T‐LAK cell‐originated protein kinase is essential for the proliferation of hepatocellular carcinoma SMMC‐7721 cells

Chen, Fang; Li, Ruwei; Wang, Chenji; Cao, Lanqing; Wang, Yingli; Liu, Yu

doi:10.1002/cbf.2964

Cited by 12 publications

(14 citation statements)

References 30 publications

(64 reference statements)

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“…August 2014 cells, [12][13][14] and we found that TOPK was significantly activated by IPostC after 2-hour ischemia/1-hour reperfusion. We, therefore, hypothesized that (1) IPostC probably reverse the increases of oxidative stress within ischemic neural cells; (2) IPostC might activate TOPK that induce neural cells to express antioxidative molecules that would contribute to the neuroprotection of IPostC; and (3) the PTEN/Akt pathway is the downstream target of TOPK, all contributing to the neuroprotection of IPostC in vivo.…”

Section: Strokementioning

confidence: 68%

“…Evidence supports that the PTEN/Akt pathway is an important downstream target of TOPK in promoting the proliferation and migration of tumor cells. [12][13][14] One notion is that overexpression of TOPK decreases the expression of PTEN and increases the activation of Akt in lung cancer cell lines. 12 Another idea is that TOPK phosphorylates PTEN at the S380 residue and inactivates PTEN, which in turn activates Akt that leads to proper G2/M progression.…”

Section: Discussionmentioning

confidence: 99%

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Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats

Zhao

Wang

Tao

et al. 2014

Stroke

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Background and Purpose-Ischemic postconditioning (IPostC) protects against ischemic brain injury. To date, no study has examined the role of T-LAK-cell-originated protein kinase (TOPK) in IPostC-afforded neuroprotection. We explored the molecular mechanism related with TOPK in antioxidant effect of IPostC against ischemia/reperfusion. Methods-Focal ischemia was induced in rats by transient middle cerebral artery occlusion. Reactive oxygen species production in the peri-infarct cortex was detected using dihydroethidium. Malondialdehyde, as a marker of lipid peroxidation, and 3-nitrotyrosine, as a marker of protein oxidation, were detected by ELISA. The expression or location of antioxidant proteins and signal molecules TOPK, phosphatase, and tensin homolog, and Akt was analyzed by Western blotting and immunofluorescence. Results-Our results revealed that IPostC relieved transient middle cerebral artery occlusion-induced oxidative damage by reducing reactive oxygen species, malondialdehyde, and 3-nitrotyrosine accumulation in the peri-infarct cortex and raised levels of antioxidants perioxiredoxin-1, peroxiredoxin-2, and thioredoxin-1. In addition, IPostC increased p-AKT and p-TOPK levels, which colocalized in neural cells. In vitro TOPK knockdown by small interfering RNA decreased the levels of antioxidants peroxiredoxin-1, thioredoxin, and manganese superoxide dismutase activity in PC12 cells. In vivo intracerebroventricular injection of TOPK small interfering RNA reversed IPostC-induced neuroprotection by increasing infarct volume and nitric oxide content and reducing manganese superoxide dismutase activity. Moreover, IPostC-evoked Akt activation was blocked by TOPK small interfering RNA in vivo, but the decreased phosphorylated phosphatase and tensin homolog level in ischemia/reperfusion was not influenced by IPostC or by TOPK small interfering RNA treatment. Conclusions-Our

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Section: Strokementioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats

Zhao

Wang

Tao

et al. 2014

Stroke

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“…Singh et al reported that TOPK mRNA were highly expressed in bladder cancer and that TOPK protein was also detected in about 65% of patients with bladder cancer . Using fresh surgical specimens of hepatocellular carcinoma (HCC), Chen et al also found that HCC cells expressed TOPK mRNA and protein. Joel et al isolated glioma‐initiating cells (GICs) from surgical specimens and found that GICs expressed TOPK mRNA and protein …”

