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Background Long non-coding RNAs (lncRNAs), which are a portion of non-protein-coding RNAs (ncRNAs), have manifested a paramount role in the pathophysiology of human diseases, particularly in pathogenesis and progression of disease. Main body of the abstract Myocardial infarction associated transcript (MIAT), which was recently found to demonstrate aberrant expression in various diseases, such as myocardial infarction, schizophrenia, ischemic stroke, diabetic complications, age-related cataract and cancers, is a novel disease-related lncRNA. This work summarize current evidence regarding the biological functions and underlying mechanisms of lncRNA MIAT during disease development. Short conclusion LncRNA MIAT likely represents a feasible cancer biomarker or therapeutic target.

Optical coherence tomography (OCT) has emerged as a transformative diagnostic tool in the realm of uncertain biliary strictures within the digestive system. Its superiority over conventional methods lies in its ability to provide submucosal assessments and real-time, wide-ranging tissue evaluations. The latest advancement in OCT technology, exemplified by the NVision Volumetric Laser Endomicroscopy (VLE) system, has significantly enhanced imaging quality and microstructure delineation, particularly in characterizing the intricate anatomy of pancreaticobiliary ducts. In recent studies, OCT has demonstrated remarkable capabilities in overcoming challenges posed by stents, inflammation, and fibrosis, setting it apart as a versatile diagnostic adjunct. Although the safety and feasibility of OCT have been extensively validated, its clinical integration demands further validation through large-scale trials and comparative studies. Ongoing technical innovations and refinements in OCT technology underscore its potential to revolutionize diagnostic precision in hepatobiliary sciences. In summary, OCT stands at the forefront of cutting-edge diagnostic methodologies for uncertain biliary strictures, offering unparalleled insights into tissue microstructures. Its seamless integration with complementary modalities, ongoing technical refinements, and the advent of ultrathin cholangioscopes collectively position OCT as a promising avenue for advancing diagnostic capabilities in hepatobiliary medicine. A literature-based review was conducted via PubMed and Web of Science to extract and synthesize diagnostic performance and structural criteria of OCT in hepatobiliary applications.

Background Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) behave as a novel class of transcription products during multiple cancer processes. However, the mechanisms responsible for their alteration in cholangiocarcinoma (CCA) are not fully understood. Methods The expression of SPRY4-IT1 in CCA tissues and cell lines was determined by RT-qPCR, and the association between SPRY4-IT1 transcription and clinicopathologic features was analyzed. Luciferase reporter and chromatin immunoprecipitation (ChIP) assays were performed to explore whether SP1 could bind to the promoter region of SPRY4-IT1 and activate its transcription. The biological function of SPRY4-IT1 in CCA cells was evaluated both in vitro and in vivo. ChIP, RNA binding protein immunoprecipitation (RIP) and luciferase reporter assays were performed to determine the molecular mechanism of SPRY4-IT1 in cell proliferation, apoptosis and invasion. Results SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p. Conclusions Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.

Akirin2 is a key regulator of embryonic development and the innate immunity response. However, this regulator’s role in tumorigenesis especially in cholangiocarcinoma (CCA) development has not been thoroughly elucidated to date. In the current work, we used RT-qPCR, western blot analysis, and immunohistochemistry (IHC) to explore the expression level of Akirin2, and the relationship between Akirin2 levels and clinicopathological characteristics was evaluated. The biological functions of Akirin2 were examined in vitro and in vivo by using a lentiviral vector system. Luciferase reporter assays were applied to detect the direct binding relationship between the 3′-UTR of Akirin2 mRNA and miR-490-3p. The results showed that Akirin2 was overexpressed in CCA and this upregulation was associated with a shorter overall survival. Silencing or overexpressing Akirin2 by lentiviral approaches significantly influenced CCA cell proliferation, migration, invasion, and angiogenesis. An in vivo tumor model further validated the oncogenic effect of Akirin2 on CCA cell growth, metastasis, and angiogenesis. Mechanistic studies demonstrated that Akirin2 induced angiogenesis by increasing the expression of VEGFA by activating the IL-6/STAT3 signaling pathway. Akirin2 promoted cell migratory and invasive potential by affecting the epithelial–mesenchymal transition (EMT) process. In addition, Akirin2 expression was negatively controlled by miR-490-3p in CCA cells, and miR-490-3p attenuated cell migration and angiogenesis in CCA cells by silencing Akirin2. Taken together, the data indicated that Akirin2 could be regulated by miR-490-3p at the posttranscriptional level and facilitate CCA cell progression via the IL-6/STAT3/VEGFA signaling pathway. The present study may expedite the development of novel therapeutic strategies for CCA.

