Roles of PLC-γ2 and PKCα in TPA-induced apoptosis of gastric cancer cells

Zhang, Bing; Wu, Qiao; Ye, Xiaofeng; Liu, Su; Lin, Xiaofeng; Chen, Mu-Chuan

doi:10.3748/wjg.v9.i11.2413

Cited by 24 publications

(30 citation statements)

References 46 publications

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“…Similarly, the DEGS1 gene encoded a member of the membrane fatty acid desaturase family [57] and was proved to participate in the activation of caspase 9 and caspase 3, which were marker proteins of cell apoptosis [58]. Moreover, PLCG2 and PRKCE genes encoded phospholipase C-(PLC)γ2 and protein kinase C(PKC)-ε, respectively, and both proteins were important elements of cellular signal transduction pathways that could regulate a chain of events either in physiological or pathological status [59][60][61]. Kajstura found that angiotensinconverting enzyme (ACE) II could induce the translocation of PKC-ε of myocytes due to an increase in intracellular free Ca…”

Section: Discussionmentioning

confidence: 99%

“…, which could lead to the initiation of apoptosis [62], while the translocation of PLC-γ2 was certified to transmit the TPA signal to its downstream molecule PKC and directly promote the process of apoptosis in MGC80-3 cells [59]. Analogously, NUAK1, also known as AMPKrelated protein kinase 5, was the downstream molecule of Akt, which participated in the classical signaling pathway with extensive consequences [63].…”

Section: +mentioning

confidence: 99%

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WITHDRAWN: Genome-wide association analysis of inguinal/scrotal hernia in pigs using specific length amplified fragment (SLAF) sequencing

Zou¹,

Zuo²,

Zhu³

et al. 2017

Oncotarget

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Inguinal and scrotal hernias are the most frequent congenital disorders in pigs, and they may cause severe economic loss in the pig breeding industry. Genetic factors play a significant role in the susceptibility to hernias, but the genetic mechanisms of inguinal/scrotal hernia are poorly understood. In this study, we performed a genome-wide association study (GWAS) with specific-locus amplified fragment sequencing (SLAF-seq) on 120 (59 cases and 61 controls) full and half sib pigs to identify genetic loci underlying variations in inguinal/scrotal hernias. A total of 218,460 high-quality SNPs were generated for further statistical analysis with casecontrols and the farmCPU model. Based on these two methods, a total of 59 SNPs were significantly (P < 0.01) associated with inguinal/scrotal hernia. Finally, 14 novel candidate genes implicated in the defect were identified, and 5 genes (CPNE5, DEGS1, PLCG2, PRKCE and NUAK1) were related to cell apoptosis, which is one of the pivotal pathogenesis factors of inguinal/scrotal hernia. In addition, 4 of them were shown strong associations with the hernia were confirmed in 270 samples (P < 0.05). This finding provides new evidence that genes related to cell apoptosis may be associated with inguinal/scrotal hernias.

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Section: Discussionmentioning

confidence: 99%

Section: +mentioning

confidence: 99%

WITHDRAWN: Genome-wide association analysis of inguinal/scrotal hernia in pigs using specific length amplified fragment (SLAF) sequencing

Zou¹,

Zuo²,

Zhu³

et al. 2017

Oncotarget

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“…Immunofluorescence analysis was performed as previously described (38). JEG-3 cells and PMTs were cultured in 1% oxygen or 21% oxygen for 24 h. The cells were washed with PBS (Sigma-Aldrich) and fixed in 4% paraformaldehyde.…”

