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Dysnatremia is common in donors and recipients of liver transplantation (LT). However, the influence of dysnatremia on LT prognosis remains controversial. This study aimed to investigate effects of donors' and recipients' serum sodium on LT prognosis. We retrospectively reviewed 248 recipients who underwent orthotopic LT at our center between January 2016 and December 2018. Donors and recipients perioperative and 3-year postoperative clinical data were included. Delta serum sodium was defined as the donors' serum sodium minus the paired recipients' serum sodium. Donors with serum sodium > 145 mmol/L had significantly higher preoperative blood urea nitrogen (BUN) (P < 0.01) and creatinine (Cr) (P < 0.01) than others. Preoperative total bilirubin (TBIL) (P < 0.01), direct bilirubin (DBIL) (P < 0.01), BUN (P < 0.01), Cr (P < 0.01) were significantly higher in the hyponatremia group of recipients than the other groups, but both of donors' and recipients' serum sodium had no effect on the LT prognosis. In the delta serum sodium < 0 mmol/L group, TBIL (P < 0.01) and DBIL (P < 0.01) were significantly higher in postoperative 1 week than the other groups, but delta serum sodium had no effect on the postoperative survival rates. Dysnatremia in donors and recipients of LT have no effect on postoperative survival rates, hepatic and renal function, but recipients with higher serum sodium than donors have significantly higher TBIL and DBIL at 1 week postoperatively.
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Transplante de Fígado , Sódio , Humanos , Transplante de Fígado/efeitos adversos , Masculino , Feminino , Sódio/sangue , Pessoa de Meia-Idade , Prognóstico , Estudos Retrospectivos , Adulto , Doadores de Tecidos , Hiponatremia/sangue , Nitrogênio da Ureia Sanguínea , Transplantados , Bilirrubina/sangue , Período Pré-Operatório , Idoso , Creatinina/sangueRESUMO
Hepatocellular carcinoma (HCC) is the third leading cause of global cancer-related deaths. Despite immunotherapy offering hope for patients with HCC, only some respond to it. However, it remains unclear how to pre-screen eligible patients. Our study aimed to address this issue. In this study, we identified 13 prognostic genes through univariate Cox regression analysis of 87 apoptosis-related genes. Subsequently, these 13 genes were analyzed using ConsensusClusterPlus, and patients were categorized into three molecular types: C1, C2, and C3. A prognostic model and RiskScore were constructed using Lasso regression analysis of 132 significant genes identified between C1 and C3. We utilized quantitative polymerase chain reaction to confirm the model's transcript level in Huh7 and THLE2 cell lines. Both molecular subtypes and RiskScores effectively predicted patients benefiting from immunotherapy. Cox regression analysis revealed RiskScore as the most significant prognosis factor, suggesting its clinical application potential and providing a foundation for future experimental research.
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Carcinoma Hepatocelular , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , Apoptose/genética , Linhagem Celular , Imunoterapia , PrognósticoRESUMO
Long non-coding RNAs (lncRNAs) play important roles in the occurrence and progression of tumors. Extensive research has contributed to the current understanding of the critical roles played by lncRNAs in various cancers. LncRNA MIR4435-2HG has been found to be crucial in many cancers, such as breast, cervical, colorectal, and gastric cancer. Expression of MIR4435-2HG is generally upregulated in cancers and MIR4435-2HG participates in many biological functions through molecular mechanism of competitive endogenous RNA networks. This review profiles recent research findings on the expression, functions, mechanism, and clinical value of MIR4435-2HG in cancer, and serves as a reference for further MIR4435-2HG-related research and clinical trials.
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MicroRNAs , RNA Longo não Codificante , Neoplasias Gástricas , Regulação Neoplásica da Expressão Gênica , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Neoplasias Gástricas/genéticaRESUMO
Genetic and epigenetic characteristics are core factors of cancer. MicroRNAs (miRNAs) are small non-coding RNAs which regulate gene expression at the post-transcriptional level via binding to corresponding mRNAs. Recently, increasing evidence has proven that miRNAs regulate the occurrence and development of human cancer. Here, we mainly review the abnormal expression of miR-625 in a variety of cancers. In summarizing the role and potential molecular mechanisms of miR-625 in various tumors in detail, we reveal that miR-625 is involved in a variety of biological processes, such as cell proliferation, invasion, migration, apoptosis, cell cycle regulation, and drug resistance. In addition, we discuss the lncRNA-miRNA-mRNA and circRNA-miRNA-mRNA networks and briefly explain the specific mechanisms of competing endogenous RNAs. In conclusion, we reveal the potential value of miR-625 in cancer diagnosis, treatment, and prognosis and hope to provide new ideas for the clinical application of miR-625.
