Cellular uptake of intracerebroventricularly administered biotin- or digoxigenin-Labeled antisense oligodeoxynucleotides in the rat

1994 ◽  
Vol 14 (5) ◽  
pp. 475-486 ◽  
Author(s):  
Frances Yee ◽  
Hans Ericson ◽  
Donald J. Reis ◽  
Claes Wahlestedt
Keyword(s):  
Cellular Uptake ◽  
Antisense Oligodeoxynucleotides

Cellular uptake of antisense oligodeoxynucleotides

1991 ◽  
Vol 6 (3) ◽  
pp. 235-250 ◽  
Author(s):  
Jerzy W. Jaroszewski ◽  
Jack S. Cohen
Keyword(s):  
Cellular Uptake ◽  
Antisense Oligodeoxynucleotides

scholarly journals Photo-reactive oligodeoxynucleotide-embedded nanovesicles (PROsomes) with switchable stability for efficient cellular uptake and gene knockdown

2020 ◽  
Vol 56 (66) ◽  
pp. 9477-9480
Author(s):  
Beob Soo Kim ◽  
Mitsuru Naito ◽  
Rimpei Kamegawa ◽  
Hyun Jin Kim ◽  
Ryo Iizuka ◽  
...  
Keyword(s):  
Cellular Uptake ◽  
Gene Knockdown ◽  
Antisense Oligodeoxynucleotides ◽  
Polyion Complex

A photo-responsive nanovesicle (PROsome) is fabricated via polyion complex between PEG-polypeptides and photo-reactive/antisense oligodeoxynucleotides (PROs/ASOs), eliciting the switchable stability for efficient cellular uptake and gene knockdown.

Water-soluble amphiphilic ruthenium(ii) polypyridyl complexes as potential light-activated therapeutic agents

2020 ◽  
Vol 56 (65) ◽  
pp. 9332-9335
Author(s):  
Sandra Estalayo-Adrián ◽  
Salvador Blasco ◽  
Sandra A. Bright ◽  
Gavin J. McManus ◽  
Guillermo Orellana ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cellular Uptake ◽  
Therapeutic Agents ◽  
Water Soluble ◽  
Polypyridyl Complexes ◽  
Cervical Cancer Cells

Two new water-soluble amphiphilic Ru(ii) polypyridyl complexes were synthesised and their photophysical and photobiological properties evaluated; both complexes showed a rapid cellular uptake and phototoxicity against HeLa cervical cancer cells.

273: Knock-Down of BCL-2 By Antisense Oligodeoxynucleotides Induces Radiosensitization and Inhibition of Angiogenesis

2007 ◽  
Vol 177 (4S) ◽  
pp. 91-92
Author(s):  
Satoshi Anai ◽  
Yoshihisa Sakai ◽  
Steve Goodison ◽  
Kathleen Shiverick ◽  
Bob Brown ◽  
...  
Keyword(s):  
Antisense Oligodeoxynucleotides ◽  
Knock Down ◽  
Inhibition Of Angiogenesis

Neuroprotective effect of antisense oligodeoxynucleotides in experimental intracerebral hemorrhage in rats

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S505-S505
Author(s):  
Huijin Yan ◽  
Mengzhou Xue ◽  
Christopher Power ◽  
Marc R Del-Bigio ◽  
James Peeling
Keyword(s):  
Intracerebral Hemorrhage ◽  
Neuroprotective Effect ◽  
Antisense Oligodeoxynucleotides

Die Anämie bei malignen Tumorerkrankungen

1989 ◽  
Vol 28 (05) ◽  
pp. 193-200 ◽  
Author(s):  
E. Aulbert
Keyword(s):  
Cellular Uptake ◽  
Tumor Tissue ◽  
Malignant Tumors ◽  
The Other ◽  
Novikoff Hepatoma ◽  
Cellular Accumulation ◽  
Tumor Mass ◽  
Proliferation Activity ◽  
Morris Hepatoma ◽  
Cellular Incorporation

Cellular uptake of 67Ga-labelled transferrin by the tumor tissue was studied in rats with tumors of different malignancy and different tumor mass using the slowly growing Morris hepatoma 5123C, the moderately growing Novikoff hepatoma and the very fast and aggressive Yoshida hepatoma AH130. The cellular accumulation of 67Ga-transferrin was found to correlate with the proliferation activity of the tumor. The 67Ga-transferrin concentration in the very fast growing Yoshida hepatoma was 4.8 times higher than the concentration in the slowly growing Morris hepatoma. The uptake of 67Ga-transferrin by the tumors resulted in a faster disappearance of circulating 67Ga-transferrin from the blood. The rate of disappearance correlated with the proliferation activity and the spread of the tumors. Using tumors of identical size the elimination of 67Ga-transferrin from the blood was much faster in the rats with Yoshida hepatoma than in those with the slowly growing Morris hepatoma. On the other hand, using tumors of different tumor size it could be demonstrated that the rate of disappearance of 67Ga-transferrin from the blood correlated directly with tumor mass. It is concluded that cellular incorporation of transferrin within the tumor cells results in a loss of circulating transferrin, which correlates with tumor mass and proliferation of tumor. This mechanism is supposed to be the cause for the hypotransferrinemia seen in patients with malignant tumors.

TARGETING CYCLIN B1 WITH ANTISENSE OLIGONUCLETOTIDES- COATED SUPERPARAMAGNETIC IRON OXIDE NANOPARTICLES

2018 ◽  
Vol 6 (10) ◽  
Author(s):  
Hosam Zaghloul ◽  
Doaa A. Shahin ◽  
Ibrahim El- Dosoky ◽  
Mahmoud E. El-awady ◽  
Fardous F. El-Senduny ◽  
...  
Keyword(s):  
Iron Oxide ◽  
Iron Oxide Nanoparticles ◽  
Cellular Uptake ◽  
Superparamagnetic Iron Oxide ◽  
Cyclin B1 ◽  
Superparamagnetic Iron Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Mcf7 Cells ◽  
M Phase ◽  
The Impact

Antisense oligonucleotides (ASO) represent an attractive trend as specific targeting molecules but sustain poor cellular uptake meanwhile superparamagnetic iron oxide nanoparticles (SPIONs) offer stability of ASO and improved cellular uptake. In the present work we aimed to functionalize SPIONs with ASO targeting the mRNA of Cyclin B1 which represents a potential cancer target and to explore its anticancer activity. For that purpose, four different SPIONs-ASO conjugates, S-M (1–4), were designated depending on the sequence of ASO and constructed by crosslinking carboxylated SPIONs to amino labeled ASO. The impact of S-M (1–4) on the level of Cyclin B1, cell cycle, ROS and viability of the cells were assessed by flowcytometry. The results showed that S-M3 and S-M4 reduced the level of Cyclin B1 by 35 and 36%, respectively. As a consequence to downregulation of Cyclin B1, MCF7 cells were shown to be arrested at G2/M phase (60.7%). S-M (1–4) led to the induction of ROS formation in comparison to the untreated control cells. Furthermore, S-M (1–4) resulted in an increase in dead cells compared to the untreated cells and SPIONs-treated cells. In conclusion, targeting Cyclin B1 with ASO-coated SPIONs may represent a specific biocompatible anticancer strategy.

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