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and FdUMP sensitivity should be considered in 5FU‑resistant cells.N6‑methyladenosine (m6A) is one of the most prevalent post‑transcriptional RNA modifications. The enzymes involved in the regulation of m6A include methyltransferase (writers), demethylase (erasers) and m6A recognition proteins (readers). Accumulating studies have demonstrated that m6A modifications have a distinct effect on various biological processes, including tumorigenesis, cell differentiation, embryonic development and neurogenic diseases, while our knowledge of the specific mechanism underlying m6A methylation in various cancer types is still limited. Various signaling pathways have an effect on tumorigenesis, invasion and apoptosis of malignant tumors. The present review summarizes the recent progress in research regarding the role of m6A in human cancer and discusses the influence of m6A on classic signaling pathways in malignant tumors.Tumor metastasis is a destructive characteristic of malignant tumors and the fundamental reason why malignant tumors are difficult to cure. The concept of a pre‑metastatic niche (PMN) provides a novel way to elucidate the molecular mechanism of tumor metastasis. At present, the PMN has been considered as a critical determinant priming distal sites for metastasis. Accumulating evidence has suggested that exosomes are cellular communicators serving a pivotal role in mediating tumor cell metastasis by establishing the PMN. Among exosomal cargos, non‑coding RNAs and proteins are two commonly studied components; however, the latter has received less attention. The present review aimed to summarize the findings regarding cargo proteins selectively loaded in malignant tumor‑derived exosomes. Metastasis‑associated proteins have been demonstrated to be selectively enriched in malignant tumor‑derived exosomes. Exosomal proteins promote PMN formation to mediate the site‑specific metastasis of tumor cells by inducing lymphangiogenesis, angiogenesis and permeability, educating stromal cells, remodeling the extracellular matrix, and suppressing the antitumor immune response. These exosomal proteins have great potential in predicting organ‑directed metastasis and prognosis, as well as in cancer therapy.Triggering receptor expressed on myeloid cells‑1 (TREM1) is a cell‑surface protein expressed on tumor‑associated macrophages (TAMs), the predominant inflammatory cells in the tumor microenvironment; however, the mechanisms for the influence of TREM1 on TAM polarization during liver cancer progression have not been investigated. In the present study, 20 patients diagnosed with hepatocellular carcinoma (HCC) who underwent surgery were enrolled, and TREM1 expression on M1/M2 macrophages and on M2 macrophages was assessed by immunohistochemical staining. Human leukemia monocytic cells (THP‑1) were differentiated into M2 macrophages using phorbol 12‑myristate 13‑acetate, IL‑4 and IL‑13. A specific short hairpin RNA was used to knockdown TREM1 expression. To investigate the effects of TREM1 downregulation in macrophages on the migration and invasion of liver cancer cells, HepG2 and MHCC97H cell lines were co‑cultured with specific conditioned media. Reverse transcription‑quantitative PCR and western blot analyses wT signaling. In addition, migration and invasion of HepG2 and MHCC97H cells were inhibited when this signaling pathway was blocked. The present findings suggest TREM1 as a novel potential therapeutic target for liver cancer management.Differentiated thyroid carcinoma (DTC) is the most common malignant neoplasm of the endocrine system. In children and adolescents, DTC usually presents as a more aggressive disease than in the adult population, but patients often have a favourable prognosis, even in cases of advanced disease. Nevertheless, certain patients have persistent or recurrent disease leading to increased morbidity. A significant challenge in the management of DTC is identifying the subgroup of patients with a high risk of unfavourable outcomes. Prognostic factors related to the patient, tumour, and stratification systems (Tumor‑Node‑Metastasis/American Joint Committee on Cancer, American Thyroid Association risk classification and dynamic risk stratification) are used in an attempt to identify the individuals at increased risk. In the present review, the current risk classification systems applied for paediatric thyroid cancer are discussed, highlighting the major differences between paediatric and adult DTC in pathophysiology, clinical presentation and long‑term outcomes. In recent years, genetic markers have also been proposed as prognostic factors for children and adolescents with DTC. Advances in the understanding of the molecular profile of paediatric DTC may aid individualized management, potentially improving diagnosis and treatment. This review article aims to critically review and update the current concepts on DTC management in children and adolescents, with an emphasis on clinical presentation, treatment, risk assessment, follow‑up and future perspectives.Recent studies have reported that gene amplified in squamous cell carcinoma 1 (GASC1) is involved in the progression of several types of cancer. However, whether GASC1 promotes glioma progression remains unknown. Therefore, the present study aimed to investigate the effect of GASC1 exposure on glioma tumorigenesis. The western blot demonstrated that grade III and IV glioma tissues exhibited a higher mRNA and protein expression of GASC1. Moreover, CD133+ U87 or U251 cells from magnetic cell separation exhibited a higher GASC1 expression. Invasion Transwell assay, clonogenic assay and wound healing assay have shown that GASC1 inhibition using a pharmacological inhibitor and specific short hairpin (sh)RNA suppressed the invasive, migratory and tumorsphere forming abilities of primary culture human glioma cells. Furthermore, GASC1‑knockdown decreased notch receptor (Notch) responsive protein hes family bHLH transcription