Heparin, including unfractionated heparin (UFH), low-molecular-weight heparin (LMWH) and heparin derivatives, are commonly used in venous thromboembolism treatment and reportedly have beneficial effects on cancer survival. Heparin can affect the proliferation, adhesion, angiogenesis, migration and invasion of cancer cells via multiple mechanisms. The main mechanisms involve inhibition of heparanase, P-/L-selectin, angiogenesis, and interference with the CXCL12-CXCR4 axis. Here we summarize the current experimental evidence regarding the anti-cancer role of heparin and its derivatives, and conclude that there is evidence to support heparin's role in inhibiting cancer progression, making it a promising anti-cancer agent.
Objective: Capecitabine is an antimetabolic fluoropyrimidine deoxynucleoside carbamate drug that can be converted to 5-FU in vivo. Currently, the role of capecitabine in the treatment of advanced breast cancer has been recognized. Also, Several meta-analyses have elucidated the role of capecitabine in the treatment of breast cancer, indicating that taxane-based regimen with capecitabine may be an effective, convenient, and well tolerated regimen in patients with early breast cancer. However, the correlation between capecitabine-based combination first-line chemotherapy and breast cancer survival remains unclear. Here, we present a meta-analysis to systematically evaluate the safety and effectiveness of capecitabine-based combination with first-line chemotherapy treatment in breast cancer.Methods: We searched Pubmed, Embase, and Medline for relevant studies evaluating pooled estimated hazard ratios of capecitabine in breast cancer patients with the eligible criteria up to June 2018. Fixed and random-effect meta-analyses were conducted based on heterogeneity of included studies.Results: Overall, 10 articles with 12,872 patients were included in the meta-analysis. Capecitabine-based combination first-line chemotherapy compared with non-combination had significant impacts on disease-free survival (HR = 0.84, 95% CI: 0.76-0.93; P = 0.000) and overall survival (HR = 0.84, 95% CI: 0.74-0.94; P = 0.001). Also, according to the 3 articles concerning neoadjuvant chemotherapy which included 2534 participants, we found that the addition of capecitabine significantly improved OS (HR = 0.89, 95% CI: 0.63-0.86; P = 0.011). In the subgroup analysis, TNBC patients got significant benefits with the addition of capecitabine in DFS (HR = 0.77, 95% CI: 0.65-0.92; P = 0.004) and OS (HR = 0.65, 95% CI: 0.51-0.81; P = 0.000). ER negative patients got significant benefits in OS (HR = 0.73, 95% CI: 0.57-0.93; P = 0.012). The association of DFS with the addition of capecitabine in Her- patients (HR = 0.84, 95% CI: 0.71-0.99; P = 0.005) was significant, as was OS (HR = 0.82, 95% CI: 0.70-0.95; P = 0.009),. Meanwhile, patients receiving capecitabine-based combination first-line chemotherapy underwent less adverse effects especially the grade 3/4 leucopenia than patients with non-combination therapy (RR=0.72 95% CI: 0.59-0.86; P = 0.000).Conclusion: Capecitabine combined with first-line chemotherapy in the treatment of breast cancer is an effective and safe treatment option and is worthy of clinical application to improve survival of breast cancer patients. In the future, we can continue to carry out relevant researches to explore the upmost appropriate dose of capecitabine for breast cancer.
Sporamin, a Kunitz-type trypsin inhibitor (TI) from sweet potato tuberous roots, has demonstrated anti-tumor activity through poorly defined mechanisms. Furthermore, the effects of sporamin on pancreatic cancer have not been explored. Herein, we studied the effects of sporamin on two human pancreatic cancer cell lines, PANC-1 and BxPC-3. Sporamin significantly inhibited the cell viability and proliferation activity and induced apoptosis in PANC-1 and BxPC-3 cells. Consistently, in sporamin-treated PANC-1 and BxPC-3 cells, the anti-apoptotic proteins Bcl-2 and Bcl-XL were downregulated and the pro-apoptotic protein Bax was upregulated. Moreover, nuclear factor kappa B activation and IκBα phosphorylation were inhibited, and total IκBα expression was increased in sporamin-treated PANC-1 and BxPC-3 cells. Thus, our results suggest that the anti-tumor effects of sporamin in pancreatic cancer cells might result partly from induction of apoptosis by downregulating nuclear factor kappa B pathway.
The physiochemical properties of the implant interface significantly influence cell growth, differentiation, cellular matrix deposition, and mineralisation, and eventually, determine the bone regeneration efficiency. Cells directly sense and respond to the physical, chemical, and mechanical cues of the implant surface, and it is increasingly recognized that surface topography can evoke specific cellular responses, conferring biological functions on substrate materials and regulating tissue regeneration. Current progress towards the fundamental understanding of the interplay between the cell and topographical surface has been made by combined advance in fabrication technologies and cell biology. Particularly, the precise fabrication and control of nano/microscale topographies can provide the fundamental knowledge of the mechanotransduction process that governs the cellular response as well as the knowledge of how the specific features drive cells towards a defined differentiation outcome. In this review, we first introduce common techniques and substrate materials for designing and fabricating micro/nano‐topographical surfaces for bone regeneration. We then illustrate the intrinsic relationship of topological cues, cellular signal transduction, and cell functions and fates in osteogenic differentiation. Finally, we discuss the challenges and the future of using topological cues as a cell therapy to direct bone tissue regeneration.
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