CK2β Is Expressed in Endometrial Carcinoma and Has a Role in Apoptosis Resistance and Cell Proliferation

Pallarés, Judit; Llobet, David; Santacana, Maria; Eritja, Núria; Velasco, Ana; Cuevas, Dolors; López, Susana; Palomar-Asenjo, Víctor; Yeramian, Andrée; Dolcet, Xavier; Matías‐Guiu, Xavier

doi:10.2353/ajpath.2009.080552

Cited by 36 publications

(23 citation statements)

References 36 publications

(34 reference statements)

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“…ECL kit (GE Healthcare, Pittsburgh, PA) was used to detect the protein band, and the band intensities were quantified by the Image J software. The specificity of the CK2 antibodies has been reported previously (Kang et al, 2009; Pallares et al, 2009). The amounts of total and membrane CK2 subunits were quantified by normalizing the optical density of their protein band to that of β-actin and GAPDH, respectively.…”

Section: Methodssupporting

confidence: 58%

Protein Kinase CK2 Increases Glutamatergic Input in the Hypothalamus and Sympathetic Vasomotor Tone in Hypertension

Ye¹,

Li²,

Li³

et al. 2011

J. Neurosci.

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Increased glutamatergic input in the paraventricular nucleus (PVN) is important for high sympathetic outflow in hypertension, but the associated molecular mechanisms remain unclear. Here we determined the role of protein kinase CK2 in increased N-methyl-D-aspartate receptor (NMDAR) activity in spinally projecting PVN neurons and sympathetic vasomotor tone in spontaneously hypertensive rats (SHR). The selective CK2 inhibitors 5,6-dichloro-1-β-D-ribofuranosylbenzimidazole (DRB) or 4,5,6,7-tetrabromobenzotriazole (TBB) significantly decreased the frequency of miniature excitatory postsynaptic currents (EPSCs) of labeled PVN neurons in SHR but not in Wistar-Kyoto (WKY) normotensive rats. Also, DRB abolished the inhibitory effect of the NMDAR antagonist AP5 on the frequency of mEPSCs in SHR. Treatment with DRB or TBB significantly reduced the amplitude of evoked NMDA-EPSCs but not AMPA-EPSCs in SHR. Furthermore, DRB significantly decreased the firing activity of PVN neurons in SHR but not in WKY rats. The membrane protein level of CK2α in the PVN, but not brainstem and prefrontal cortex, was significantly higher in SHR than in WKY rats. Lowering blood pressure with celiac ganglionectomy in SHR did not alter the increased CK2α level and the effects of DRB on mEPSCs and NMDA-EPSCs. In addition, intracerebroventricular injection of DRB not only significantly reduced blood pressure and lumbar sympathetic nerve discharges but also eliminated the inhibitory effect of AP5 microinjected into the PVN on sympathetic nerve activity in SHR. Our findings suggest that augmented CK2 activity critically contributes to increased pre- and postsynaptic NMDAR activity in the PVN and elevated sympathetic vasomotor tone in essential hypertension.

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Section: Methodssupporting

confidence: 58%

Protein Kinase CK2 Increases Glutamatergic Input in the Hypothalamus and Sympathetic Vasomotor Tone in Hypertension

Ye¹,

Li²,

Li³

et al. 2011

J. Neurosci.

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“…Ongoing and completed phase I and phase II clinical trials with TRAIL are showing clinically promising outcomes with no apparent toxicity (5,6). However, recent studies have indicated that a variety of cancer cells are resistant to the apoptotic effects of TRAIL (7)(8)(9), and it is notable that the majority of breast cancer cells are resistant to TRAIL-mediated apoptosis (10). The mechanisms underlying resistance to TRAIL are not fully understood, and the identification of TRAIL resistance factors could facilitate the development of more effective TRAILbased cancer therapies.…”

mentioning

confidence: 99%

The Oncogene Metadherin Modulates the Apoptotic Pathway Based on the Tumor Necrosis Factor Superfamily Member TRAIL (Tumor Necrosis Factor-related Apoptosis-inducing Ligand) in Breast Cancer

Zhang

Wang

Huo

et al. 2013

Journal of Biological Chemistry

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Background: MTDH is overexpressed in breast cancers and promotes resistance to multiple chemotherapeutic agents. We hypothesized that MTDH may contribute to TRAIL resistance in breast cancer. Results: MTDH modulated TRAIL resistance in breast cancer cells through caspase-8 down-regulation and Bcl-2 up-regulation. Conclusion:The findings uncovered novel mechanisms of TRAIL resistance mediated by MTDH. Significance: MTDH can be considered as a novel target for overcoming TRAIL resistance in breast cancer.

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“…Moreover, an important protein responsible for apoptosis resistance in endometrial carcinoma is FLICE-like inhibitory protein (FLIP), which shares a high degree of homology with caspase-8 but lacks protease activity and [4]. FLIP is frequently expressed in endometrial carcinomas and is regulated by CK2 [13,26]. However, it is evident that FLIP overexpression does not explain, alone, by itself, resistance of TRAIL-induced apoptosis in endometrial carcinoma.…”

Section: Discussionmentioning

confidence: 99%

DcR1 expression in endometrial carcinomas

et al. 2009

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The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family, which mediates apoptosis by the extrinsic pathway. Up-regulation of decoy receptors, DcR1 and DcR2, may result in diminished binding of TRAIL to their functional receptors. DcR1 expression was assessed in normal endometrial tissue (NE) and endometrial carcinoma (EC) samples by immunohistochemistry (IHC) and quantitative real-time polymerase chain reaction (PCR). IHC was performed in two tissue microarrays; one composed of 80 samples of NE and a second one constructed from paraffin-embedded blocks of 62 EC. For quantitative real-time RT-PCR analysis, RNA was obtained from 19 NE and 28 EC samples using Trizol. mRNA expression of DcR1 was assessed with Taqman-based assays in an Abi-Prism 700 SDS. Results were correlated with stage, histological type, and grade. By IHC, cytoplasmic expression of DcR1 was frequently seen in NE (79.6%) and varied according to the menstrual cycle. Positive DcR1 immunostaining was also detected in EC (98.1% of the cases) without any specific statistical association with histological type, grade, and stage. By quantitative real-time PCR, all NE had similar levels of DcR1expression (0.8-1.7 RQ), which were considered the basal levels of DcR1 expression in NE. Increased DcR1 expression (> or =5-fold higher than the basal levels) was detected in 13 of 28 EC (46.4%). High DcR1 expression levels were found in ECs of different stages: IA, four of 12 (33%); IB, two of four (50%); IC, four of six (66%); and IIA and IIB three of six (50%). Results suggest that DcR1 expression occurs in a subset of EC and may contribute to resistance to TRAIL-induced apoptosis.

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CK2β Is Expressed in Endometrial Carcinoma and Has a Role in Apoptosis Resistance and Cell Proliferation

Cited by 36 publications

References 36 publications

Protein Kinase CK2 Increases Glutamatergic Input in the Hypothalamus and Sympathetic Vasomotor Tone in Hypertension

Protein Kinase CK2 Increases Glutamatergic Input in the Hypothalamus and Sympathetic Vasomotor Tone in Hypertension

The Oncogene Metadherin Modulates the Apoptotic Pathway Based on the Tumor Necrosis Factor Superfamily Member TRAIL (Tumor Necrosis Factor-related Apoptosis-inducing Ligand) in Breast Cancer

DcR1 expression in endometrial carcinomas

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