Pancreatic cancer has been becoming the second cause of cancer death in the western world, and its disease burden has increased. Neoadjuvant therapy is one of the current research hotspots in the field of pancreatic cancer, aiming to improve the surgical rate and prognosis of pancreatic cancer. Based on the latest evidence, this review discussed neoadjuvant therapy in pancreatic cancer from the following three aspects: patient selection, protocols selection of neoadjuvant therapy, and treatment response evaluation and resectability prediction. A big controversy existed on the indications of neoadjuvant treatment, but it was agreed that any patient who is likely to achieve R0 resection due to neoadjuvant therapy should be the targeted population. A variety of chemotherapy regimens were tried for neoadjuvant therapy in pancreatic cancer, and FOLFIRINOX and Nab-Paclitaxel plus Gemcitabine are two preferred regimens at present. It was challenging to evaluate treatment response and predict resectability after neoadjuvant therapy, although imaging by CT is widely used. Based on new findings of the remarkable performance of several chemotherapy regimens with or without radiotherapy, the neoadjuvant indications of pancreatic cancer have extended in recent years. However, it is still a challenge to assess the neoadjuvant treatment response and determine the timing of surgery.
Hepatocellular carcinoma (HCC) is different from other solid tumors because it is commonly associated with the occurrence of intrahepatic metastasis. Additionally, the liver, unlike other organs, is the main site of coagulation and fibrinolytic factor production. Therefore, it was speculated that coagulation and fibrinolytic factors could be associated with intrahepatic metastasis of HCC. Do the coagulation and fibrinolytic systems protect HCC cells against anoikis during infiltration and metastasis? Conversely, do the coagulation and fibrinolytic systems lead to immune escape of HCC cells by affecting the immune microenvironment of patients? The current review aimed to present a number of novel hypotheses for the treatment of HCC by exploring the mechanisms of coagulation and fibrinolytic factors in the regulation of cancer growth. Contents1. Introduction 2. Coagulation characteristics of cancer 3. Regulation of the coagulation and fibrinolytic systems in HCC 4. Role of the coagulation system in resistance of HCC cells to anoikis 5. uPA system and immunotherapy for HCC 6.
BackgroundDysregulated expression of long non-coding RNAs (lncRNAs) has been reported in the pathogenesis and progression of multiple cancers, including hepatocellular carcinoma (HCC). LncRNA CTD-2547G23.4 is a novel lncRNA, and its role in HCC is still unknown. Here, we aimed to clarify the expression pattern and clinical value of CTD-2547G23.4 and to investigate the prospective regulatory mechanism via bioinformatics analysis in HCC.MethodsTo identify differentially expressed lncRNAs in HCC, we downloaded RNA-Seq data for HCC and adjacent non-tumour tissues via The Cancer Genome Atlas (TCGA). CTD-2547G23.4 was selected by using the R language and receiver operating characteristic curve analysis. Furthermore, we validated the differential expression of CTD-2547G23.4 via Gene Expression Omnibus (GEO), ArrayExpress, Oncomine databases and quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between the CTD-2547G23.4 level and clinic pathological parameters was also assessed. To further probe the role of CTD-2547G23.4 in HCC cell cycle, lentivirus-mediated small interfering RNA was applied to silence CTD-2547G23.4 expression in Huh-7 cell line. In addition, the related genes of CTD-2547G23.4 gathered from The Atlas of Noncoding RNAs in Cancer (TANRIC) database and Multi Experiment Matrix (MEM) were assessed with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes, Protein Analysis Through Evolutionary Relationships and protein–protein interaction (PPI) networks.ResultsCTD-2547G23.4 expression was remarkably higher in 370 HCC tissue samples than that in adjacent non-tumour liver tissues (48.762 ± 27.270 vs. 14.511 ± 8.341, P < 0.001) from TCGA dataset. The relative expression level of CTD-2547G23.4 in HCC was consistently higher than that in adjacent non-cancerous tissues (2.464 ± 0.833 vs. 1.813 ± 0.784, P = 0.001) as assessed by real time RT-qPCR. The area under the curve of the summary receiver operating characteristic curve was 0.8720 based on TCGA, qRT-PCR and GEO data. Further analysis indicated that the increased expression levels of CTD-2547G23.4 were associated with the neoplasm histologic grade and vascular tumour cell type. The expression of CTD-2547G23.4 was significantly downregulated in CTD-2547G23.4 knockdown cells. Moreover, cell cycle analysis revealed that CTD-2547G23.4 depletion in Huh-7 cell line led to S phase arrest. Furthermore, 314 related genes identified by TANRIC and MEM databases were processed with a pathway analysis. The bioinformatics analysis indicated that CTD-2547G23.4 might play a key role in the progress of HCC through four hub genes, SRC, CREBBP, ADCY8 and PPARA.ConclusionsCollectively, we put forward the hypothesis that the novel lncRNA CTD-2547G23.4 may act as an exceptional clinical index and promote the HCC tumourigenesis and progression via various related genes.Electronic supplementary materialThe online version of this article (10.1186/s12935-018-0566-3) contains supplementary material, which is available to authorized users.
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