Background The gains in survival outcomes of US patients with hepatocellular carcinoma (HCC) have come at the expense of developing non‐cancer‐related morbidities, such as cardiovascular diseases (CVDs) and infections. However, population‐based data on causes of death (CODs) in patients with HCC are scarce. Methods A cancer registry database in the United States was used to analyze the CODs among patients with HCC. Death cause distribution and standardized mortality ratios were calculated to quantify the disease‐specific death burden. Results A total of 40,094 patients with a histological diagnosis of HCC were identified from the SEER‐18 database between 2000 and 2018, of which 30,796 (76.8%) died during the follow‐up period. The majority of these deaths (25,153, 81.7%) occurred within 2 years after diagnosis, 13.2% (4075) occurred within 2–5 years, and 5.1% (1568) occurred after 5 years. All age groups had a lower burden of female deaths than of male deaths during the study period. With respect to CODs, 23,824 (77.4%), 2289 (7.4%), and 4683 (15.2%) were due to HCC, other cancers, and non‐cancer causes, respectively. Non‐cancer‐related deaths were more common among older patients and those with longer latency periods since diagnosis. The major causes of non‐cancer‐related deaths are other infectious and parasitic diseases, including HIV and CVDs. Conclusions CODs during HCC survivorship varied, and a growing number of survivors tended to die from causes other than HCC, with an increasing latency period since diagnosis. Comprehensive analyses of mortality patterns and temporal trends could underpin strategies to reduce these risks.

BackgroundOwing to advances in diagnostic technology, the diagnosis of T1 colorectal cancers (CRCs) continues to increase. However, the optimal management of T1 CRCs in the Western Hemisphere remains unclear due to limited population-based data directly comparing the efficacy of endoscopic therapy (ET) and surgical resection (SR). The purpose of this study was to report outcome data from a large Western cohort of patients who underwent ET or SR for early CRCs.MethodsThe SEER-18 database was used to identify patients with T1 CRCs diagnosed from 2004 to 2018 treated with ET or SR. Multivariable logistic regression models were employed to identify variables related to lymph node metastasis (LNM). Rates of ET and 1-year relative survival were calculated for each year. Effect of ET or SR on overall survival and cancer-specific survival was compared using Kaplan–Meier method stratified by tumor size and site.ResultsA total of 28,430 T1 CRCs patients were identified from 2004 to 2018 in US, with 22.7% undergoing ET and 77.3% undergoing SR. The incidence of T1 CRCs was 6.15 per 100,000 person-years, with male patients having a higher incidence. Left-sided colon was the most frequent location of tumors. The utilization of ET increased significantly from 2004 to 2018, with no significant change in 1-year relative survival rate. Predictors of LNM were age at diagnosis, sex, race, tumor size, histology, grade, and location. The 5-year relative survival rates were 91.4 and 95.4% for ET and SR, respectively. Subgroup analysis showed that OS and CSS were similar between ET and SR in T1N0M0 left-sided colon cancers with tumors 2 cm or less and in rectal cancers with tumors 1 cm or less.ConclusionOur study showed that ET was feasible and safe for patients with left-sided T1N0M0 colon cancers and tumors of 2 cm or less, as well as T1N0M0 rectal cancers and tumors of 1 cm or less. Therefore, the over- and under-use of ET should be avoided by carefully selecting patients based on tumor size and site.

