Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.108 (TAT)
 2,389 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glioblastoma with high mortality has been one of the most serious cancers threatening human health. Because of the present treatment limitations, there is an urgent need to construct a multifunctional vesicle for enhancing the treatment of in situ malignant glioblastoma. In our study, drug and gene co-loaded magnetic PLGA/multifunctional polymeric liposome (magnetic PLGA/MPLs) core-shell nanospheres were constructed. They were mainly self-assembled from two parts: hydrophobic PLGA cores that can load drugs and magnetic nanocrystals; and polymeric lipid shells anchored with functional molecules such as PEG chains, TAT peptides and RGD peptides that can help the vectors to condense the gene, prolong the circulation time, cross the blood brain barrier and target delivery to the cancer tissue. The results showed that the magnetic PLGA/MPLs nanosphere has a nanosized core-shell structure, can achieve sustained drug release and has good DNA binding abilities. Importantly, compared with the control group and other groups with single functionality, it can co-deliver the drug and gene into the same cell in vitro and show the strongest inhibiting effect on the growth of the in situ malignant glioblastoma in vivo. All of these results indicated that the different functional components of magnetic PLGA/MPLs, can form an organic whole and none of them can be dispensed with. The magnetic PLGA/MPLs nanosphere may be another option for treatment of glioblastoma.
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PMID:Smart multifunctional core-shell nanospheres with drug and gene co-loaded for enhancing the therapeutic effect in a rat intracranial tumor model. 2296 Oct 67

Glioblastoma is the most lethal brain cancer in adults. Despite advances in surgical techniques, radiotherapy, and chemotherapy, their therapeutic effect is far from significant, since the detailed underlying pathological mechanism of this cancer is unclear. The establishment of molecular interaction networks has laid the foundation for the exploration of these mechanisms with a view to improving therapy for glioblastoma. In the present study, to further explore the cellular role of DCF1 (dendritic cell-derived factor 1), the proteins bound to TAT-DCF1 (transactivator of transcription-dendritic cell-derived factor 1) were identified, and biosystem analysis was employed. Functional enrichment analyses indicate that TAT-DCF1 induced important biological changes in U251 cells. Furthermore, the established molecular interaction networks indicated that TAT-DCF1 directly interacted with TAF6 in glioma cells and with UBC in HEK293T (human embryonic kidney 293T) cells. In addition, further biological experiments demonstrate that TAT-DCF1 induced the activation of the RPS27A/TOP2A/HMGB2/BCL-2 signaling pathway via interaction with TAF6 in U251 cells. Taken together, these findings suggest that the TAT-DCF1 peptide possesses great potential for the development of glioblastoma therapy through the interaction with TAF6-related pathways and provides further theoretic evidence for the mechanisms underlying the antitumor effects of TAT-DCF1.
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PMID:Proteomics and molecular network analyses reveal that the interaction between the TAT-DCF1 peptide and TAF6 induces an antitumor effect in glioma cells. 3189 68