Section: Discussionmentioning

confidence: 99%

Impact of a novel biomarker, T‐LAK cell‐originating protein kinase (TOPK) expression on outcome in malignant glioma

et al. 2017

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This study aimed to evaluate the biological features of T-lymphokine-activated killer cell-originating protein kinase (TOPK) in vitro and to assess clinical impact of TOPK on the outcome in patients with malignant glioma. TOPK protein level and TOPK mRNA and protein levels in six glioma cell lines were examined using Western blot and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Immunohistochemistry was performed to examine their subcellular localization of TOPK. Using surgical specimens from 57 patients with gliomas, TOPK and Ki-67 expressions were examined by immunohistochemistry. Their co-localization was also examined with double immunofluorescence immunohistochemistry. Impacts of TOPK/Ki-67 expression on the overall survival (OS) and progression-free survival (PFS) in 32 patients with glioblastoma multiforme (GBM) were examined, using Kaplan-Meier and Cox proportion hazard models. Immunohistochemistry revealed that approximately 20-30% of glioma cells were positive for TOPK in vitro. TOPK mRNA was identified in all glioma cell lines on RT-PCR. The value of TOPK/GAPDH was 0.27 ± 0.11. TOPK and Ki-67 expressions were significantly higher in GBM patients than in non-GBM patients. A majority of TOPK-positive cells were also positive for Ki-67 and vice versa. Multivariate analysis revealed that a low TOPK expression (≤ 12.7%) was an independent predictor of longer OS (P = 0.0372), and that gross total removal and a low TOPK expression (≤ 12.7%) were independent predictors of longer PFS (P = 0.0470 and P = 0.0189, respectively). The findings strongly suggest biological and clinical importance of TOPK expression in gliomas, indicating a novel therapeutic potential of TOPK inhibitors to treat malignant gliomas.

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“…Since the identification of TOPK as a novel MAPKK‐like protein kinase , further studies have been conducted with respect to downstream targets . TOPK has been reported to phosphorylate and inactivate PTEN, which in turn activates Akt, leading to proper G 2 /M progression in HeLa cells .…”

Section: Discussionmentioning

confidence: 99%

Activation of T‐LAK‐cell‐originated protein kinase‐mediated antioxidation protects against focal cerebral ischemia–reperfusion injury

et al. 2014

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T-LAK-cell-originated protein kinase (TOPK), a MAPKK-like kinase, is crucial for neural progenitor cell proliferation; however, the function of TOPK and the molecular mechanism underlying cerebral ischemia-reperfusion injury remains unknown. Therefore, we investigated the role of TOPK in experimental stroke. Sprague-Dawley rats underwent transient middle cerebral artery occlusion (tMCAO) and reperfusion, and TOPK small interfering RNA (siRNA) was delivered by intracerebroventricular injection at the beginning of MCAO. After TOPK overexpression and H 2 O 2 stimulation in PC12 neuronal cells, antioxidative proteins, apoptosis-related proteins and signal pathways were detected by western blot analysis, the levels of the peroxidation products (malondialdehyde and 3-nitrotyrosine) were measured with ELISA. Phosphorylation of TOPK was increased in rat cortical neurons following tMCAO. TOPK overexpression in PC12 cells augmented levels of antioxidative proteins (peroxiredoxin 1 and 2, heme oxygenase 1 and manganese superoxide dismutase), as well as total superoxide dismutase activity, along with inhibition of malondialdehyde and 3-nitrotyrosine upon H 2 O 2 stimulation. TOPK overexpression increased cell viability and reduced expression of caspase 3 and caspase 12 in PC12 cells in response to H 2 O 2 . The p-ERK level was increased by TOPK overexpression, and antioxidative protection afforded by TOPK was abolished by blocking the extracellular signal-regulated kinase pathway in PC12 cells. TOPK siRNA increased the infarct volume and reduced total superoxide dismutase activity in the cortex in vivo after MCAO. These data reveal that activating TOPK confers neuroprotection against focal cerebral ischemiareperfusion injury by antioxidative function, in part through activation of the extracellular signal-regulated kinase pathway.Abbreviations 3-NT, 3-nitrotyrosine; Akt, protein kinase B; ERK, extracellular signal-regulated kinase; HO-1, heme oxygenase 1; MDA, malondialdehyde; Prx-1, peroxiredoxin 1; siRNA, small interfering RNA; tMCAO, transient middle cerebral artery occlusion; TOPK, T-LAK-cell-originated protein kinase; TTC, 2,3,5-triphenyltetrazolium chloride.

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T‐LAK cell‐originated protein kinase is essential for the proliferation of hepatocellular carcinoma SMMC‐7721 cells

Cited by 12 publications

References 30 publications

Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats

Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats

Impact of a novel biomarker, T‐LAK cell‐originating protein kinase (TOPK) expression on outcome in malignant glioma

Activation of T‐LAK‐cell‐originated protein kinase‐mediated antioxidation protects against focal cerebral ischemia–reperfusion injury

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