Phosphorylation of Ribosomal Protein S3 and Antiapoptotic TRAF2 Protein Mediates Radioresistance in Non-small Cell Lung Cancer Cells

Yang, Hee Jung; Youn, HyeSook; Seong, Ki Moon; Jin, Young Woo; Kim, Joon; Youn, BuHyun

doi:10.1074/jbc.m112.385989

Cited by 58 publications

(65 citation statements)

References 39 publications

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“…Signaling through TRAF2, but not TRAF1 or TRAF3, is known to promote NF-B activity, and TRAF2 is also responsible for promoting JNK/SAPK activity, inflammation, cell migration, and chemo-and radioresistance of cancer cells (41)(42)(43)(44)(45)(46)(47). Moreover, specific depletion of TRAF2 in GB has been shown to inhibit growth and confer radiosensitization to tumor cells (48).…”

Section: Discussionmentioning

confidence: 99%

The Src Homology 3 Domain-containing Guanine Nucleotide Exchange Factor Is Overexpressed in High-grade Gliomas and Promotes Tumor Necrosis Factor-like Weak Inducer of Apoptosis-Fibroblast Growth Factor-inducible 14-induced Cell Migration and Invasion via Tumor Necrosis Factor Receptor-associated Factor 2

Ensign

Mathews

Eschbacher

et al. 2013

Journal of Biological Chemistry

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Background: Glioblastoma is characterized by heightened cell invasion and therapeutic resistance. Results: The Src homology 3 domain-containing GEF (SGEF) promotes fibroblast growth factor-inducible 14 (Fn14) proinvasive signaling in glioblastoma via TNF receptor-associated factor 2 (TRAF2). Conclusion: SGEF is an important regulator of glioblastoma cell invasion downstream of Fn14. Significance: Therapy directed at mediators of invasion may confer increased chemotherapeutic and radiologic susceptibility in glioblastoma.

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Section: Discussionmentioning

confidence: 99%

The Src Homology 3 Domain-containing Guanine Nucleotide Exchange Factor Is Overexpressed in High-grade Gliomas and Promotes Tumor Necrosis Factor-like Weak Inducer of Apoptosis-Fibroblast Growth Factor-inducible 14-induced Cell Migration and Invasion via Tumor Necrosis Factor Receptor-associated Factor 2

Ensign

Mathews

Eschbacher

et al. 2013

Journal of Biological Chemistry

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“…Following the experimental treatment, Western blot analysis, immunoprecipitation (IP), and in vivo kinase assay studies were performed as previously described (4,6,23). Detailed procedures are described in Supplementary Materials and Methods.…”

Section: Northern Blot Analysismentioning

confidence: 99%

“…Nevertheless, therapeutic outcomes are not fully satisfactory due to the emergence of radioresistance that is considered to be a critical obstacle that leads to the failure of radiotherapy and consequently increases mortality in patients with NSCLC (2). So far, a large number of studies have been conducted to find a way to control radioresistance and develop potent adjuvants for radiotherapy that enhance treatment efficacy (3,4). A profound understanding of the molecular events associated with therapeutic resistance would greatly advance the discovery of drugs enabling to modulate radiation-induced signaling responses to improve the prognosis of patients with NSCLC (5-7).…”

Section: Introductionmentioning

confidence: 99%

PAK1 Tyrosine Phosphorylation Is Required to Induce Epithelial–Mesenchymal Transition and Radioresistance in Lung Cancer Cells

et al. 2014

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The p21-activated Ser/Thr kinase 1 (PAK1) kinase has an essential role in tumorigenesis and cell survival in many cancers, but its regulation is not fully understood. In this study, we showed that in response to irradiation of lung cancer cells, PAK1 was upregulated, tyrosine phosphorylated, and translocated to the nucleus. Tyrosine phosphorylation relied upon JAK2 kinase activity and was essential for PAK1 protein stability and binding to Snail. This radiation-induced JAK2-PAK1-Snail signaling pathway increased epithelial-mesenchymal transition (EMT) by regulating epithelial and mesenchymal cell markers. Notably, JAK2 inhibitors mediated radiosensitization and EMT blockade in a mouse xenograft model of lung cancer. Taken together, our findings offered evidence that JAK2 phosphorylates and stabilizes functions of PAK1 that promote EMT and radioresistance in lung cancer cells, with additional implications for the use of JAK2 inhibitors as radiosensitizers in lung cancer treatment.

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“…As the functional organelle for protein synthesis, ribosomes bound to the endoplasmic reticulum (ER) perform complex surveillance of various pathologic stresses [33] [34]. Ribosomal alteration by endogenous and external insults can be a trigger of a variety of pathogenic processes, including inflammatory responses [35] [36] [37].…”

Section: Discussionmentioning

confidence: 99%

Trivalent Chromium Promotes Healing of Experimental Colitis in Mice by Suppression of Inflammation and Oxidative Stress

Odukanmi¹,

Salami²,

Koda³

et al. 2017

JBM

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Ulcerative colitis (UC) has reactive oxygen species (ROS) and immunologic pathways implicated in its pathogenesis. The search for new therapeutic protocols in managing UC is tailored in suppressing or preventing these pathways. The influence of trivalent chromium (Cr 3+ ), an essential mineral on experimental colitis was investigated. Mice were grouped into 3; group 1 (control) received clean drinking water while groups 2 and 3 received 10 and 100 ppm Cr 3+ respectively for 12 weeks through drinking water. After Cr 3+ administration, 5 animals per group were sacrificed on day 0. Thereafter, experimental colitis was induced intra-rectally using acetic acid (4%, 0.3mL) and 5 mice per group were subsequently sacrificed on days 3, 7 and 14. Blood and colonic tissues were obtained and processed appropriately. Blood Cr 3+ level, haematological variables, gross and microscopic colitis scores, colonic myeloperoxidase (MPO), Superoxide Dismutase (SOD) and malondialdehyde (MDA) levels were determined using standard methods. Colon cytokine mRNA genes were quantified using real-time PCR. There was a significant decrease in colon gross and histology scores on days 3 and 7 in chromium treated compared with control. The MPO and MDA in chromium groups reduced significantly compared with control while SOD activities increased significantly in Cr 3+ groups compared with control. Total RNA increased in chromium groups compared with control on day 3 post-colitis. There was up-regulation of IL-10, down-regulation of TNF-α and IFN-λ in chromium administered groups compared with control. Chromium enhanced healing of colitis by suppression of ROS, inflammation and promotion of antioxidant activities.

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Phosphorylation of Ribosomal Protein S3 and Antiapoptotic TRAF2 Protein Mediates Radioresistance in Non-small Cell Lung Cancer Cells

Cited by 58 publications

References 39 publications

PAK1 Tyrosine Phosphorylation Is Required to Induce Epithelial–Mesenchymal Transition and Radioresistance in Lung Cancer Cells

Trivalent Chromium Promotes Healing of Experimental Colitis in Mice by Suppression of Inflammation and Oxidative Stress

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