Reduction in Cyclin D1/Cdk4/Retinoblastoma Protein Signaling by CRE-Decoy Oligonucleotide

Park, Yun Gyu; Park, Serk In; Lim, Seoung Ok; Lee, Moon Seop; Ryu, Chong Kun; Kim, Insun; Cho‐Chung, Yoon S.

doi:10.1006/bbrc.2001.4521

Cited by 25 publications

(18 citation statements)

References 26 publications

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“…Therefore, a potential strategy in the treatment of ER-positive breast cancer would be to combine hormonal treatment and blockade of cyclin D1 function. Several strategies have already been successfully used to block cyclin D1 expression, such as antisense oligonucleotides, a CREdecoy oligonucleotide, a novel DNA-binding ligand, or siRNA (37,39,40). An important lesson learned from knocking out cyclin D1 in the mouse genome was that cyclin D1 expression was required for full mammary gland development but not required for normal development and function of most tissues (41).…”

Section: Discussionmentioning

confidence: 99%

Cyclin D1 Is Necessary for Tamoxifen-Induced Cell Cycle Progression in Human Breast Cancer Cells

Kilker

Planas-Silva²

2006

Cancer Research

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Despite the success of tamoxifen in treating hormoneresponsive breast cancer, its use is limited by the development of resistance to the drug. Understanding the pathways involved in the growth of tamoxifen-resistant cells may lead to new ways to treat tamoxifen-resistant breast cancer. Here, we investigate the role of cyclin D1, a mediator of estrogendependent proliferation, in growth of tamoxifen-resistant cells using a cell culture model of acquired resistance to tamoxifen. We show that tamoxifen and 4-hydroxytamoxifen (OHT) promoted cell cycle progression of tamoxifen-resistant cells after growth-arrest mediated by the estrogen receptor downregulator ICI 182,780. Down-regulation of cyclin D1 with small interfering RNA blocked basal cell growth of tamoxifenresistant cells and induction of cell proliferation by OHT. In addition, pharmacologic inhibition of phosphatidylinositol 3-kinase/Akt or mitogen-activated protein kinase/extracellular signal-regulated kinase 1/2 pathways decreased basal cyclin D1 expression and impaired OHT-mediated cyclin D1 induction and cell cycle progression. These findings indicate that cyclin D1 expression is necessary for proliferation of tamoxifen-resistant cells and for tamoxifen-induced cell cycle progression. These results suggest that therapeutic strategies to block cyclin D1 expression or function may inhibit development and growth of tamoxifen-resistant tumors.

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Section: Discussionmentioning

confidence: 99%

Cyclin D1 Is Necessary for Tamoxifen-Induced Cell Cycle Progression in Human Breast Cancer Cells

Kilker

Planas-Silva²

2006

Cancer Research

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“…CRE decoy OGN (5′-TGACGTCAGAGAGCGCTCTCTGACGTCA-3′) and control OGN (5′- TGACGTCATGACGTCATGACGTCA-3′) were converted to phosphorothioate OGNs (Invitrogen Carlsbad, CA, USA) as previous described [5], [6], [10].…”

Section: Methodsmentioning

confidence: 99%

Cyclic AMP-Response Element Regulated Cell Cycle Arrests in Cancer Cells

et al. 2013

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Recently, we have demonstrated that trichosanthin (TCS), a promising agent for the treatment of cervical adenocarcinoma, inhibited HeLa cell proliferation through the PKC/MAPK/CREB signal pathway. Furthermore, TCS down-regulated Bcl-2 expression was abrogated by a decoy oligonucleotide (OGN) to the cyclic AMP-responsive element (CRE). The decoy OGN blocked the binding of CRE-binding protein (CREB) to Bcl-2. These results suggested that CRE-mediated gene expression may play a pivotal role in HeLa cell proliferation. However, little is known about the effect of TCS on cell cycle arrests, particularly, whether the genes involved in cell cycle were regulated by CRE. Our present study shows that the arrests of S, G1 and G2/M phases were accompanied by the significant down-regulation of cyclin A, D1 and CDK 2, 4 in HeLa cells, cyclin D1, E and CDK 2, 4 in Caski and C33a cells, and cyclin A, B1, E and CDK 2 in SW1990 cells. However, the cell cycle arrests were reversed via the significant up-regulation of cyclin A and D1, by the combined treatment of TCS and CRE. In conclusion, these data demonstrate for the first time that specific cell cycle arrests in cancer cells can be induced by TCS by inhibiting the binding of CREB to CRE on genes related to cell proliferation.

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“…A subsequent study sought to illuminate the pathway of CRE decoy inhibition [78] by assessing protein expression of CRE target genes. In breast cancer cells treated with decoy, both cyclin D1 reduction and growth inhibition were demonstrated to be dose and time-dependent.…”

Section: Cyclic Amp Response Element (Cre)mentioning

confidence: 99%

Oligonucleotides as Anticancer Agents: From the Benchside to the Clinic and Beyond

Coppelli

Grandis²

2005

CPD

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Prevention, improved screening, and better treatment regimens have improved cancer incidence and mortality in the last decade. Chemoradiation continues to cause high morbidity in patients undergoing treatment. DNA therapeutics have the potential to modify the genes that cause tumor progression in order to produce a response that is tumor-specific, efficacious and systemic without toxicity to normal cells. The most widely used and most experimentally advanced DNA therapeutic is the antisense oligonucleotide. These oligomers are predominantly used to inhibit mRNA expression. For cancer chemotherapy, the Bcl-2 antisense oligonucleotide is currently in phase III clinical trials. Transcription factor decoys form DNA:protein heteroduplexes and produce cellular responses at the genomic rather than transcriptional level. The use of other transcription factor decoys as oncologic reagents is now being developed. The phenomenon of RNA interference has only recently been discovered to occur in plants as a response to viral infection. Small interfering RNAs cause mRNA inhibition. siRNAs also inhibit expression of mRNA, however the intracellular cascade is quite different. siRNA could prove to be more powerful and longer lasting than antisense. Several DNA therapeutics are currently being studied. This review will focus on antisense oligonucleotides, transcription factor decoys and siRNA with an emphasis on how they can be employed as anticancer agents. Mechanism of action and design strategies will be summarized, as well as therapeutic targets and demonstrated clinical efficacy for each reagent.

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Reduction in Cyclin D1/Cdk4/Retinoblastoma Protein Signaling by CRE-Decoy Oligonucleotide

Cited by 25 publications

References 26 publications

Cyclin D1 Is Necessary for Tamoxifen-Induced Cell Cycle Progression in Human Breast Cancer Cells

Cyclin D1 Is Necessary for Tamoxifen-Induced Cell Cycle Progression in Human Breast Cancer Cells

Cyclic AMP-Response Element Regulated Cell Cycle Arrests in Cancer Cells

Oligonucleotides as Anticancer Agents: From the Benchside to the Clinic and Beyond

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