Radiotherapy characterized by invasive, localization and low toxicity has been recognized as one of the standard cancer therapy regimes, especially for non-surgically resectable advanced cancers. However, inherent and acquired resistance of cancer cells has significantly impeded the efficacy of radiotherapy. Of all the resistance determinants, varieties of anti-apoptotic signaling pathways or anti-survival proteins aberrant activation in malignant tumor cells play crucial roles in radiation insensitivity. This paper mainly focuses on clarifying the roles of the interesting key molecular signals including Ras, insulin-like growth factor type 1 receptor, transforming growth factor-beta, histone deacetylase and heat shock protein 90 in regulating radiotherapy sensitivity, in order to find the potential targets to improve the efficacy of radiotherapy.

Ionizing radiation (IR) including X-ray and X-ray can induce apoptosis of cancer cells, mainly due to telomere damage and genome DNA breaks caused by IR. Although IR has been used clinically to cure some types of malignant tumors, the inherent or acquired resistance of cancer cells to IR has increasingly been an impediment for its usage. Overwhelming evidence has shown that telomerase is able to repair IR-induced telomere and chromosome damages, which may play key roles in mediating IR resistance. Unfortunately, the underlying mechanisms remain poorly known. This paper reviews the advances in research on telomerase-mediated regulation of IR sensitivity in recent 10 years, in order to clarify the molecular mechanism and the roles of telomerase-mediated regulation of IR sensitivity in cancer therapy and hope to provide useful clues and instructions for IR in cancer therapy.

P53 abnormality or mutation is commonly seen in patients with hepatocellular carcinoma (HCC), and therefore, restoration of P53 function has become a research hotspot in the treatment of HCC.This article reviews the association of P53 with Bcl-2 protein family, microRNA, TGFβ, HBV, HCV, and AKT and the role of P53 in regulating cell apoptosis, in order to provide clues for improving the therapeutic outcome of HCC.

Objective The objective of this study was to investigate effects of miR-34a on the proliferation,invasion and migration of colon cancer SW480 cell and its possible mechanism.Methods miR-34a overexpressed lentivirus and empty virus vector were transfected into SW480 cells and untreated cells were used as blank control group.Real-time PCR was used to detect the expression of miR-34a in each group.The cell proliferation was detected by CCK8 assay.The cell migration and invasion ability were detected by wound healing and transwell assays.The expression of E-cadherin and Vimentin protein was detected by Western blotting.Results Compared with the empty virus vector group and the blank control group,the expression of miR-34a was increased in the transfected cells,and the cell proliferation efficiency,invasion and migration ability were decreased in the transfected cells (P ＜ 0.05).miR-34a significantly increased the expression of E-cadherin protein and decreased Vimentin protein expression in the transfected cells.Conclusion miR-34a can inhibit the proliferation,invasion and migration of colon cancer SW480 cells,and affect the expression of E-cadherin and Vimentin.MR-34a is expected to be a potential molecular target for the metastasis and recurrence of colorectal cancer.

Hepatocellular carcinoma ( HCC ) is one of the most malignant tumors, transcatheter arterial chemoembolization( TACE) is a new treatment for HCC,which is currently considered as the standard care for pa-tients with unresectable HCC.MicroRNAs( miRNAs) ,a class of small non-coding RNAs,the correlations within miRNA dictions and tumor prognosis have been documented,and a part of miRNAs has been proposed as biomar-kers to reliably predict the outcomes before HCC patients being treated with TACE.

Pancreatic adenocarcinoma ( PAC) is still a refractory human digest malignancies due to multi-faceted causes ,late diagnosis and insensitive to traditional chemo -and radio-therapy .Resistance to apoptosis could be one of the most relevant mechanisms for PAC to escape any non -surgical therapy .This review aims to clear up the main deregulated apoptosis signal pathways over the years and to find out the abnormal molecule tar -get(s),and therefore,provide novel concepts for PAC molecular targeting therapy .

Hepatocellular carcinoma ( HCC ) is one of the commonest malignant tumors in China .The therapeutic effects of conventional therapies including surgery resection at early stage ,chemotherapy or radiothera-py are greatly less than expected .One of the most possible reasons is the blockage of apoptosis in HCC cells .This review collects literatures about the studies on the roles of key signal pathways including RA ,STAT3,PDT,p53,β-catenin,TRAIL,microRNA and RAS in HCC therapy .This study may contribute greatly to providing outline in-sights for using apoptosis induction in liver cancer therapy .We hope it can promote the development liver cancer therapy in China .

In recent years, studies have shown that the expression of pyruvate kinase muscle isozyme 2 (PKM2) is increased significantly in various tumor cells. PKM2 acts like a signal molecule in tumor cells and participates in the expression and regulation of genes related to tumor cell proliferation, cell autophagy, and cell cycle progression. This article summarizes the expression of PKM2 in liver cancer tissues and cell lines, elaborates on the role of PKM2 in the proliferation, differentiation, and metastasis of liver cancer cells and prognostic evaluation, and points out that PKM2 can be used in the clinical diagnosis, treatment, and prognostic evaluation of liver cancer.

Currently, sorafenib is the multi-target inhibitor for the treatment of advanced primary liver cancer, and can effectively prolong the progression-free survival and overall survival in patients with advanced primary liver cancer. The application of sorafenib in the targeted therapy for liver cancer has become a hot topic. Major targets or signaling pathways include Raf/Mek/Erk, Jak/Stat, PI3K/Akt/mTOR, VEGFR and PDGFR, STAT, microRNA, Wnt/β-catenin, autolysosome, and tumor-related proteins, and sorafenib can regulate the proliferation, differentiation, metastasis, and apoptosis of liver cancer cells through these targets. This article reviews the current research on the action of sorafenib on these targets or signaling pathways to provide useful references for further clinical research on sorafenib.

Liver fibrosis is the final outcome of various chronic liver diseases, and various cells, cytokines, and miRNAs are involved in the development and progression of liver fibrosis and liver cirrhosis. Hepatic fibrosis and pathologic angiogenesis are interdependent processes and promote each other, but the physiopathological mechanism of arterial capillary proliferation in liver fibrosis remains unknown. Aquaporins not only transport water molecules, but also promote angiogenesis. This article briefly introduces the expression of aquaporins in the hepatobiliary system and their physiological and biochemical characteristics and summarizes the role of aquaporins in the progression of liver fibrosis and liver cirrhosis, in order to provide new thoughts and guidance for aquaporins as the target in the treatment of liver fibrosis and liver cirrhosis.