The Involvement of the Fcεri Signaling Pathway in the Pathogenesis of Lacrimal Gland Benign Lymphoepithelial Lesions

2021 ◽  
Author(s):  
Jing Li ◽  
Rui Liu ◽  
Mei Sun ◽  
Jinjin Wang ◽  
Nan Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Western Blotting ◽  
Lacrimal Gland ◽  
Immunohistochemical Staining ◽  
Proteome Analysis ◽  
Control Group ◽  
Rt Pcr ◽  
Expression Levels ◽  
Benign Lymphoepithelial Lesion ◽  
Medical University

Abstract Objective: Benign lymphoepithelial lesion of lacrimal gland (LGBLEL) is a common orbital inflammatory disease with unknown pathogenesis. T his paper analyzed the role of the FcepsilonRI (FcεRI) signaling pathway in the pathogenesis of LGBLEL.Methods: Transcriptome sequencing and proteome sequencing were performed on LGBLEL and orbital CH diag nosed by histopathology in Beijing Tongren Hospital, Capital Medical University, between July 2010 and October 2013. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to jointly analyze the differentially expressed ge nes and proteins related to FcεRI signaling pathway. Four LGBLEL and three orbital CH diagnosed by histopathology in Beijing Tongren Hospital, Capital Medical University, between October 2018 and August 2019 were randomly selected as the experimental group and the control group, respectively. RT PCR, immunohistochemical staining, and western blotting were used to verify the genes and proteins related to the FcεRI signaling pathway.Results: Combined transcriptome and proteome analysis showed that the FcεRI signaling pathway was up regulated in LGBLEL (P=0.0040), and that the important proteins such as SYK, p38, JNK, PI3K, and ERK were highly expressed in LGBLEL tissues. RT PCR results showed that the mRNA expression levels of SYK, p38, JNK, PI3K, and ERK wer e significantly increased in the LGBLEL group (P=0.0066, P=0.0002, P=0.0003, P<0.0001, P<0.0001, respectively). Immunohistochemical staining results showed that the protein expression levels of SYK, p38, JNK, PI3K, and ERK in LGBLEL tissues were significan tly higher than in orbital CH. Western Blotting showed that the protein contents of p SYK, p p38, p JNK, p PI3K, and p ERK were significantly higher than in orbital CH (P=0.0169, P=0.0074, P=0.0046, P=0.0157, P=0.0156, respectively). Conclusion: The genes and proteins related to the FcεRI signaling pathway are up regulated in LGBLEL, indicating that the FcεRI signaling pathway participates in the pathogenesis of LGBLEL.

The Role of the Complement System Classical and Alternative Pathways in the Pathogenesis of Lacrimal Gland Benign Lymphoepithelial Lesions

2021 ◽  
Author(s):  
Rui Liu ◽  
Jing Li ◽  
Mei Sun ◽  
Jinjin Wang ◽  
Nan Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Lacrimal Gland ◽  
Complement System ◽  
Immunohistochemical Staining ◽  
Rt Pcr ◽  
Alternative Pathways ◽  
Medical University ◽  
The Complement System ◽  
Lymphoepithelial Lesions

