Construction and validation of somatic mutation-derived long non-coding RNAs signatures of genomic instability to predict prognosis of hepatocellular carcinoma.

BACKGROUND: Long non-coding RNAs (LncRNAs) have been found to be a potential prognostic factor for cancers, including hepatocellular carcinoma (HCC). Some LncRNAs have been confirmed as potential indicators to quantify genomic instability (GI). Nevertheless, GI-LncRNAs remain largely unexplored. This study established a GI-derived LncRNA signature (GILncSig) that can predict the prognosis of HCC patients. AIM: To establish a GILncSig that can predict the prognosis of HCC patients. METHODS: Identification of GI-LncRNAs was conducted by combining LncRNA expression and somatic mutation profiles. The GI-LncRNAs were then analyzed for functional enrichment. The GILncSig was established in the training set by Cox regression analysis, and its predictive ability was verified in the testing set and TCGA set. In addition, we explored the effects of the GILncSig and TP53 on prognosis. RESULTS: A total of 88 GI-LncRNAs were found, and functional enrichment analysis showed that their functions were mainly involved in small molecule metabolism and GI. The GILncSig was constructed by 5 LncRNAs (miR210HG, AC016735.1, AC116351.1, AC010643.1, LUCAT1). In the training set, the prognosis of high-risk patients was significantly worse than that of low-risk patients, and similar results were verified in the testing set and TCGA set. Multivariate Cox regression analysis and stratified analysis confirmed that the GILncSig could be used as an independent prognostic factor. Receiver operating characteristic curve analysis of the GILncSig showed that the area under the curve (0.773) was higher than the two LncRNA signatures published recently. Furthermore, the GILncSig may have a better predictive performance than TP53 mutation status alone. CONCLUSION: We established a GILncSig that can predict the prognosis of HCC patients, which will help to guide prognostic evaluation and treatment decisions.

The effects of propranolol on the biology and Notch signaling pathway of human umbilical vein endothelial cells.

BACKGROUND: Propranolol is the first choice for treating infantile hemangioma (IH). How propranolol works in IH remains unclear. Infantile hemangioma endothelial cells (HemECs) express Notch1, Jagged, Hey1, and other molecules in the Notch pathway, suggesting that Notch pathway-related molecules play an important role in affecting vascular endothelial cell proliferation. Whether propranolol can affect the Notch signaling pathway in IH treatment is unclear. METHODS: We performed this study to observe the effect of propranolol on the expression of Notch signaling pathway molecules in human umbilical vein endothelial cells (HUVECs) and to explore the therapeutic mechanism of propranolol on IH. HUVECs cultured in vitro were exposed to 60, 120, 240, 360, or 480 µM propranolol. The morphological changes of the HUVECs were observed under an inverted microscope. HUVECs proliferation was detected with Cell Counting Kit-8 (CCK-8). The effects of propranolol on HUVECs apoptosis were detected by flow cytometry. The role of Notch in propranolol inhibition of HUVEC proliferation was analyzed with real-time polymerase chain reaction (PCR) and western blotting. RESULTS: Propranolol reduced HUVECs numbers and altered their morphology. The inhibitory effect of propranolol on cell proliferation was dependent on the reaction time and drug concentration. Propranolol upregulated Jagged1, Notch1, and Hey1 expression and downregulated delta-like ligand4 (DLL4) expression. CONCLUSIONS: Propranolol may play a role in IH treatment by increasing Jagged1 expression in endothelial cells, activating the Notch pathway and inducing the upregulation of the downstream target gene HEY1.

Progress of Psf1 and prospects in the tumor: A review.

Partner of Sld5-1(Psf1) is a member of Gins complex, which was discovered in 2003. It consists of the predominantly α-helical A-domain and the massively ß-stranded B-domain. Some researches indicate that Psf1 plays a prominent part in DNA replication through cell cycle regulation, and plays a key role in early embryo development and tissue regeneration. The overexpression of Psf1 in active proliferating cells is closely correlated with the occurrence of tumors. On the side, tumor cells with high Psf1 expression showed high heterogeneity and poor clinical prognosis. In this review, we will review the research progress of Psf1 in cell cycle regulation, immature cell proliferation and oncology.

A rare case report of obstructive jaundice caused by mucus-producing cholangiocarcinoma.

RATIONALE: Cholangiocarcinoma is a common cause of obstructive jaundice but is mainly associated with solid mass and not semisolid secretion. In this report, the patient was admitted to the hospital with obstructive jaundice; however, no solid mass was found to lead to jaundice. PATIENT CONCERNS: The patient developed symptoms of obstructive jaundice for 10 days, including fatigue and yellow skin staining. DIAGNOSES: Postoperative pathological examination of the bile duct wall revealed cholangioadenocarcinoma, and the jelly like contents were inflammatory secretions. INTERVENTIONS: The patient underwent laparotomy and was diagnosed with obstructive jaundice. An exploratory laparotomy revealed that the content in the biliary duct tree was a jelly like inflammatory secretion. OUTCOMES: Follow-up data revealed that the levels of total bilirubin and aminotransferase were normal, and a computed tomography scan showed no tumor mass. LESSONS: There are very few reports about obstructive jaundice caused by inflammatory secretion that almost filled up the biliary tree. Internal drainage of the cholestatic bile can be achieved through endoscopic retrograde cholangiopancreatograpy, or external drainage can be achieved through percutaneous transhepatic biliary drainage, which can relieve the symptoms of biliary obstruction and improve the patient's quality of life.