scholarly journals Zinc Metallochaperones Reactivate Mutant p53 Using an ON/OFF Switch Mechanism: A New Paradigm in Cancer Therapeutics

2018 ◽  
Vol 24 (18) ◽  
pp. 4505-4517 ◽  
Author(s):  
Xin Yu ◽  
Samuel Kogan ◽  
Ying Chen ◽  
Ashley T. Tsang ◽  
Tracy Withers ◽  
...  
Keyword(s):  
Cancer Therapeutics ◽  
Mutant P53 ◽  
New Paradigm ◽  
Switch Mechanism

scholarly journals Zinc Metallochaperones as Mutant p53 Reactivators: A New Paradigm in Cancer Therapeutics

Cancers ◽  
2018 ◽  
Vol 10 (6) ◽  
pp. 166 ◽  
Author(s):  
Samuel Kogan ◽  
Darren Carpizo
Keyword(s):  
Cancer Therapeutics ◽  
Mutant P53 ◽  
New Paradigm

scholarly journals Aptamers: Novel Therapeutics and Potential Role in Neuro-Oncology

Cancers ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2889
Author(s):  
Paola Amero ◽  
Soumen Khatua ◽  
Cristian Rodriguez-Aguayo ◽  
Gabriel Lopez-Berestein
Keyword(s):  
Brain Tumors ◽  
Targeted Delivery ◽  
Cancer Therapeutics ◽  
Pediatric Brain Tumors ◽  
Surface Proteins ◽  
New Paradigm ◽  
Preclinical Research ◽  
Current State ◽  
Potential Therapeutic Role ◽  
Diagnostic Applications

A relatively new paradigm in cancer therapeutics is the use of cancer cell–specific aptamers, both as therapeutic agents and for targeted delivery of anticancer drugs. After the first therapeutic aptamer was described nearly 25 years ago, and the subsequent first aptamer drug approved, many efforts have been made to translate preclinical research into clinical oncology settings. Studies of aptamer-based technology have unveiled the vast potential of aptamers in therapeutic and diagnostic applications. Among pediatric solid cancers, brain tumors are the leading cause of death. Although a few aptamer-related translational studies have been performed in adult glioblastoma, the use of aptamers in pediatric neuro-oncology remains unexplored. This review will discuss the biology of aptamers, including mechanisms of targeting cell surface proteins, various modifications of aptamer structure to enhance therapeutic efficacy, the current state and challenges of aptamer use in neuro-oncology, and the potential therapeutic role of aptamers in pediatric brain tumors.

Effect of long non-coding RNA EIF3J-AS1 on multi-drug resistance and autophagy in gastric cancer.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e15581-e15581
Author(s):  
Yuhao Luo ◽  
Rui Zhou ◽  
Na Huang ◽  
Li Sun ◽  
Wangjun Liao
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Treatment Options ◽  
Cancer Therapeutics ◽  
Underlying Mechanism ◽  
Multi Drug Resistance ◽  
New Paradigm ◽  
Gastric Cancer Cells ◽  
Non Coding Rna ◽  
Long Non Coding Rna

e15581 Background: Gastric cancer (GC) is a leading cause of cancer mortality worldwide, oxaliplatin and epirubicin based chemotherapy are one of the most important treatment options for GC patients. However, drug resistance, especially multi-drug resistance remains a major obstacle for successful chemotherapy. Recently, long non-coding RNAs (lncRNAs) have been widely identified to play emerging roles in diverse physiological and pathophysiological processes including drug resistance. Our previous bioinformatics analysis showed long non-coding RNA EIF3J-AS1 was a potential multi-drug resistance gene, but the underlying mechanism is still unknown. Methods: We generated oxaliplatin resistance cells (MGC803/OXA) and epirubicin resistance cells(MGC803/EPI) based on parental gastric cancer cells MGC803. Relative expression levels of EIF3J-AS1 were measured by qRT-PCR. Transmission electron microscopy was used to measure autophagosomes. Rapamycin was applied to inducing autophagy while chloroquine and 3-methyladenine were used to block autophagy. Protein level of autophagy related genes were examined by Western Blot. Coexpression genes of EIF3J-AS1 from TCGA RNA-seq datas were analyzed by cBiportal. RNA immunoprecipitation was used to analyze endogenous microRNAs and mRNAs. Results: EIF3J-AS1 was significantly upregulated in MGC803/OXA and MGC803/EPI cells compared with parental cells MGC803. EIF3J-AS1 inhibition increased chemosensitivity to both oxaliplatin and epirubicin. Moreover, EIF3J-AS1 silence lead to the decrease of autophagy. Autophagy related gene ATG14 was identified as a downstream target gene. EIF3J-AS1 promoted ATG14 expression by directly interacting with and increasing stability of ATG14 mRNA, On the other hand, EIF3J-AS1 competitively sponged miR-188-3p and promoted ATG14 expression in a ceRNA-dependent way. Conclusions: LncRNA EIF3J-AS1 is a crucial regulator of multi-drug resistance by inducing autophagy in gastric cancer. Targeting EIF3J-AS1/ATG14 axis might be a new paradigm for cancer therapeutics.

Methods to Screen Compounds Against Mutant p53 Misfolding and Aggregation for Cancer Therapeutics

2018 ◽  
pp. 265-277
Author(s):  
Giulia Diniz da Silva Ferretti ◽  
Danielly C. Ferraz da Costa ◽  
Jerson L. Silva ◽  
Luciana Pereira Rangel
Keyword(s):  
Cancer Therapeutics ◽  
Mutant P53

Abstract 3432: Zinc metallochaperones for mutant p53 reactivation in cancer therapeutics

2020 ◽  
Author(s):  
Xin Yu ◽  
Bing Na ◽  
Saif Zaman ◽  
Tracy Withers ◽  
John Gilleran ◽  
...  
Keyword(s):  
Cancer Therapeutics ◽  
Mutant P53 ◽  
P53 Reactivation

Solar Filaments as Tracers of Subsurface Processes

2000 ◽  
Vol 179 ◽  
pp. 177-183
Author(s):  
D. M. Rust
Keyword(s):  
Magnetic Fields ◽  
Magnetic Flux ◽  
Coronal Mass Ejections ◽  
Interplanetary Space ◽  
Intermediate Stage ◽  
Coronal Plasma ◽  
Magnetic Helicity ◽  
The Sun ◽  
New Paradigm ◽  
Solar Filaments

AbstractSolar filaments are discussed in terms of two contrasting paradigms. The standard paradigm is that filaments are formed by condensation of coronal plasma into magnetic fields that are twisted or dimpled as a consequence of motions of the fields’ sources in the photosphere. According to a new paradigm, filaments form in rising, twisted flux ropes and are a necessary intermediate stage in the transfer to interplanetary space of dynamo-generated magnetic flux. It is argued that the accumulation of magnetic helicity in filaments and their coronal surroundings leads to filament eruptions and coronal mass ejections. These ejections relieve the Sun of the flux generated by the dynamo and make way for the flux of the next cycle.

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