and collagen catabolic processes. Kyoto Encyclopedia of Genes and Genomes analysis demonstrated that these differentially expressed genes were mainly enriched in the focal adhesion pathway, ECM‑receptor interaction pathway, phosphoinositide 3‑kinase (PI3K)‑Akt pathway, and cell adhesion molecules. Comprehensive analyses of the gene tree and pathway network revealed that the majority of cell cycle genes were upregulated, while the majority of the genes associated with intracellular response, cell adhesion and cell differentiation were downregulated. The ECM‑receptor interaction, focal adhesion kinase (FAK) and PI3K‑Akt pathways were closely associated with one another and held key positions in differential signaling pathways. The ECM‑receptor, FAK and PI3K‑Akt signaling pathways were found to synergistically promote tongue cancer occurrence and progression, and may serve as potential diagnostic and therapeutic targets for this type of cancer.The emergence of new drugs is a major feature of the treatment history of multiple myeloma (MM), which also reflects the current incurability of MM. As a unique member of cyclin dependent kinase (CDK) family, CDK5 participates in numerous tumorigenic or non‑tumorigenic processes. The aim of this study is to investigate the effects of CDK5 on the viability of MM cells and bortezomib resistance using western blotting, immunohistochemistry, transient transfection, MTT assays, cell cycle analysis, apoptosis assays and a myeloma xenograft mouse model. The present study found that MM patients with high CDK5 expression in the bone marrow do not respond well to bortezomib, have higher DS stage and worse prognosis. Genetic and pharmacological (dinaciclib) inhibition of CDK5 triggers MM cell viability inhibition. Dinaciclib induces G2/M arrest and apoptosis of MM cells. In vivo experiments with myeloma xenograft mice indicate that dinaciclib significantly reduces the volume of tumors with good tolerance. Dinaciclib combined with bortezomib exerts a synergistic anti‑myeloma activity accompanied by inhibiting the activation of the nuclear factor‑κB pathway.