Cancer tumor Jurkat

The DNA-damaging agent bleomycin arrests the cell cycle of Jurkat cells defective in the G1 checkpoint in the G2 phase, and microtubule-affecting colchicine arrests it in the M phase [40]. Boromycin showed no effect on the cell cycle status of Jurkat cells at least up to 340 nM but potentiated anti-tumor activity of bleomycin in SCID mice inoculated with Jurkat cells. These data suggest that boromycin disrupts the cell cycle at the G2 checkpoint of cancer cells selectively, leading to sensitization of cancer cells to anti-cancer reagents. 

Studies on some cell lines have shown that in tumor models such as mouse epidermal 1B6 cells and MCF-7, ROS were observed to stimulate cell growth in monolayers. In other cell lines, ROS can also be involved in the pathogenesis of cancer. By promoting cell proliferation in the transformed cancer cell lines MCF-7, HeLa, and Jurkat cells, reduced antioxidant levels were implicated in malignant transformation. Overexpression of manganese superoxide dismutase (MnSOD), a normal cellular antioxidant, enzyme was reported to revert transformation or tumor-promotion response in these and other transformed cell tines, such as human melanoma (UACC-903) cells, human breast cancer (MCF-7) cells, and mouse epidermal JB6 cells. ... 

Eucalyptus ben ianui Maiden et Cambage yrtaceae) Jurkat (T leukemia cells) J774A (murine macrophage tumor) HeLa (cervical cancer) Doll-Boscardin et al. (2012... 

It has been shown that tannic acid (TA) exerts cancer chemopreventive activity in various animal models (61). TA induced either growth arrest or apoptotic death (62). TA induced apoptosis more in human oral squamous cell carcinoma and salivary gland tumor cell lines than in normal human gingival fibroblasts, whereas gallic acid, a component unit of TA, showed much weaker selective cytotoxicity (63). Recently, it was shown that inhibition of the proteosome of living Jurkat cells results in accumulation of two natural proteosome substrates, the cyclin-dependent kinase inhibitor p27 and the proapoptotic protein Bax, followed growth arrest in G1 and induction of apoptotic cell death (d ). 

---