br In addition to the e ect
In addition to the eﬀect on endothelial cells, we also examined the eﬀect of ANGPTL6 on tumor cells. Diﬀerent types of cytokines, che-mokines, and other secretory proteins in the surrounding micro-environment were secreted into the tumor bed, and these proteins not only aﬀect the activity of stromal cells, such as endotheliocytes, fibro-blasts, immune PCI32765 and inflammatory cells, but also modulate the biological behavior of the tumor cells themselves. ANGPTL2 loss sup-presses gastric cell growth, invasion, and migration. ANGPTL2 is a pro-inflammatory factor whose overexpression leads to EMT and promotes the aggressiveness in pancreatic cancer . ANGPTL2 accelerated the invasiveness and metastasis of colorectal cells, contributing to tumor development via the promotion of vessel formation and epithelial-me-senchymal transition. ANGPTL3 knockdown decreased oral cancer proliferation with inactivated extracellular regulated kinase, increased cyclin-dependent kinase inhibitors and arrested the cell-cycle.
Nevertheless, ANGPTL4 plays a completely diﬀerent role depending on the tumor type. ANGPTL4 can restore the melanoma metastasis process by decreasing vascular activity and tumor cell activity and mobility, through dual eﬀects on blood vessels and tumor compartments. More-over, ANGPTL4 accelerates venous invasion and tumor metastasis in colorectal cancer  and gastric cancer . Substantial experimental evidence indicated that downregulation of ANGPTL6 in cancer cells leads to cell apoptosis and migration. We investigated whether knock-down of ANGPTL6 induced cell apoptosis. Regarding cell viability and invasiveness, the numbers of migratory and invasive of cells were re-markably decreased by shRNA-ANGPTL6 compared with corresponding controls. The tumor volume and size were significantly inhibited after knockdown of ANGPLT6 in vivo. The above findings suggest that ANGPTL6 promotes not only tumor endotheliocyte angiogenesis but also the malignancy of the tumor cells themselves. r> In conclusion, our study describes the role of ANGPTL6 in AFPGC angiogenesis and progression. The features of ANGTL6-endothelial cell-angiogenesis are not only an eﬀective biomarker for AFPGC diagnosis but also an attractive therapeutic intervention for future studies.
The authors disclose no competing interests in this research.
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Anions reversibly responsive luminescent nanocellulose hydrogels for cancer spheroids culture and release
Jun Haia, Xiaofan Zengb, Yanhong Zhub, Baodui Wanga,∗
a State Key Laboratory of Applied Organic Chemistry and Key Laboratory of Nonferrous Metal Chemistry and Resources Utilization of Gansu Province, Lanzhou University, Gansu, Lanzhou, 730000, China b College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, 430074, China
Artificial stimuli-responsive hydrogels that can mimic natural extracellular matrix for growth and release of cancer spheroids (CSs) have attracted much attention. However, such hydrogels still face a challenge in reg-ulating CSs growth and controlled release as well as keeping CSs integrity. Herein, a new class of ClO−/SCN− reversibly responsive nanocellulose hydrogel with fluorescence on-off reporter is developed. Upon addition of ClO−, the gel network of nanocellulose hydrogel was destructed, accompanying by the fluorescent quenching. Notably, when introducing of SCN−, a red fluorescence filamentous hydrogel was recovered by coordination cross-linking. The hydrogel reforms in a completely reversible process through the regulation of ClO −/SCN−. Benefit from the above response features of the hydrogel, the growth of cancer spheroids (CSs) in the hydrogel and on demand release of CSs from the hydrogel could be easily achieved through ClO−/SCN− regulation. Importantly, the growth and release of CSs can be monitored in real time by fluorescence imaging. Overall, such design strategy based on ClO−/SCN−-responsive fluorescent hydrogels provided a new type of multi-responsive hydrogels as main scaffolds for cancer research and cancer drug screening.