PDCD5 promotes cisplatin-induced apoptosis of glioma cells via activating mitochondrial apoptotic pathway

Li, Haiyan S.; Zhang, Xia; Song, Xingguo; Zhu, Faliang; Wang, Qun; Guo, Chun; Liu, Chunmei; Shi, Yongyu; Ma, Chao; Wang, Xiaoyan; Zhang, Lining

doi:10.4161/cbt.20565

Cited by 22 publications

(12 citation statements)

References 26 publications

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“…The diffuse cell death combined with accumulation of large quantities of programmed cell death protein 5 (PDCD5) (more than 1,000-fold) and some apoptosis-associated cytoskeletal proteins indicated that apoptotic cell death may have occurred in the explants. PDCD5 (TFAR19) is a proapoptotic factor (60), and its expression is increased during apoptosis (61)(62)(63). It functions in apoptosis either through direct interaction with p53 (63) or via indirect acetylation of p53 (64).…”

Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus Induces Hypoxia and Cellular Damage in Porcine Dermal Explants

et al. 2015

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fWe developed a porcine dermal explant model to determine the extent to which Staphylococcus aureus biofilm communities deplete oxygen, change pH, and produce damage in underlying tissue. Microelectrode measurements demonstrated that dissolved oxygen (DO) in biofilm-free dermal tissue was 4.45 ؎ 1.17 mg/liter, while DO levels for biofilm-infected tissue declined sharply from the surface, with no measurable oxygen detectable in the underlying dermal tissue. Magnetic resonance imaging demonstrated that biofilm-free dermal tissue had a significantly lower relative effective diffusion coefficient (0.26 ؎ 0.09 to 0.30 ؎ 0.12) than biofilm-infected dermal tissue (0.40 ؎ 0.12 to 0.48 ؎ 0.12; P < 0.0001). Thus, the difference in DO level was attributable to biofilm-induced oxygen demand rather than changes in oxygen diffusivity. Microelectrode measures showed that pH within biofilm-infected explants was more alkaline than in biofilm-free explants (8.0 ؎ 0.17 versus 7.5 ؎ 0.15, respectively; P < 0.002). Cellular and nuclear details were lost in the infected explants, consistent with cell death. Quantitative label-free shotgun proteomics demonstrated that both proapoptotic programmed cell death protein 5 and antiapoptotic macrophage migration inhibitory factor accumulated in the infected-explant spent medium, compared with uninfected-explant spent media (1,351-fold and 58-fold, respectively), consistent with the cooccurrence of apoptosis and necrosis in the explants. Biofilm-origin proteins reflected an extracellular matrix-adapted lifestyle of S. aureus. S. aureus biofilms deplete oxygen, increase pH, and induce cell death, all factors that contribute to impede wound healing.

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Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus Induces Hypoxia and Cellular Damage in Porcine Dermal Explants

et al. 2015

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“…Overexpression of BCL-2 rendered chondrosarcoma cells resistant to cisplatin treatments, while BCL-2 inhibition can reverse chemoresistance of chondrosarcoma in vitro. Moreover, recombinant human PDCD5 (rhPDCD5) was also shown to sensitize chondrosarcoma cells to cisplatinbased chemotherapy, with inhibition of cell growth and apoptosis (Li et al, 2012).…”

Section: Microrna-100 Resensitizes Resistant Chondrosarcoma Cells To mentioning

confidence: 99%

MicroRNA-100 Resensitizes Resistant Chondrosarcoma Cells to Cisplatin through Direct Targeting of mTOR

Zhu

Wang²,

Zhang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Chondrosarcomas are malignant cartilage-forming tumors of bone which exhibit resistance to both chemotherapy and radiation treatment. miRNAs have been well demonstrated to regulate gene expression and play essential roles in a variety of biological processes, including proliferation, differentiation, migration, cell cycling and apoptosis. In this study, we obtained evidence that miR-100 acts as a tumor suppressor in human chondrosarcomas. Interestingly, cisplatin resistant chondrosarcoma cells exhibit decreased expression of miR-100 compared with parental cells. In addition, we identified mTOR as a direct target of miR-100. Overexpression of miR-100 complementary pairs to the 3' untranslated region (UTR) of mTOR, resulted in sensitization of cisplatin resistant cells to cisplatin. Moreover, recovery of the mTOR pathway by overexpression of S6K desensitized the chondrosarcoma cells to cisplatin, suggesting the miR-100-mediated sensitization to cisplatin dependent on inhibition of mTOR. In summary, the present studies highlight miR-100 as a tumor suppressor in chondrosarcoma contributing to anti-chemoresistance. Overexpression of miR-100 might be exploited as a therapeutic strategy along with cisplatin-based combined chemotherapy for the treatment of clinical chondrosarcoma patients.

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“…In their recent study, novel evidence demonstrated that PDCD5 is a p53 regulator during gene expression and cell cycle (15). Li et al (16) found that PDCD5 promotes cisplatininduced apoptosis of glioma cells via activating mitochondrial apoptotic pathway. Han et al (17) confirmed that PDCD5 shows a greater inhibitory effect on the Ras/Raf/MEK/ERK signaling pathway in the human osteosarcoma cell line MG-63.…”

Section: Introductionmentioning

confidence: 99%

PDCD5 expression predicts a favorable outcome in patients with hepatocellular carcinoma

Cheng

et al. 2013

International Journal of Oncology

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Liver cancer in men is the fifth most frequently diagnosed cancer worldwide. Programmed cell death 5 (PDCD5) is an apoptosis related gene and plays an important role in the pathogenesis and development of cancer. In this study, we confirmed that the levels of PDCD5 mRNA and protein were lower in hepatocellular carcinoma (HCC) tissue compared to normal tissue. PDCD5 expression was significantly associated with HBV infection, tumor number, lymph node metastasis and the survival time of the patients with HCC. In addition, the serum levels of PDCD5 and AFP in the patients were significantly positively correlated. We also confirmed that upregulation of PDCD5 was able to inhibit cell proliferation and mobility, induce apoptosis and G1 arrest. Interestingly, PDCD5 also inhibited proteasome activity similarly to the proteosome inhibitor MG132. PDCD5 could be considered as a reliable marker of favorable prognosis of HCC patients.

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PDCD5 promotes cisplatin-induced apoptosis of glioma cells via activating mitochondrial apoptotic pathway

Cited by 22 publications

References 26 publications

Staphylococcus aureus Induces Hypoxia and Cellular Damage in Porcine Dermal Explants

Staphylococcus aureus Induces Hypoxia and Cellular Damage in Porcine Dermal Explants

MicroRNA-100 Resensitizes Resistant Chondrosarcoma Cells to Cisplatin through Direct Targeting of mTOR

PDCD5 expression predicts a favorable outcome in patients with hepatocellular carcinoma

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