Cancer Cell Research (Online ISSN: 2161-2609)

by  Jie Yu, Fen Yu, Lin Shi, Nianrong Luo, Yongxia Chen, Xia Liu, Yongfeng Jia

Cancer Cell Research 2019 6(21) 529-535; published online  7 January 2019

Abstract: Tumor is an increasingly common disease in today's society, it is also one of the major serious diseases do harm to human beings. But people still know little about how tumor cells work after lots of efforts were put to understand them. There is one primarily interrelated theme found on a combination of clinical and experimental observations of phenotypic plasticity. Changes of phenotypic plasticity might be induced by Epithelial-mesenchymal transition (EMT), cancer stem cells (CSCs), and vasculogenic mimicry (VM), or they interacted together, at least partly. Although they have important impacts on tumor biology, the clinical relevance of these concepts remains to be recapitulated. In this review, we will update the current state of correlations between EMT, CSCs, and VM formation with a focus on their contributions to phenotypic plasticity, their clinical implications for the design of therapeutic strategies will also be discussed.

by  Bowen Zhu, Yu Huang, Jing Zheng, Lili Yan, Hui Lin, Qingyu Zhang

Cancer Cell Research 2019 6(21) 536-543; published online  27  January 2019

Abstract: To study the inhibitory effects of blocking chemokine pathways CXCL12/CXCR4, CXCR7 and intracellular ERK signaling pathway on human endometrial carcinoma in nude mice. Ishikawa cells suspension (7.5×107/ml) of endometrial cancer were used to establish animal models. 30 nude mice were randomly divided into the following five groups: AMD3100 (6 mg/kg), PD98059 (50 mg/kg), Anti-CXCR7 (1 ul/mouse), AMD3100+Anti-CXCR7 (6 mg/kg+1 ul/mouse) and Nacl (etc. volume of saline). These small molecule inhibitors were intraperitoneally injected into the body. Tumor length and short diameter to calculate tumor volume were measured every three days for three weeks. At the end of the treatment period, completely stripped the all tumors, weigh them and the expression of Survivin in subcutaneous xenografts was detected by western blotting and RT-PCR. The growth curve and weight of the tumors in the experimental groups were significantly lower than those in the control group (P<0.01). The results of western blotting and RT-PCR revealed that the expression levels of Survivin protein and mRNA in subcutaneous xenografts of experimental groups were down regulated compared with control group (P<0.01). There were no significant difference in growth curves, weights, tumor inhibition rates, Survivin protein and mRNA expression of tumors between experimental groups (P>0.05). Blocking CXCL12-specific receptors CXCR4, CXCR7 and intracellular ERK signaling pathway can inhibit the growth of endometrial carcinoma cells in vivo, this condition may be related to the down-regulation of the apoptosis-inhibiting gene Survivin.

by  Yash Lalit Samtani

Cancer Cell Research 2019 6(21) 544-550; published online  27  January 2019

Abstract: For long, it was believed that we are at the mercy of our genes, that our genetic makeup is beyond our influence. However, in recent years, the developing field of epigenetics have proven otherwise. The epigenome is highly susceptible to changes in environmental factors. Altered epigenetic marks are responsible for altered gene expression. Numerous studies suggest that deregulated epigenetic modifications are present ubiquitously in virtually all types of malignancies including cancer. In fact, epigenetic changes appear to be present in nearly every stage of cancer development. Thus, epigenetic therapy for medicinal or chemopreventive purposes has grown to become a subject of huge importance. A number of bioactive dietary components are of particular interest in the field of epigenetics (Nutriepigenomics). Many of these compounds display anticancer properties and may play a role in cancer prevention. Numerous studies suggest that a number of nutritional compounds have epigenetic targets in cancer cells. Importantly, emerging evidence strongly suggests that consumption of dietary agents can alter normal epigenetic states as well as reverse abnormal gene activation or silencing. Epigenetic modifications induced by bioactive food compounds are thought to be beneficial in cancer prevention and therapy. This article will primarily focus on dietary factors that have been demonstrated to influence the epigenome and that may be used in conjunction with other cancer prevention and chemotherapeutic therapies. Another focus shall include how different stages of life affect the influence of these factors on the epigenome.

