Gadolinium uptake by brain cancer cells: Quantitative analysis with X-PEEM spectromicroscopy for cancer therapy

Author(s):  
Gelsomina De Stasio
2019 ◽  
Vol 7 (5) ◽  
pp. 2102-2122 ◽  
Author(s):  
Sandhra M. Carvalho ◽  
Alice G. Leonel ◽  
Alexandra A. P. Mansur ◽  
Isadora C. Carvalho ◽  
Klaus Krambrock ◽  
...  

Magnetopolymersomes for potential multimodal brain cancer therapy – “nanoheaters meet drug nanocarriers”.


Author(s):  
Menghan Gao ◽  
Hong Deng ◽  
Weiqi Zhang

: Hyaluronan (HA) is a natural linear polysaccharide that has excellent hydrophilicity, biocompatibility, biodegradability, and low immunogenicity, making it one of the most attractive biopolymers used for biomedical researches and applications. Due to the multiple functional sites on HA and its intrinsic affinity for CD44, a receptor highly expressed on various cancer cells, HA has been widely engineered to construct different drug-loading nanoparticles (NPs) for CD44- targeted anti-tumor therapy. When a cocktail of drugs is co-loaded in HA NP, a multifunctional nano-carriers could be obtained, which features as a highly effective and self-targeting strategy to combat the cancers with CD44 overexpression. The HA-based multidrug nano-carriers can be a combination of different drugs, various therapeutic modalities, or the integration of therapy and diagnostics (theranostics). Up to now, there are many types of HA-based multidrug nano-carriers constructed by different formulation strategies including drug co-conjugates, micelles, nano-gels and hybrid NP of HA and so on. This multidrug nano-carrier takes the full advantages of HA as NP matrix, drug carriers and targeting ligand, representing a simplified and biocompatible platform to realize the targeted and synergistic combination therapy against the cancers. In this review, recent progresses about HA-based multidrug nano-carriers for combination cancer therapy are summarized and its potential challenges for translational applications have been discussed.


Nanoscale ◽  
2020 ◽  
Vol 12 (18) ◽  
pp. 10189-10195 ◽  
Author(s):  
Xin Zhao ◽  
Dongyang Tang ◽  
Ying Wu ◽  
Shaoqing Chen ◽  
Cheng Wang

The artifical cell system for the gene therapy of cancer might be a promising approach for the reversal of neoplastic progress of cancer cells.


2021 ◽  
Vol 27 ◽  
pp. 101071
Author(s):  
Michael Merrick ◽  
Michael J. Mimlitz ◽  
Catherine Weeder ◽  
Haris Akhter ◽  
Allie Bray ◽  
...  
Keyword(s):  

Author(s):  
Xiao Lei ◽  
Kun Cao ◽  
Yuanyuan Chen ◽  
Hui Shen ◽  
Zhe Liu ◽  
...  

Abstract Background To block repairs of DNA damages, especially the DNA double strand break (DSB) repair, can be used to induce cancer cell death. DSB repair depends on a sequential activation of DNA repair factors that may be potentially targeted for clinical cancer therapy. Up to now, many protein components of DSB repair complex remain unclear or poorly characterized. In this study, we discovered that Transglutaminase 2 (TG2) acted as a new component of DSB repair complex. Methods A bioinformatic analysis was performed to identify DNA damage relative genes from dataset from The Cancer Genome Atlas. Immunofluorescence and confocal microscopy were used to monitor the protein localization and recruitment kinetics. Furthermore, immunoprecipitation and mass spectrometry analysis were performed to determine protein interaction of both full-length and fragments or mutants in distinct domain. In situ lung cancer model was used to study the effects cancer therapy in vivo. Results After DSB induction, cytoplasmic TG2 was extensively mobilized and translocated into nucleus after phosphorylated at T162 site by DNA-PKcs. Nuclear TG2 quickly accumulated at DSB sites and directly interacting with Topoisomerase IIα (TOPOIIα) with its TGase domain to promote DSB repair. TG2 deficient cells lost capacity of DSB repair and become susceptible to ionizing radiation. Specific inhibition of TG2-TOPOIIα interaction by glucosamine also significantly inhibited DSB repair, which increased sensitivity in lung cancer cells and engrafted lung cancers. Conclusions These findings elucidate new mechanism of TG2 in DSB repair trough directly interacting with TOPOIIα, inhibition of which provided potential target for overcoming cancer resistance.


2021 ◽  
Author(s):  
Wooram Park ◽  
Seok-Jo Kim ◽  
Paul Cheresh ◽  
Jeanho Yun ◽  
Byeongdu Lee ◽  
...  

Mitochondria are crucial regulators of the intrinsic pathway of cancer cell death. The high sensitivity of cancer cells to mitochondrial dysfunction offers opportunities for emerging targets in cancer therapy. Herein,...


2021 ◽  
Vol 259 ◽  
pp. 117741
Author(s):  
Xiaoxiao Guo ◽  
Sara M. Elkashef ◽  
Anjana Patel ◽  
Goreti Ribeiro Morais ◽  
Steven D. Shnyder ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1201
Author(s):  
Garri Manasaryan ◽  
Dmitry Suplatov ◽  
Sergey Pushkarev ◽  
Viktor Drobot ◽  
Alexander Kuimov ◽  
...  

The PARP family consists of 17 members with diverse functions, including those related to cancer cells’ viability. Several PARP inhibitors are of great interest as innovative anticancer drugs, but they have low selectivity towards distinct PARP family members and exert serious adverse effects. We describe a family-wide study of the nicotinamide (NA) binding site, an important functional region in the PARP structure, using comparative bioinformatic analysis and molecular modeling. Mutations in the NA site and D-loop mobility around the NA site were identified as factors that can guide the design of selective PARP inhibitors. Our findings are of particular importance for the development of novel tankyrase (PARPs 5a and 5b) inhibitors for cancer therapy.


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