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Cisplatinspecific responses have been observed in other cell lines from tumor types that are commonly refractory to cisplatin treatment such as the human nonsmall cell lung carcinoma lines A. Moreover, hafter treatment with cisplatin, but not transplatin, JNK activity of TG cells or lung carcinoma cells M remains elevated, suggesting that treatment with cisplatin leads to a prolonged response.Extended titrations revealed IC values of and M for the parental cells and empty vector control cells, respectively or over fold more sensitive to cisplatin than the control cells. In fact, the viability of these cells when treated with cisplatin is somewhat increased relative to parental or empty vector control cells for all viability determinations in the range M cisplatin, suggesting that increased JNK substrate augmented viability following treatment with cisplatin. Viability studies show that parental or empty vector control cells are largely insensitive to cisplatin at concentrations M. Extended titrations revealed IC values of and M for the parental and empty vector control cells, respectively. The addition of zinc acetate alone has no effect on the viability of parental or empty vector control cells. None of the cell lines examined here were made cisplatinresistant prior to analysis.Similar results have been observed with an additional human glioblastoma line, U, and an additional epithelial tumor line, MCF. Inhibition of this response sensitizes cells to the cellkilling properties of cisplatin.Thus, this assay provides a direct assessment of the extent of cisplatininduced DNA damage.A, PCR results for TG parental cells either immediately or hafter treatment with cisplatin.The results are the averages of three assays for each of two independent preparations of DNA for the three concentrations of cisplatin.Following the h recovery period, DNA damage remained unrepaired,   and total DNA damage was substantially increased.Sensitization to cisplatin is also observed in PC prostate carcinoma cells modified to express TAM, a known dominant negative inhibitor of AP. Moreover, transcription of these genes is known to be activated through the ATFCREB sites upon stimulation by genotoxic agents. In view of the common regulatory mechanism involving ATFCREB sites, a concerted induction of genes with a related function, DNA repair, is suggested.Biol. Chem. doi. jbc. Access the most updated version of this article at http:www.jbc.orgcontent When a correction for this article is posted Click here to choose from all of JBCs email alerts This article cites references, of which can be accessed free at http:www.jbc.orgcontent.full.htmlreflist Downloadedfromhttp: www.jbc.orgbyguestonSeptember, The polymerase bdependent pathway could also use FEN for excision of the synthetic AP sites, which were not susceptible to belimination.In this pathway, FEN was functional without PCNA and replication factor C but required the DNA synthesis, which led to a flap <a href="http://www.thechemlibrary.com/archives/320">buy Rivastigmine</a> structure formation.Base excision repair is a major mechanism for repair of damaged bases in DNA. Major lesions to be repaired by this mechanism are bases with a relatively small modification or apurinicapyrimidinic sites.These types of damage are induced by ionizing radiation and exposure to various chemicals, such as alkylating agents, as well as by attack from reactive species generated during normal cellular metabolism.

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