Splicing Out the West?

Guo, Jerry; Xin, Hao

doi:10.1126/science.314.5803.1232

Cited by 51 publications

(26 citation statements)

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“…Strategies have focused on inactivation of mutant p53 or reactivation of wild-type function in the mutant p53 protein. Gene therapy using administration of wt-p53 had been proved in clinical trial in China [32]. Other biologic approaches Although some studies in cell culture and in animal models demonstrated their effectiveness in the application to p53-defective cancers, their efficacy and safety in clinical trials are currently debated.…”

Section: Discussionmentioning

confidence: 99%

CP-31398 inhibits the growth of p53-mutated liver cancer cells in vitro and in vivo

Zhang

Yan

et al. 2015

Tumor Biol.

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The tumor suppressor p53 is one of the most frequently mutated genes in hepatocellular carcinoma (HCC). Previous studies demonstrated that CP-31398 restored the native conformation of mutant p53 and trans-activated p53 downstream genes in tumor cells. However, the research on the application of CP-31398 to liver cancer has not been reported. Here, we investigated the effects of CP-31398 on the phenotype of HCC cells carrying p53 mutation. The effects of CP-31398 on the characteristic of p53-mutated HCC cells were evaluated through analyzing cell cycle, cell apoptosis, cell proliferation, and the expression of p53 downstream genes. In tumor xenografts developed by PLC/PRF/5 cells, the inhibition of tumor growth by CP-31398 was analyzed through gross morphology, growth curve, and the expression of p53-related genes. Firstly, we demonstrated that CP-31398 inhibited the growth of p53-mutated liver cancer cells in a dose-dependent and p53-dependent manner. Then, further study showed that CP-31398 re-activated wild-type p53 function in p53-mutated HCC cells, which resulted in inhibitive response of cell proliferation and an induction of cell-cycle arrest and apoptosis. Finally, in vivo data confirmed that CP-31398 blocked the growth of xenografts tumors through transactivation of p53-responsive downstream molecules. Our results demonstrated that CP-31398 induced desired phenotypic change of p53-mutated HCC cells in vitro and in vivo, which revealed that CP-31398 would be developed as a therapeutic candidate for HCC carrying p53 mutation.

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Section: Discussionmentioning

confidence: 99%

CP-31398 inhibits the growth of p53-mutated liver cancer cells in vitro and in vivo

Zhang

Yan

et al. 2015

Tumor Biol.

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“…Among other biological activities of therapeutic value, the human chaperone Hsp70 (monomer, 70 kDa) has shown an important anti-tumoral value, [ 30 ] being one of the fi rst agents approved in China for the viral gene therapy of cancer. [ 31 ] In addition, Hsp70 is a potent inhibitor of cell apoptosis, [ 32 ] making the testing of their biological activity feasible under cell culture conditions. The antiapoptotic activity of Hsp70 is relevant both in the cytoplasm and in mitocondria.…”

Section: Doi: 101002/adma201104330mentioning

confidence: 99%

Functional Inclusion Bodies Produced in Bacteria as Naturally Occurring Nanopills for Advanced Cell Therapies

et al. 2012

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Inclusion bodies (50-500 nm in diameter) produced in recombinant bacteria can be engineered to contain functional proteins with therapeutic potential. Upon exposure, these protein particles are efficiently internalized by mammalian cells and promote recovery from diverse stresses. Being fully biocompatible, inclusion bodies are a novel platform, as tailored nanopills, for sustained drug release in advanced cell therapies.

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“…In head and neck cancer, p53 mutations are frequent, and the incidence of p53 mutations increases with progression of head and neck cancer (46,47). Therefore, a recombinant human adenovirus that expresses functional wild-type p53 has been approved by the Chinese government for the treatment of head and neck carcinoma (48)(49)(50). Treatments showed that antitumor efficacy was associated with the expression and activity of functional p53, and adverse effects were also significant (51)(52)(53)(54).…”

Section: Current Strategies To Target the P53 Pathway In Tumor Metabomentioning

confidence: 99%

The Fundamental Role of the p53 Pathway in Tumor Metabolism and Its Implication in Tumor Therapy

Shen

Sun

et al. 2012

Clinical Cancer Research

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It is well established that the altered metabolism exhibited by cancer cells, including high rates of glycolysis, lactate production, and biosynthesis of lipids, nucleotides, and other macromolecules, and which may occur either as a consequence or as a cause of tumorigenesis, plays an essential role in cancer progression. Recently, the tumor suppressor p53 was found to play a central role in this process. Here, we review the role of p53 in modulating tumor metabolism. Specifically, we focus on the functions of p53 in regulating aerobic glycolysis, oxidative phosphorylation, the pentose phosphate pathway, fatty acid synthesis and oxidation, and glutamine metabolism, and we discuss the therapeutic strategy whereby p53 helps to prevent malignant progression.

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Splicing Out the West?

Cited by 51 publications

References 0 publications

CP-31398 inhibits the growth of p53-mutated liver cancer cells in vitro and in vivo

CP-31398 inhibits the growth of p53-mutated liver cancer cells in vitro and in vivo

Functional Inclusion Bodies Produced in Bacteria as Naturally Occurring Nanopills for Advanced Cell Therapies

The Fundamental Role of the p53 Pathway in Tumor Metabolism and Its Implication in Tumor Therapy

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