Thrombospondin-1 mediates oncogenic Ras–induced senescence in premalignant lung tumors

Baek, Kwan-Hyuck; Bhang, Dong-Ha; Zaslavsky, Alexander; Wang, Liang-Chuan; Vachani, Anil; Kim, Carla F.; Albelda, Steven Μ.; Evan, Gérard I.; Ryeom, Sandra

doi:10.1172/jci67465

Cited by 51 publications

(56 citation statements)

References 68 publications

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“…Little attention has been given to the effect of TSP-1 on tumor malignancy and immune response in a cell-extrinsic or -intrinsic manner. In fact, an increasing number of papers have reported the role of TSP-1 in these aspects (20,47). As we have shown in the present study, TSP-1 treatment helped tumor cells restore the capacity of CD47 to inhibit the expression of stemness factors.…”

Section: Discussionsupporting

confidence: 73%

Photodynamic Therapy-mediated Cancer Vaccination Enhances Stem-like Phenotype and Immune Escape, Which Can Be Blocked by Thrombospondin-1 Signaling through CD47 Receptor Protein

Zheng¹,

Zou²,

Wang³

et al. 2015

Journal of Biological Chemistry

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Background: Photodynamic therapy (PDT)-mediated vaccination has shown poor clinical outcomes in tumor treatment. Results: Tumor cells that escaped from PDT-mediated vaccination exhibited enhanced stem-like phenotypes and undermined immunogenicity, which were prevented by interfering TSP-1/CD47/SIRP-␣ signal axis. Conclusion: TSP-1/CD47/SIRP-␣ signal axis is associated with the malignant evolution of tumor cells upon tumor vaccination. Significance: This study provides new evidence for improving the clinical outcome of immunotherapy.

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Section: Discussionsupporting

confidence: 73%

Photodynamic Therapy-mediated Cancer Vaccination Enhances Stem-like Phenotype and Immune Escape, Which Can Be Blocked by Thrombospondin-1 Signaling through CD47 Receptor Protein

Zheng¹,

Zou²,

Wang³

et al. 2015

Journal of Biological Chemistry

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“…4A). These are genuine target genes for p53 in response to stress signaling (4, 5, 66, 67). Wild type and p53 -null mice (6-week-old) were injected via tail vein with 0.6 mg DOX/30 g of a mouse, thymi were harvested at 0 and 4 hrs, and binding of Dmp1 to p53 target gene promoters ( p21, Bbc3 ) or intron ( Thbs1 ) was studied by chromatin immunoprecipitation.…”

Section: Resultsmentioning

confidence: 99%

Stabilization of the p53-DNA Complex by the Nuclear Protein Dmp1α

Kendig

Kai

Fry

et al. 2017

Cancer Investigation

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We recently reported the existence of a physical interaction between the Myb-like transcription factor Dmp1 (Dmtf1) and p53 in which Dmp1 antagonized polyubiquitination of p53 by Mdm2 and promoted its nuclear localization. Dmp1 significantly stabilized p53-DNA complexes on promoters that contained p53-consensus sequences, which were either supershifted or disrupted with antibodies to Dmp1. Lysates from mice injected with doxorubicin showed that Dmp1 bound to p21Cip1, Bbc3, and Thbs1 gene regulatory regions in a p53-dependent fashion. Our data suggest that acceleration of DNA-binding of p53 by Dmp1 is a critical process for Dmp1 to increase the p53 function in Arf-deficient cells.

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“…Using lung- or pancreas-specific systems, researchers were able to visualize senescence in premalignant tumors using SA-β-Gal staining and BrdU incorporation, as well as with antibodies toward OIS effectors (including p16 INK4a and p15 INK4b ) (128, 129). …”

Section: Detection Of Senescence In Vivomentioning

confidence: 99%

The Immortal Senescence

Bianchi‐Smiraglia

Lipchick

Nikiforov

2016

Methods in Molecular Biology

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Activation of oncogenic signaling paradoxically results in the permanent withdrawal from cell cycle and induction of senescence (oncogene-induced senescence (OIS)). OIS is a fail-safe mechanism used by the cells to prevent uncontrolled tumor-growth and, as such, it is considered as the first barrier against cancer. In order to progress, tumor cells thus need to first overcome the senescent phenotype. Despite the increasing attention gained by OIS in the past 20 years, this field is still rather young due to continuous emergence of novel pathways and processes involved in OIS. Among the many factors contributing to incomplete understanding of OIS are the lack of unequivocal markers for senescence and the complexity of the phenotypes revealed by senescent cells in in vivo and in vitro. OIS has been shown to play major roles at both the cellular and organismal levels in biological processes ranging from embryonic development to barrier to cancer progression. Here we will briefly outline major advances in methodologies that are being utilized for induction, identification and characterization of molecular processes in cells undergoing oncogene-induced senescence. The full description of such methodologies is provided in the corresponding chapters of the Book.

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Thrombospondin-1 mediates oncogenic Ras–induced senescence in premalignant lung tumors

Cited by 51 publications

References 68 publications

Photodynamic Therapy-mediated Cancer Vaccination Enhances Stem-like Phenotype and Immune Escape, Which Can Be Blocked by Thrombospondin-1 Signaling through CD47 Receptor Protein

Photodynamic Therapy-mediated Cancer Vaccination Enhances Stem-like Phenotype and Immune Escape, Which Can Be Blocked by Thrombospondin-1 Signaling through CD47 Receptor Protein

Stabilization of the p53-DNA Complex by the Nuclear Protein Dmp1α

The Immortal Senescence

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