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RNA methylation is considered a significant epigenetic modification, a process that does not alter gene sequence but may play a necessary role in multiple biological processes, such as gene expression, genome editing, and cellular differentiation. With advances in RNA detection, various forms of RNA methylation can be found, including N6-methyladenosine (m6A), N1-methyladenosine (m1A), and 5-methylcytosine (m5C). Emerging reports confirm that dysregulation of RNA methylation gives rise to a variety of human diseases, particularly hepatocellular carcinoma. We will summarize essential regulators of RNA methylation and biological functions of these modifications in coding and noncoding RNAs. In conclusion, we highlight complex molecular mechanisms of m6A, m5C, and m1A associated with hepatocellular carcinoma and hope this review might provide therapeutic potent of RNA methylation to clinical research.
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Long non-coding RNAs (lncRNAs) are RNAs with a length of no less than 200 nucleotides that are not translated into proteins. Accumulating evidence indicates that lncRNAs are pivotal regulators of biological processes in several diseases, particularly in several malignant tumors. Long intergenic non-protein coding RNA 1116 (LINC01116) is a lncRNA, whose aberrant expression is correlated with a variety of cancers, including lung cancer, gastric cancer, colorectal cancer, glioma, and osteosarcoma. LINC01116 plays a crucial role in facilitating cell proliferation, invasion, migration, and apoptosis. In addition, numerous studies have recently suggested that LINC01116 has emerged as a novel biomarker for prognosis and therapy in malignant tumors. Consequently, we summarize the clinical significance of LINC01116 associated with biological processes in various tumors and provide a hopeful orientation to guide clinical treatment of various cancers in future studies.
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Long non-coding RNAs (lncRNAs) are transcribed by RNA polymerase II and are longer than 200 nucleotides. Several studies have revealed that lncRNAs are important regulators of cancer progression. The lncRNA FGD5-AS1, first identified in 2018, has emerged as a crucial regulator of processes related to carcinogenesis. The expression levels of FGD5-AS1 are known to be significantly up-regulated in a variety of human cancers. Moreover, FGD5-AS1 expression closely correlates with clinical features and poor prognosis and its expression has been shown to attenuate cell proliferation, cell migration, cell invasiveness, drug resistance, and the epithelial-mesenchymal transition through several pathways. Here, we provide an overview of the role of FGD5-AS1 in various cancers and discuss its potential clinical utility in tumor progression. In addition, we used a gene expression profiling interactive analysis dataset to explore associations between FGD5-AS1 pan-cancer expressions and prognoses.
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Pancreatic cancer is one of the malignant tumors with the worst prognosis in the world. As a new way of programmed cell death, ferroptosis has been proven to have potential in tumor therapy. In this study, we used the TCGA-PAAD cohort combined with the previously reported 60 ferroptosis-related genes to construct and validate the prognosis model and in-depth analysis of the differences in the function and immune characteristics of different RiskTypes. The results showed that the six-gene signature prognostic model that we constructed has good stability and effectiveness. Further analysis showed that the upregulated genes in the high-risk group were mainly enriched in extracellular matrix receptor-related pathways and other tumor-related pathways and the infiltration of immune cells, such as B, T, and NK cells, was suppressed. In short, our model shows good stability and effectiveness. Further studies have found that the prognostic differences between different RiskTypes may be due to the changes in the ECM-receptor pathway and activation of the immune system. Additionally, ICI drugs can treat pancreatic cancer in high-risk groups.
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Pancreatic adenocarcinoma (PAAD) is the most malignant digestive tumor. The global incidence of pancreatic cancer has been rapidly trending upwards, necessitating an exploration of potential prognostic biomarkers and mechanisms of disease development. One of the most prevalent RNA modifications is 5-methylcytosine (m5C); however, its contribution to PAAD remains unclear. Data from The Cancer Genome Atlas (TCGA) database, including genes, copy number variations (CNVs), and simple nucleotide variations (SNVs), were obtained in the present study to identify gene signatures and prognostic values for m5C regulators in PAAD. Regulatory gene m5C changes were significantly correlated with TP53, BRCA1, CDKN2A, and ATM genes, which play important roles in PAAD pathogenesis. In particular, there was a significant relationship between m5C regulatory gene CNVs, especially in genes encoding epigenetic "writers". According to m5C-regulated gene expression in clinically graded cases, one m5C-regulated genes, DNMT3A, showed both a strong effect on CNVs and a significant correlation between expression level and clinical grade (P < 0.05). Furthermore, low DNMT3A expression was not only associated with poor PAAD patient prognosis but also with the ribosomal processing. The relationship between low DNMT3A expression and poor prognosis was confirmed in an International Cancer Genome Consortium (ICGC) validation dataset.
