Enhanced cytotoxicity from deoxyguanosine-enriched T-oligo in prostate cancer cells.
Enhanced cytotoxicity from deoxyguanosine-enriched T-oligo in prostate cancer cells.
复制标题
富含脱氧鸟苷的 T-oligo 在前列腺癌细胞中增强细胞毒性。
DOI：
10.1089/nat.2013.0420
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发表时间：
2013
影响因子：
4
通讯作者：
Faller,DouglasV
中科院分区：
文献类型：
--
作者：
Rankin,AndrewM;Forman,Lora;Sarkar,Sibaji;Faller,DouglasV
Prostate cancer represents approximately 10 percent of all cancer cases in men and accounts for more than a quarter of all cancer types. Advances in understanding the molecular mechanisms of prostate cancer progression, however, have not translated well to the clinic. Patients with metastatic and hormone-refractory disease have only palliative options for treatment, as chemotherapy seldom produces durable or complete responses, highlighting the need for novel therapeutic approaches. T-oligo, a single-stranded deoxyribonucleic acid with partial sequence homology to human telomeric DNA, has elicited cytostatic and/or cytotoxic effects in multiple cancer cell types. In contrast, normal primary cells of varying tissue types are resistant to cytotoxic actions of T-oligo, underscoring its potential utility as a novel targeted cancer therapeutic. Mechanistically, T-oligo is hypothesized to interfere with normal telomeric structure and form G-quadruplex structures, thereby inducing genomic stress in addition to aberrant upregulation of DNA damageresponse pathways. Here, we present data demonstrating the enhanced effectiveness of a deoxyguanosine-enriched sequence of T-oligo, termed (GGTT)4, which elicits robust cytotoxic effects in prostate cancer cells at lower concentrations than the most recent T-oligo sequence (5′-pGGT TAG GTG TAG GTT T 3′) described to date and used for comparison in this study, while exerting no cytotoxic actions on nontransformed human prostate epithelial cells. Additionally, we provide evidence supporting the T-oligo induced activation of cJun N-terminal kinase (JNK) signaling in prostate cancer cells consistent with G-quadruplex formation, thereby significantly advancing the understanding of the T-oligo mechanism of action.
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影响因子：
5.6
作者：
Rankin, Andrew M.;Sarkar, Sibaji;Faller, Douglas V.
通讯作者：
Faller, Douglas V.
影响因子：
11.2
作者：
Qi, Haiyan;Lin, Chao-Po;Liu, Leroy F.
通讯作者：
Liu, Leroy F.
c-myc 反义硫代磷酸寡核苷酸中的连续四鸟苷序列抑制人肺癌细胞的细胞生长：可能涉及细胞粘附抑制
DOI：
--
发表时间：
1997
期刊：
Japanese journal of cancer research : Gann
影响因子：
--
作者：
Y. Saijo;B. Uchiyama;T. Abe;K. Satoh;T. Nukiwa
通讯作者：
T. Nukiwa
影响因子：
158.5
作者：
Petrylak, DP;Tangen, CM;Crawford, ED
通讯作者：
Crawford, ED
影响因子：
2
作者：
S. Sarkar;A. Abujamra;J. E. Loew;L. Forman;S. Perrine;D. Faller
通讯作者：
S. Sarkar;A. Abujamra;J. E. Loew;L. Forman;S. Perrine;D. Faller