Cancer cell cytoplasm

Figure 7.1 Drug targets at the level of cellular structure. The mammalian cell presents a variety of druggable targets. The most important ones are located at the level of the cell membrane. Within the cell, cytoplasmic organelles, such as mitochondria, are beginning to be exploited as potential drug targets. The nucleus, at the center of the cell, is an important target for the development of antineoplastic agents for the treatment of cancer.

Kam et al. [38-40] SW CNT-r cytochrome C,RNA, DNA CNT transferred cytochrome C to the cancer cells accumulation of SW CNT-RNA conjugates in cytoplasm and nucleus of HeLa cells... 

The effect of prolonged fixation with formaldehyde on the antigenicity of the nucleus may differ from that of the cytoplasm. This phenomenon is exemplified by Bcl-2 and Bax, members of the same family of proteins involved in apoptosis regulation these proteins reside in the cytoplasm as well as in the nucleus. It was recently demonstrated that prolonged fixation with formaldehyde alone irreversibly reduced nuclear or mitotic Bcl-2 immunoreactivity even after heat-mediated antigen retrieval in monolayers of MCF-7 human breast cancer cells (Hoetelmans et al., 2001). 

While the effect on tests requiring the interaction of the tumour cells with extra cellular matrix components suggest that the interaction of RAPTA compounds with cell surface molecules may be responsible for part of their activity, the compounds also accumulate within cancer cells and interact to a significant extent with proteins in the cytoplasm. Adduct formation of RAPTA compounds with proteins has been studied using mass spectrometric methods [10, 25, 26]. In general, rapid and irreversible binding has been observed. In a recent study the reactivity of cisplatin and RAPTA-C with a mixture of proteins was probed without using any... 

It is clear how normal, wild-type APC downregulates the level of p-catenin, but why are higih levels of p-catenin in the cytoplasm of the cell cancerogenic The answer is that when APC is mutated in the colon cell and no longer can order the phosphorylation and destruction of p-catenin, the monomeric form of P-catenin accumulates first in the cytoplasm and subsequently moves to the nucleus, where it interacts with Tcf and Lef, forming transcriptionally active complexes. Uncontrolled activation of Tcf-controlled genes, by the p-catenin-Tcf-Lef complexes, is a likely cause of cancer, as shown in melanoma cell lines. Malignant transformation of colon cells also occurs when p-catenin is mutated and becomes unresponsive to GSK-3p-mediated phosphorylation. In this case, p-catenin remains unphosphorylated and cannot be destroyed. Thus, a mutant p-catenin, which is not properly phosphorylated, may cause cancer even when a functional, wild-type APC is present. (P-Catenins with abnormal phosphorylation patterns have been found in cancer cells.)... 

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