factor 1 (Hes1) signaling. GASC1 inhibition reduced notch receptor 1 (NOTCH1) expression, and a NOTCH1 inhibitor enhanced the effects of GASC1 inhibition on the CD133+ U87 or U251 cell tumorsphere forming ability, while NOTCH1 overexpression abrogated these effects. In addition, the GASC1 inhibitor caffeic acid and/or the NOTCH1 inhibitor DAPT (a γ‑Secretase Inhibitor), efficiently suppressed the human glioma xenograft tumors. Thus, the present results demonstrated the importance of GASC1 in the progression of glioma and identified that GASC1 promotes glioma progression, at least in part, by enhancing NOTCH signaling, suggesting that GASC1/NOTCH1 signaling may be a potential therapeutic target for glioma treatment.Radioactive iodine (RAI, 131I) therapy is the main treatment for thyroid carcinoma (TC). Long noncoding RNA (lncRNA)/microRNA (miR) competing endogenous RNA (ceRNA) networks have aroused great interest for their roles in gene expression. The present study aimed to investigate the effect of lncRNA SNHG7 on the growth and 131I resistance of TC. Differentially expressed lncRNAs in TC and paracancerous tissues were analyzed. The binding of miR‑9‑5p with small nucleolar RNA host gene 7 (SNHG7) and dipeptidyl‑peptidase 4 (DPP4) was identified. Gain‑ and loss‑of‑function analyses of SNHG7 and miR‑9‑5p were performed to determine their effects on the growth and 131I resistance of TC cells. The activity of the PI3K/Akt pathway was evaluated. Consequently, upregulated SNHG7 was revealed in TC tissues and correlated with 131I resistance. Silencing of SNHG7 or overexpressing miR‑9‑5p inhibited the growth and 131I resistance of TC cells. SNHG7 acted as a ceRNA of miR‑9‑5p to enhance DPP4 expression. Overexpressed SNHG7 increased DPP4 expression and activated the PI3K/Akt signaling pathway by sponging miR‑9‑5p. The in vitro results were reproduced in vivo. see more In summary, the present study provided evidence that the SNHG7/miR‑9‑5p/DPP4 ceRNA network could promote the growth and 131I resistance of TC cells via PI3K/Akt activation. The present study may offer novel options for TC treatment.Hepatic fibrosis, a common pathological manifestation of chronic liver injury, is generally considered to be the end result of an increase in extracellular matrix produced by activated hepatic stellate cells (HSCs). The aim of the present study was to target the mechanisms underlying HSC activation in order to provide a powerful therapeutic strategy for the prevention and treatment of liver fibrosis. In the present study, a high‑throughput screening assay was established, and the histone deacetylase inhibitor givinostat was identified as a potent inhibitor of HSC activation in vitro. Givinostat significantly inhibited HSC activation in vivo, ameliorated carbon tetrachloride‑induced mouse liver fibrosis and lowered plasma aminotransferases. Transcriptomic analysis revealed the most significantly regulated genes in the givinostat treatment group in comparison with those in the solvent group, among which, dermokine (Dmkn), mesothelin (Msln) and uroplakin‑3b (Upk3b) were identified as potential regulators of HSC activation. Givinostat significantly reduced the mRNA expression of Dmkn, Msln and Upk3b in both a mouse liver fibrosis model and in HSC‑LX2 cells. Knockdown of any of the aforementioned genes inhibited the TGF‑β1‑induced expression of α‑smooth muscle actin and collagen type I, indicating that they are crucial for HSC activation. In summary, using a novel strategy targeting HSC activation, the present study identified a potential epigenetic drug for the treatment of hepatic fibrosis and revealed novel regulators of HSC activation.Circular RNAs (circRNAs) are a class of non‑coding RNAs formed by covalently closed loops through back‑splicing and exon‑skipping. circRNAs have been confirmed to play a vital role in various biological functions, acting as microRNA sponges and reservoirs, as well as combining with RNA‑binding proteins during the progression of multiple cancer types. Therefore, the present review evaluated recent research articles in PubMed that were published between November 2017 and September 2020. Key word search strings included 'Circular RNA (circRNA) AND bladder cancer (BC)', 'circular RNA (circRNA) AND prostate cancer (PCa)' and 'circular RNA (circRNA) AND renal cell cancer (RCC)'. In total, >58 circRNAs were found to be implicated in urological cancers, with several of the circRNAs targeting common carcinogenic pathways, such as the AKT, TGF‑β, MAPK, VEGF and even metabolic pathways. circRNAs are important modulators of BC, PCa and RCC. circRNAs are functionally implicated in the pathogenesis of these cancer types, and have been found to act as biomarkers for the diagnosis and prognosis of urological cancer. However, to the best of our knowledge, the functions of circRNAs in tumors of the urinary system remain largely unknown and require further research.Pituitary tumors do not pose a threat to life but can cause visual disturbances and serious clinical syndromes, such as infertility and metabolic syndrome. Therefore, screening of key genes involved in the occurrence and development of pituitary tumors can provide new targets for the treatment of pituitary tumors. The aim of the present study was to investigate the molecular mechanism of long non‑coding (lnc.) RNA maternally expressed 3 (MEG3) in cell proliferation, apoptosis and epithelial‑mesenchymal transition (EMT) processes of pituitary tumor. Tissue samples were obtained from 34 patients who underwent surgical treatment of pituitary tumors. Pituitary tumor cells (GH3 and MMQ) were transfected with pcDNA3.1(+)‑MEG3, short hairpin (sh)MEG3, microRNA (miR)‑23‑3p inhibitor or their controls using Lipofectamine® 2000. Reverse transcription‑quantitative PCR and western blot analyses were used to detect the levels of MEG3, miR‑23b‑3p and FOXO4, as well as proliferation‑, apoptosis‑ and EMT‑associated genes and proteins.
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