دورية أكاديمية
Overcoming temozolomide resistance in glioblastoma via dual inhibition of NAD+ biosynthesis and base excision repair.
| العنوان: | Overcoming temozolomide resistance in glioblastoma via dual inhibition of NAD+ biosynthesis and base excision repair. |
|---|---|
| المؤلفون: | Goellner EM; Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, and University of Pittsburgh Cancer Institute, Hillman Cancer Center, Pittsburgh, Pennsylvania 15213-1863, USA., Grimme B, Brown AR, Lin YC, Wang XH, Sugrue KF, Mitchell L, Trivedi RN, Tang JB, Sobol RW |
| المصدر: | Cancer research [Cancer Res] 2011 Mar 15; Vol. 71 (6), pp. 2308-17. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Association for Cancer Research Country of Publication: United States NLM ID: 2984705R Publication Model: Print Cited Medium: Internet ISSN: 1538-7445 (Electronic) Linking ISSN: 00085472 NLM ISO Abbreviation: Cancer Res Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Baltimore, Md. : American Association for Cancer Research Original Publication: Chicago [etc.] |
| مواضيع طبية MeSH: | DNA Repair/*drug effects , Dacarbazine/*analogs & derivatives , Drug Resistance, Neoplasm/*drug effects , NAD/*biosynthesis, Acrylamides/pharmacology ; Adenosine Triphosphate/metabolism ; Antineoplastic Agents, Alkylating/pharmacology ; Cell Line, Tumor ; Cell Survival/drug effects ; DNA Glycosylases/genetics ; DNA Glycosylases/metabolism ; Dacarbazine/pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Glioblastoma/genetics ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Hydroxylamines/pharmacology ; Immunoblotting ; Methyl Methanesulfonate/pharmacology ; Piperidines/pharmacology ; Poly(ADP-ribose) Polymerases/genetics ; Poly(ADP-ribose) Polymerases/metabolism ; RNA Interference ; Temozolomide |
| مستخلص: | Glioblastoma multiforme (GBM) is a devastating brain tumor with poor prognosis and low median survival time. Standard treatment includes radiation and chemotherapy with the DNA alkylating agent temozolomide (TMZ). However, a large percentage of tumors are resistant to the cytotoxic effects of the TMZ-induced DNA lesion O(6)-methylguanine due to elevated expression of the repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) or a defect in the mismatch repair (MMR) pathway. Although a majority of the TMZ-induced lesions (N7-methylguanine and N3-methyladenine) are base excision repair (BER) substrates, these DNA lesions are also readily repaired. However, blocking BER can enhance response to TMZ and therefore the BER pathway has emerged as an attractive target for reversing TMZ resistance. Our lab has recently reported that inhibition of BER leads to the accumulation of repair intermediates that induce energy depletion-mediated cell death via hyperactivation of poly(ADP-ribose) polymerase. On the basis of our observation that TMZ-induced cell death via BER inhibition is dependent on the availability of nicotinamide adenine dinucleotide (NAD(+)), we have hypothesized that combined BER and NAD(+) biosynthesis inhibition will increase TMZ efficacy in glioblastoma cell lines greater than BER inhibition alone. Importantly, we find that the combination of BER and NAD(+) biosynthesis inhibition significantly sensitizes glioma cells with elevated expression of MGMT and those deficient in MMR, two genotypes normally associated with TMZ resistance. Dual targeting of these two interacting pathways (DNA repair and NAD(+) biosynthesis) may prove to be an effective treatment combination for patients with resistant and recurrent GBM. (© 2011 AACR.) |
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| معلومات مُعتمدة: | R44 GM087798 United States GM NIGMS NIH HHS; CA148629 United States CA NCI NIH HHS; P30 CA047904 United States CA NCI NIH HHS; P20 CA132385 United States CA NCI NIH HHS; P20 CA132385-03 United States CA NCI NIH HHS; CA132385 United States CA NCI NIH HHS; R01 CA148629 United States CA NCI NIH HHS; R01 CA148629-01A1 United States CA NCI NIH HHS; GM087798 United States GM NIGMS NIH HHS; R43 GM087798 United States GM NIGMS NIH HHS; R44 GM087798-02 United States GM NIGMS NIH HHS |
| المشرفين على المادة: | 0 (Acrylamides) 0 (Antineoplastic Agents, Alkylating) 0 (Hydroxylamines) 0 (N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide) 0 (Piperidines) 0U46U6E8UK (NAD) 7GR28W0FJI (Dacarbazine) 8L70Q75FXE (Adenosine Triphosphate) 9TZH4WY30J (methoxyamine) AT5C31J09G (Methyl Methanesulfonate) EC 2.4.2.30 (Poly(ADP-ribose) Polymerases) EC 3.2.2.- (DNA Glycosylases) YF1K15M17Y (Temozolomide) |
| تواريخ الأحداث: | Date Created: 20110317 Date Completed: 20110725 Latest Revision: 20220310 |
| رمز التحديث: | 20221213 |
| مُعرف محوري في PubMed: | PMC3077901 |
| DOI: | 10.1158/0008-5472.CAN-10-3213 |
| PMID: | 21406402 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1538-7445 |
|---|---|
| DOI: | 10.1158/0008-5472.CAN-10-3213 |