Abstract Objective: The complement system plays an important role in chronic inflammation and autoimmune diseases. On the basis of previous studies, this paper further analyzed the role of the complement system classical pathway and alternative pathway in the pathogenesis of lacrimal gland benign lymphoepithelial lesions (LGBLEL).Methods: Six cases of LGBLEL and six cases of orbital cavernous hemangioma (CH), diagnosed by histopathology in Beijing Tongren Hospital, Capital Medical University, between July 2010 and October 2013 were randomly selected for proteomic analysis. Gene ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to analyze the signaling pathways of differentially expressed genes and proteins. Four LGBLEL and three orbital CH cases, diagnosed by histopathology in Beijing Tongren Hospital, Capital Medical University, between October 2018 and August 2019, were randomly selected as the experimental group and the control group, respectively. RT-PCR, immunohistochemical staining and western blotting were used to verify the genes and proteins related to the complement system signaling pathway.Results: The expression of complement system signaling pathway in LGBLEL tissue was significantly different (P<0.0001) compared with orbital CH, and C3, C5 and C9 were differentially expressed genes. RT-PCR results showed that mRNA expression levels of C1qA, C3, C5 and C9 related to the complement signaling pathway were higher in LGBLEL tissues than in orbital CH (P<0.0001). Immunohistochemical staining results showed that C1qA, C3, C5 and C9 protein expression was significantly higher in LGBLEL tissues than in orbital CH. Western blotting showed that the levels of C1qA, C3, C5 and C9 proteins were significantly higher in LGBLEL tissues than in orbital CH (P=0.0008; P=0.0375; P=0.0306; P=0.0073, respectively).Conclusion: Both the classical and alternative pathways of complement system are involved in the pathogenesis of LGBLEL.

scholarly journals The FcεRI signaling pathway is involved in the pathogenesis of lacrimal gland benign lymphoepithelial lesions as shown by transcriptomic analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jing Li ◽  
Rui Liu ◽  
Mei Sun ◽  
Jinjin Wang ◽  
Nan Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Lacrimal Gland ◽  
Immunohistochemical Staining ◽  
Transcriptomic Analysis ◽  
Control Groups ◽  
Benign Lymphoepithelial Lesion ◽  
Medical University ◽  
And Control ◽  
Lymphoepithelial Lesions

AbstractThis study aimed to analyze the role of the FcepsilonRI (FcεRI) signaling pathway in the pathogenesis of benign lymphoepithelial lesion of lacrimal gland (LGBLEL). Transcriptomic analysis was performed on LGBLEL and orbital cavernous hemangioma (CH) patients diagnosed via histopathology in Beijing Tongren Hospital, Capital Medical University, between July 2010 and October 2013. Four LGBLEL and three orbital CH patients, diagnosed between October 2018 and August 2019, were randomly selected as experimental and control groups, respectively. RT-PCR, immunohistochemical staining, and western blotting were used to verify genes and proteins related to the FcεRI signaling pathway. Transcriptomic analysis showed that the FcεRI signaling pathway was upregulated in the LGBLEL compared with the CH group. The mRNA expression levels of important genes including SYK, p38, JNK, PI3K, and ERK were significantly increased in the LGBLEL group (P = 0.0066, P = 0.0002, P = 0.0003, P < 0.0001, P < 0.0001, respectively). Immunohistochemical staining results showed that SYK, p38, and ERK were positively expressed in LGBLEL, while JNK and PI3K were not. The protein contents of P-SYK, P-p38, P-JNK, P-PI3K, and P-ERK were significantly higher in the LGBLEL than in the CH group (P = 0.0169, P = 0.0074, P = 0.0046, P = 0.0157, P = 0.0156, respectively). The FcεRI signaling pathway participates in the pathogenesis of LGBLEL.

scholarly journals Effects of Polygonatum sibiricum Polysaccharides (PSP) on Human Esophageal Squamous Cell Carcinoma (ESCC) via NF-κB Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Weizheng Zhou ◽  
Jiang Hong ◽  
Ji Zhu ◽  
Xiaowei Wang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Control Group ◽  
Dependent Manner ◽  
Rt Pcr ◽  
Expression Levels