Background Pyrimidine metabolism is critical for tumour progression. Uridine–cytidine kinase 2 (UCK2), a key regulator of pyrimidine metabolism, is elevated during hepatocellular carcinoma (HCC) development and exhibits carcinogenic effects. However, the key mechanism of UCK2 promoting HCC and the therapeutic value of UCK2 are still undefined. The aim of this study is to investigate the potential of UCK2 as a therapeutic target for HCC. Methods Gene expression matrices were obtained from public databases. RNA-seq, co-immunoprecipitation and RNA-binding protein immunoprecipitation were used to determine the mechanism of UCK2 promoting HCC. Immune cell infiltration level and immune-related functional scores were evaluated to assess the link between tumour microenvironment and UCK2. Results In HCC, the expression of UCK2 was upregulated in part by TGFβ1 stimulation. UCK2 promoted cell cycle progression of HCC by preventing the degradation of mTOR protein and maintaining the stability of PDPK1 mRNA. We also identified UCK2 as a novel RNA-binding protein. Downregulation of UCK2 induced cell cycle arrest and activated the TNFα/NFκB signalling pathway-related senescence-associated secretory phenotype to modify the tumour microenvironment. Additionally, UCK2 was a biomarker of the immunosuppressive microenvironment. Downregulated UCK2 induced a secretory phenotype, which could improve the microenvironment, and decreased UCK2 remodelling metabolism could lower the resistance of tumour cells to T-cell-mediated killing. Conclusions Targeting UCK2 inhibits HCC progression and could improve the response to immunotherapy in patients with HCC. Our study suggests that UCK2 could be an ideal target for HCC.

Growing evidence suggests that long non-coding RNAs (lncRNAs) could function as important regulators in carcinogenesis and cancer progression. Nicotinamide nucleotide transhydrogenase antisense RNA 1 (lncRNA NNT-AS1) is up-regulated in some human tumors and functions as a tumor promoter. This study aimed to detect the effect of NNT-AS1 on cholangiocarcinoma (CCA) prognosis. In this study, we detected NNT-AS1 expression in CCA tissue samples and cell lines, and analyzed the association between NNT-AS1 expression levels and clinical parameters of CCA patients. Moreover, we conducted loss-of-function studies in CCA cancer cells to explore the biological function and molecular mechanism of NNT-AS1. NNT-AS1 was downregulated by using RNAi technology. Cell proliferation was examined by CCK8 and clone formation assays. Cell migration and invasion were determined by wound healing and transwell assays. Western blot assays were used to explore protein expression. In this study, NNT-AS1 was expressed at high levels in CCA and closely associated with poor prognosis of patients with CCA. NNT-AS1 knockdown impaired cell proliferation, suppressed CCA cell migration and invasion, and restrained tumor growth in vitro. Moreover, NNT-AS1 directly bounded to miR-485 and further regulated BCL9. Finally, rescue assays verified that NNT-AS1 modulated the tumorigenesis of CCA by regulating miR-485. Taken together, NNT-AS1 played a critical biological role in the development of CCA. Our results elucidated NNT-AS1/miR-485/BCL9 axis might lead to a further understanding of the molecular mechanism of CCA.

BackgroundThe purpose of current study was to examine the incidence, characteristics, treatment, and survival of splenic marginal zone lymphoma (SMZL).MethodsUsing SEER-18 database, patients diagnosed with SMZL between 2000 and 2018 were included. Effect of splenectomy on survival was evaluated after balancing the confounding factors by propensity score matching. Rates of splenectomy and 1-year relative survival were calculated for each year. A logistic regression model identified factors related to splenectomy, and a Cox regression model assessed factors linked to overall survival (OS).ResultsA total of 2790 patients with SMZL were analyzed. The majority were older than 60 years, female, and white. The age-adjusted incidence of SMZL was 0.17/100,000 person-years, with higher incidence in males. Incidence increased by 0.68%/year and peaked at 80–84 years for both genders. The SMZL-specific survival rates at 3 and 5 years were 89.6% and 85.3%, respectively. Meanwhile, the relative survival rates for the same periods were 88.6% and 85.9%, respectively. Splenectomy patients were more likely to be younger, male, and diagnosed with early-stage disease. Despite the decreasing utilization rate of splenectomy from 59.4% in 2000 to 16.2% in 2018, the 1-year relative survival rate remained relatively stable with minor fluctuations over time. Whether or not the patient underwent splenectomy was not found to be a significant prognostic indicator for OS.ConclusionsOur study demonstrated a decreasing use of splenectomy but a relatively stable survival in patients with SMZL, highlighting the urgency to better understand the role of splenectomy and its associated outcomes.