by  Xuemei Zhao, Cuiping Liu, Chen Chen, Yang Song, Yifan Ci, Qianqian Li, Yang Meng, Xiaohan Liu

Cancer Cell Research 2019 6(21) 551-557; published online  28  January 2019

Abstract: Butyric acid is produced by endogenous intestinal bacteria during the fermentation of dietary fiber, and has been found to have anticancer effects. The aim of the present study was to identify that if sodium butyrate (NaB) affects proliferation, migration, invasion, adhesion abilities and epithelial-mesenchymal transition (EMT) in CRC cells (SW620), and explore its possible mechanisms.In this study SW620 cells were cultured in RPMl l640 medium containing 10% fetal bovine serum in a 5% CO2 incubator at 37°C. SW620 cells were divided into 5 groups: control group, 1.25mM NaB group, 2.5mM NaB group, 5mM NaB group and 10 mM NaB group. The effect of NaB treatment on SW620 cells proliferation was detected by CCK-8 assay. The functional role of NaB on SW620 cells motility was evaluated by wound healing assay and transwell migration assay. In addition, a Matrige invasion assay was performed to characterize the invasion ability. The adhesion ability between cells and extracellular matrix was examined by cell-interstitial adhesion test. The protein expression level of TGF-β, E-Cadherin and Vimentin were measured by Western-Blot. The results demonstrated that after treated by different concentrations (1.25mM, 2.5 mM, 5mM,10mM) of NaB for 24h, the proliferation rates of SW620 cells were inhibited significantly (P<0.05). Compared to the control group, the abilities of migration, invasion and adhesion of SW620 cells lines in other groups were gradually decreased, respectively (P<0.05). Western-Blot assay showed that NaB could significantly inhibit the expression of TGF-β and Vimentin protein and promote the expression of E-Cadherin in SW620 cells (P<0.05). There was a dose-effect relationship between the concentration and effect of NaB on SW620 cells in all the above experiments. These findings indicate that NaB can inhibit the abilities of migration, invasion and adhesion of SW620 cells. In addition, NaB can inhibit the EMT of CRC cells by down-regulating the expression of TGF-β and Vimentin protein and up-regulating the expression of E-Cadherin protein.

by  Lang He

Cancer Cell Research 2019 6(21) 558-564; published online  8 March 2019

Abstract: Anti-angiogenic therapy has emerged as the research frontier of cancer treatment with the concept of starving tumor cells by suppressing tumor neovascularization. It is well known that tumor blood vessels are different from regular blood vessels in terms of structure and function. With the advance of anti-angiogenic research, it was discovered that anti-angiogenic agents could transiently normalize tumor blood vessels to be structurally and functionally similar to regular blood vessels. This short period is called normalization time window of tumor vasculature. Accumulating evidence supports that administering anti-angiogenic drugs combined with radiotherapy or chemotherapy in the normalization time window enhances efficacy of cancer therapeutics. Recombinant human endostatin (rh-ES) is a novel anti-angiogenic agent with complete independent intellectual property rights in China. It is of vital importance to determine the normalization time window of rh-ES to guide clinical planning and treatment in the future. The recent progress in normalization time window of rh-ES was comprehensively reviewed.

by  Xiaotong Liu, Shuo Sun, Dongyang Zhang, Zhaoyun Sun, Jianwei Du, Wenjie Jiao, Linhao Xu

Cancer Cell Research 2019 6(21) 565-568; published online  8 March 2019

Abstract: Esophageal cancer is one of the six major malignant tumors worldwide. Radical resection is regarded as an effective treatment method for patients with good general condition and no proof of metastasis. Because esophageal cancer is separated from the location of the left descending aorta, the operative approach is divided into the following three main types: triple incision approach (trans-cervix, right thorax and abdomen) for upper esophageal cancer, double incision approach (trans-right thorax and abdomen) for middle esophageal cancer and single incision approach (trans-left thorax) for lower esophageal or cardia cancer. A right aortic arch is a rare vascular malformation, and the incidence of a right aortic arch associated with esophageal cancer is even rarer. This anatomical abnormality has driven thoracic surgeons worldwide to explore and discuss the best choice of surgical method. Here, we introduce one case of surgical treatment of esophageal cancer associated with right aortic arch (RAA) that has been integrated with the theory of enhanced recovery after surgery (ERAS).