Objective. To explore the effects of different concentrations of Polygonatum sibiricum polysaccharides (PSP) on human esophageal squamous cell carcinoma (ESCC) cell line Eca109 and explore the new approach for the treatment of ESCC. Methods. Eca109 cells were divided into 5 groups, including one control group and 4 experimental groups where the concentrations of PSP used were 50, 100, 200, and 400 μg/mL. The proliferation rate of Eca109 cells in each group was measured with the CCK8 assay, and the apoptosis rate in each group was analyzed by flow cytometry; the in vitro scratch assay was used to determine the migration ability of Eca109 cells after PSP treatment; the expression levels of IL-1, IL-6, IL-10, TNF-α, and TGF-β were measured by RT-PCR, and the expression levels of TLR4 and proteins that are related to NF-κB signaling pathways were determined by Western blot. Results. PSP significantly inhibited the proliferation of Eca109 cells (p<0.05) on a time- and dose-dependent manner; the apoptosis rates of Eca109 cells in experimental groups were significantly increased after 48 h of culture (p<0.05); PSP significantly reduced the migration and invasion ability of Eca109 cells (p<0.05); RT-PCR results showed that the expression of IL-10 in Eca109 cells increased significantly after treatment with PSP (p<0.05), while the expression of IL-1, IL-6, TNF-α, and TGF-β decreased significantly (p<0.05). Compared with the control group, the expression level of TLR4, NF-κB/p50, and NF-κB/p65 protein in each experimental group was significantly lower than that in the control group (p<0.05). Conclusions. PSP significantly inhibited the proliferation, invasion, and migration of Eca109 cells and promoted cell apoptosis. These observed effects were probably due to the PSP’s inhibition on the NF-κB signaling pathway in Eca109 cells via the regulation of the TLR4 expression.

scholarly journals Expression of β-catenin in human trophoblast and its role in placenta accreta and placenta previa

2018 ◽  
Vol 47 (1) ◽  
pp. 206-214
Author(s):  
Qing Han ◽  
Lianghui Zheng ◽  
Zhaodong Liu ◽  
Jinying Luo ◽  
Rongxin Chen ◽  
...  
Keyword(s):  
Western Blotting ◽  
Cell Invasion ◽  
Placenta Accreta ◽  
Placenta Previa ◽  
Control Group ◽  
Rt Pcr ◽  
Lesion Area ◽  
Human Trophoblast ◽  
Chorionic Villi ◽  
Pcr Techniques

Objectives To investigate the expression of β-catenin in chorionic villi, and to explore its roles in placenta accreta and placenta previa. Methods We compared β-catenin expression in the control group, placenta accreta group (lesion area and normal zones), and placenta previa group (placental central and placental edge zones) by immunohistochemistry, Western blotting, and RT-PCR techniques. Results Compared with the normal group, the placenta accreta group had a longer length of stay, greater bleeding volume, and lower newborn birth weight. Further, the expression of β-catenin was lower in both placenta previa and placenta accreta groups than in the control group, as measured by immunohistochemistry. Compared with the control group, expression of β-catenin was significantly lower in the placenta previa and placenta accreta groups by Western blotting and RT-PCR. Importantly, the level of placental β-catenin was significantly different when compared between the lesion and normal zones of placenta. Conclusion The expression of β-catenin in placenta accreta might play an important role in the regulation of placental cell invasion; low expression of β-catenin in placenta accreta might be responsible for excessive trophoblastic invasion.

Celastrol Inhibits the Proliferation and Decreases Drug Resistance of Cisplatin-Resistant Gastric Cancer SGC7901/DDP Cells

2021 ◽  
Vol 21 ◽  
Author(s):  
Dongmei Zhan ◽  
Tengyang Ni ◽  
Haibo Wang ◽  
Mengying Lv ◽  
Masataka Sunagawa ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Signaling Pathway ◽  
Resistance Index ◽  
Mtor Signaling ◽  
Control Group ◽  
Human Gastric Cancer ◽  
Cancer Resistance ◽  
Mtor Signaling Pathway ◽  
Expression Levels

