Extra-pancreatic metastasis is a difficult problem for surgical intervention in pancreatic cancer. CXC chemokine receptor 4 (CXCR4) was considered to have an important role in this process. We hypothesized it may contribute to the pancreatic cancer progression through influencing canonical Wnt pathway. The purpose of this study was to examine the functional role of CXCR4 in the progression of pancreatic cancers and explore the possible mechanism. To this end, the relation between CXCR4 and clinical characteristics was analysed. shRNA against CXCR4 was applied to disrupt the SDF-1/CXCR4 signal transduction pathways in pancreatic cancer cell lines. Our results showed that overall survival in the case of patients positive for CXCR4 expression was significantly lower than that in the case of patients negative for CXCR4 expression. Notably, in vitro studies we observed that the abrogation of CXCR4 could obviously influence the pancreatic cancer cell phenotype including cell proliferation, colony formation, cell invasion and also inhibit the TOPflash activity. In addition, Wnt target genes and mesenchymal markers such as Vimentin and Slug were also inhibited in CXCR4 knockdown cells. Collectively, these data reported here demonstrate CXCR4 could modulate the canonical Wnt pathway and perhaps be a promising therapeutic target for pancreatic cancer progression.

Expression of lymphoid enhancer factor 1 (LEF1) is frequently altered in different human cancers. This study aimed to assess LEF1 expression in colon cancer tissues and to explore changed phenotypes, gene expressions, and the possible mechanism after knocked down LEF1 expression in colon cancer cell lines. A total of 106 colon cancer and matched paratumorous normal tissues were used to assess LEF1 expression using immunohistochemistry and qRT-PCR. LEF1 lentivirus was used to knockdown LEF1 expression for the assessment of cell viability, cell cycle distribution, apoptosis, and gene expressions. The nude mouse xenograft assay was performed to detect the effects of LEF1 knockdown in vivo. The data showed that the levels of LEF1 mRNA and protein were significantly increased in human colon cancer tissues compared to the matched paratumorous normal tissues and were associated with infiltration depth, lymph node and distant metastases, advanced TNM (tumor-node-metastasis) stages, and shorter overall survival. Furthermore, LEF1 knockdown reduced tumor cell viability, invasion capacity, MMP2 and MMP-9 expression, but induced apoptosis. Nude mouse xenograft assay showed that LEF1 knockdown suppressed tumor formation and growth in vivo. In addition, the expression of Notch pathway-related proteins RBP-jκ and Hes1 was reduced in LEF1 knockdown cells. Taken together, LEF1 protein was overexpressed in colon cancer tissues and knockdown of LEF1 expression inhibited colon cancer growth in vitro and in vivo. These data suggest that targeting of LEF1 expression should be further evaluated for colon cancer prevention and therapy.

ObjectiveSelf-compassion is consistently found to be related to better psychological outcomes.As most studies were cross-sectional, little is known about the predictive role of selfcompassion for future psychological outcomes. This longitudinal study in cancer patients investigated the predictive role of self-compassion at the time of cancer diagnosis for the course of symptoms of depression, anxiety, and fatigue in the period of receiving cancer treatment. Methods: This longitudinal study was conducted at the Shaanxi Provincial TumourHospital in Xi'an, China. A total of 153 heterogeneous cancer patients were assessed within 1 week after cancer diagnosis (T1) as well as at the start (T2) and the end (T3) of medical treatment. Hierarchical linear regression analyses were conducted to examine the research questions.Results: Cross-sectional regression analyses at T1 showed that a self-compassion total score and negative self-compassion (and to a lesser extent positive selfcompassion) were significantly related to symptoms of depression, anxiety, and fatigue. When controlling for symptoms at T1, positive self-compassion significantly predicted all three outcomes at T3. A self-compassion total score only predicted symptoms of anxiety at T2, controlling for T1 symptoms. In contrast, we found no significant predictive value of negative self-compassion. Conclusions: This study suggests that the positive aspects of self-compassion are beneficial for cancer patients for their future functioning, in terms of fewer symptoms of depression, anxiety, and fatigue over time. Future interventions should test how and to what extent self-compassion can be cultivated and whether increases in self-compassion are associated with better outcomes. KEYWORDS cancer, oncology, positive and negative self-compassion, depression, anxiety, fatigue, longitudinal study Lei Zhu and Juntao Yao share the first coauthorship.

This study demonstrates the existence of 4 patterns of unmet supportive needs in Chinese cancer patients. Patients with few unmet needs reported the best QoL.

ABCB5 belongs to the ATP-binding cassette (ABC) superfamily, which is recognized for playing a role in the failure of chemotherapy. ABCB5 has also been found to be overexpressed at the transcriptional level in a number of cancer subtypes, including breast cancer. However, the exact mechanism ABCB5 uses on cancer cell metastasis is still unclear. In the present study, we demonstrate that ABCB5 expression was increased in metastatic tissues when compared with nonmetastatic tissues. ABCB5 can significantly enhance metastasis and epithelial-mesenchymal transition (EMT), while knockdown of ABCB5 inhibited these processes. Microarray analysis indicated that ZEB1 may function as a downstream factor of ABCB5. Furthermore, the expression of ZEB1 in tissues is positively relevant to ABCB5 in breast cancer. Knocking down ZEB1 inhibits ABCB5 ectopic expression-induced migration and invasion, as well as EMT. Taken together, these results helped to realize the oncogene functions of ABCB5 in breast cancer cells and provided a new direction in treating breast cancer.