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5-Metilcitosina/química , Adenocarcinoma/patologia , Biomarcadores Tumorais/metabolismo , Epigênese Genética , Regulação Neoplásica da Expressão Gênica , Neoplasias Pancreáticas/patologia , Transcriptoma , Adenocarcinoma/genética , Adenocarcinoma/metabolismo , Biomarcadores Tumorais/genética , Seguimentos , Perfilação da Expressão Gênica , Humanos , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/metabolismo , Prognóstico , Estudos Retrospectivos , Taxa de SobrevidaRESUMO
Pancreatic cancer consists one of tumors with the highest degree of malignancy and the worst prognosis. To date, immunotherapy has become an effective means to improve the prognosis of patients with pancreatic cancer. Long non-coding RNAs (lncRNAs) have also been associated with the immune response. However, the role of immune-related lncRNAs in the immune response of pancreatic cancer remains unclear. In this study, we identified immune-related lncRNA pairs through a new combinatorial algorithm, and then clustered and deeply analyzed the immune characteristics and functional differences between subtypes. Subsequently, the prognostic model of 3 candidate lncRNA pairs was determined by multivariate COX analysis. The results showed significant prognostic differences between the C1 and C2 subtypes, which may be due to the differential infiltration of CTL and NK cells and the activation of tumor-related pathways. The prognostic model of the 3 lncRNA pairs (AC244035.1_vs._AC063926.1, AC066612.1_vs._AC090124.1, and AC244035.1_vs._LINC01885) was established, which exhibits stable and effective prognostic prediction performance. These 3 lncRNA pairs may regulate the anti-tumor effect of immune cells through ion channel pathways. In conclusion, our research demonstrated the panoramic differences in immune characteristics between subtypes and stable prognostic models, and identified new potential targets for immunotherapy.
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BACKGROUND: 5-Methylcytosine (m5C) is a reversible modification to both DNA and various cellular RNAs. However, its roles in developing human cancers are poorly understood, including the effects of mutant m5C regulators and the outcomes of modified nucleobases in RNAs. METHODS: Based on The Cancer Genome Atlas (TCGA) database, we uncovered that mutations and copy number variations (CNVs) of m5C regulatory genes were significantly correlated across many cancer types. We then assessed the correlation between the expression of individual m5C regulators and the activity of related hallmark pathways of cancers. RESULTS: After validating m5C regulators' expression based on their contributions to cancer development and progression, we observed their upregulation within tumor-specific processes. Notably, our research connected aberrant alterations to m5C regulatory genes with poor clinical outcomes among various tumors that may drive cancer pathogenesis and/or survival. CONCLUSION: Our results offered strong evidence and clinical implications for the involvement of m5C regulators.
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Variações do Número de Cópias de DNA , Epigênese Genética , Neoplasias , 5-Metilcitosina , Metilação de DNA , Regulação Neoplásica da Expressão Gênica , Genes Reguladores , Humanos , Mutação , Neoplasias/genética , PrognósticoRESUMO
Long noncoding RNAs (lncRNAs), are transcripts longer than 200 nucleotides that are considered to be vital regulators of many cellular processes, particularly in tumorigenesis and cancer progression. long intergenic non-protein coding RNA 261 (LINC00261), a recently discovered lncRNA, is abnormally expressed in a variety of human malignancies, including pancreatic cancer, gastric cancer, colorectal cancer, lung cancer, hepatocellular carcinoma, breast cancer, laryngeal carcinoma, endometrial carcinoma, esophageal cancer, prostate cancer, choriocarcinoma, and cholangiocarcinoma. LINC00261 mainly functions as a tumor suppressor that regulates a variety of biological processes in the above-mentioned cancers, such as cell proliferation, apoptosis, motility, chemoresistance, and tumorigenesis. In addition, the up-regulation of LINC00261 is closely correlated with both favorable prognoses and many clinical characteristics. In the present review, we summarize recent research documenting the expression and biological mechanisms of LINC00261 in tumor development. These findings suggest that LINC00261, as a tumor suppressor, has bright prospects both as a biomarker and a therapeutic target.
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Long non-coding RNAs (lncRNA), as key regulators of cell proliferation and death, are involved in the regulation of various processes in the nucleus and cytoplasm, involving biological developmental processes in the fields of immunology, neurobiology, cancer, and stress. There is great scientific interest in exploring the relationship between lncRNA and tumors. Many researches revealed that lymph enhancer-binding factor 1-antisense RNA 1 (LEF1-AS1), a recently discovered lncRNA, is downregulated in myeloid malignancy, acting mainly as a tumor suppressor, while it is highly expressed and carcinogenic in glioblastoma (GBM), lung cancer, hepatocellular carcinoma (HCC), osteosarcoma, colorectal cancer (CRC), oral squamous cell carcinoma (OSCC), prostatic carcinoma, retinoblastoma, and other malignant tumors. Furthermore, abnormal LEF1-AS1 expression was associated with tumorigenesis, development, survival, and prognosis via the regulation of target genes and signaling pathways. This review summarizes the existing data on the expression, functions, underlying mechanism, relevant signaling pathways, and clinical significance of LEF1-AS1 in cancer. It is concluded that LEF1-AS1 can serve as a novel biomarker for the diagnosis and prognosis of various tumors, thus deserves further attention in the future.