Section: Immunofluorescence Analysismentioning

confidence: 99%

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Jiang¹,

Cai

Zhu

et al. 2014

The Journal of Immunology

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High mobility group box 1 (HMGB1) plays an important role in the pathologic processes of endothelial permeability under oxidative stress. Trophoblast oxidative stress has been implicated in the pathophysiology of preeclampsia (PE). HMGB1 serum levels are increased in PE. However, the potential roles of HMGB1 in endothelial permeability in PE remain unclear. We assessed the effects of the hypoxic trophoblast on the permeability of the endothelial monolayer. Our results showed that the hypoxic trophoblast displayed higher HMGB1 mRNA, intracellular HMGB1 protein, and HMGB1 in conditioned medium than those of the normoxic trophoblast did. The hypoxic trophoblast conditioned medium increased the endothelial monolayer permeability and increased TLR 4 and caveolin-1 (CAV-1) protein expression in endothelial cells, which was inhibited by glycyrrhizic acid and HMGB1 small interfering RNA transfection to trophoblasts before hypoxia. The increased endothelial permeability induced by hypoxic trophoblast conditioned medium could be inhibited with TLR4 or CAV-1 gene silencing in endothelial cells. Immunoprecipitation showed that CAV-1 and TLR4 are colocalized in HUVECs and C57BL/6 mouse kidney. TLR4 small interfering RNA suppressed CAV-1 protein expression in endothelial cells upon stimulation of hypoxic trophoblast conditioned medium or HMGB1. We conclude that hypoxic trophoblasts play an important role in the mechanism of general edema (including protein urine) in PE via increasing endothelial monolayer permeability through the HMGB1/TLR4/CAV-1 pathway.

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“…For example, in a study by Tomlinson et al (2001), PLCg2 was found to be essential for the Bruton's tyrosine kinase (BTK):ER-induced apoptosis response. Zhang et al (2003) also found that PLCg2 was significantly upregulated during TPA (12-O-tetradecanoylphorbol-1, 3-acetate)-induced apoptosis in gastric cancer cells, suggesting that PLCg2 has an essential role in the induction of apoptosis. However, little is known about the contribution of PLCg2 to the induction of apoptosis during LR.…”

Section: Introductionmentioning

confidence: 77%

“…These then activate downstream signaling pathways thus regulating various biological events, such as cell growth and differentiation (Ozdener et al, 2002). Recently, several studies have identified PLCg2 as an important regulator of apoptosis, and it has been reported to induce the apoptosis of gastric cancer cells (Zhang et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Construction of recombinant adenovirus Ad-rat PLCg2-shRNA and successful suppression of PLCg2 expression in BRL-3A cells

Chen

Zhou

2016

Genet. Mol. Res.

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ABSTRACT. Phospholipase Cg2 (PLCg2) induces apoptosis of immune and tumor cells; however, it remains unclear whether PLCg2 promotes hepatocyte apoptosis during liver regeneration (LR). Therefore, to establish a framework for further exploring the function of PLCg2, we generated recombinant adenoviruses carrying a template encoding short hairpin (sh)-RNA targeting PLCg2 (Ad-PLCg2-shRNA), which were used to silence the expression of PLCg2 in BRL-3A cells. First, three pairs of PLCg2-shRNAs were designed, synthesized, and cloned into a shuttle vector, pHBAd-U6-GFP, after annealing. The recombinant shuttle plasmids were co-transfected with the backbone vector pHBAd-BHG into HK293 cells to package the recombinant Ad-PLCg2-shRNAs used to infect BRL-3A cells. with the highest silencing efficiency, levels of PLCg2 mRNA were evaluated by qRT-PCR. DNA sequencing confirmed that the correct shRNA coding sequences were inserted into the shuttle vectors and adenoviral plasmids. The titers of three recombinant adenoviruses were at least 1 x 10 10 PFU/mL. The most effective adenoviral construct, with interference efficiency of 77%, was determined by qRT-PCR. These results show that a recombinant adenovirus, Ad-PLCg2-shRNA, was developed and was effective at silencing the rat PLCg2 gene. This construct may contribute to the study of PLCg2 in hepatocyte apoptosis during LR.

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Roles of PLC-γ2 and PKCα in TPA-induced apoptosis of gastric cancer cells

Abstract: AIM:To investigate the roles of PLCγ2 and PKCα in TPAinduced apoptosis of gastric cancer cells.

Cited by 24 publications

References 46 publications

WITHDRAWN: Genome-wide association analysis of inguinal/scrotal hernia in pigs using specific length amplified fragment (SLAF) sequencing

WITHDRAWN: Genome-wide association analysis of inguinal/scrotal hernia in pigs using specific length amplified fragment (SLAF) sequencing

Hypoxic Trophoblast HMGB1 Induces Endothelial Cell Hyperpermeability via the TRL-4/Caveolin-1 Pathway

Construction of recombinant adenovirus Ad-rat PLCg2-shRNA and successful suppression of PLCg2 expression in BRL-3A cells

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