Background: This study aimed to determine the effect and mechanism of Celastrol inhibiting the proliferation and decreases drug resistance of cisplatin-resistant gastric cancer cells. Objective: To explore the effect and mechanism of Celastrol on proliferation and drug resistance of human gastric cancer cisplatin-resistant cells SGC7901/DDP. Methods: The thiazole blue (MTT) method was used to detect the sensitivity of human gastric cancer cisplatin-resistant cells SGC7901/DPP to cisplatin and Celastrol to determine the Drug resistance index (DRI). According to the half inhibitory concentration (IC50) value, the action concentration of the following experimental drugs was set to reduce the cytotoxicity; Annexin V-FITC/PI double staining method was used to detect the apoptosis of SGC7901/DDP cells induced by Celastrol; Western Blot was used to examine the expression levels of P-glycoprotein (P-gp), Multidrug Resistance Associated Protein 1 (MRP1), Breast Cancer Resistance Associated Protein (Breast Cancer Resistance)-relative protein (BCRP), and mechanistic Target of Rapamycin (mTOR) pathway related proteins; Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the mRNA expression levels of P-gp, MRP1, and BCRP. Results: (1) Compared with the control group (We set the untreated group as the control group), the proliferation of the SGC7901/DPP cells was significantly inhibited after treating with 0.1-6.4μmol/L Celastrol in a time- and concentration-dependent manner (P<0.05). The Drug resistance index DRI of the SGC7901/DPP cells to DDP was 5.64. (2) Compared with the control group, Celastrol could significantly inhibit the proliferation and induce the apoptosis of the SGC7901/DPP cells (P<0.05). (3) The mRNA and protein expression levels of P-gp, MRP1, and BCRP in the SGC7901/DPP cells were significantly higher than those in the SGC7901 cells. However, after treating with Celastrol, the expression levels of P-gp, MRP1, and BCRP in the SGC7901/DPP cells were significantly reduced (P<0.05). (4) Compared with the control group, the Celastrol treatment also reduced the expression of the mTOR signaling pathway related proteins, suggesting that the mTOR signaling pathway may be involved in the process of Celastrol inhibiting the proliferation of the SGC7901/DDP cells and reducing their drug resistance. (5) Significantly, the combination of Celastrol and DDP reduced the expression of P-gp, MRP1, and BCRP in the SGC7901/DPP cells. Conclusion: Celastrol can inhibit the proliferation of the SGC7901/DDP cells, induce their apoptosis, and reduce the expression of drug resistance genes, probably by inhibiting the expression of the proteins related to the mTOR signaling pathway.

scholarly journals Expression of Notch–Hif-1α signaling pathway in liver regeneration of rats

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052094379
Author(s):  
Yanshan Li ◽  
Yunxiuxiu Xu ◽  
Ruomei Wang ◽  
Wenxin Li ◽  
Wenguang He ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Body Weight ◽  
Protein Expression ◽  
Liver Regeneration ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Saline Control ◽  
Control Group ◽  
Mrna Levels ◽  
Ki 67

Objective To investigate whether the Notch–Hif-1α signaling pathway is involved in liver regeneration. Methods Rats were divided into two groups and treated with daily intraperitoneal injections of saline (control) or the gamma-secretase inhibitor, Fli-06, for 2 days. Two-thirds of the rat livers were resected and rats were later euthanized at specific time points post-resection to analyze the remnant livers. Each group's liver/body weight ratio was calculated, and immunostaining and western blotting were used to determine the cell proliferation marker, PCNA and Ki-67 expression. Real-time PCR and western blotting were used to compare the mRNA expression of Notch homolog-1 ( Notch1), hairy and enhancer of split-1 ( Hes1), and vascular endothelial growth factor ( Vegf), and the protein expression of NICD and HIF-1α, respectively. Results The liver/body weight ratios and number of Ki-67- and PCNA-positive cells were significantly lower in the experimental group than the control group, indicating lower levels of liver regeneration following the disruption of Notch signaling by Fli-06. The Hes1 and Vegf mRNA levels and NICD and HIF-1α protein expression levels were all down-regulated by Fli-06 treatment. Conclusion Notch–Hif-α signaling pathway activation plays an important role in liver regeneration, where it may contribute toward liver cell proliferation.

scholarly journals Regulation and Mechanism of miR-518d through the PPARα-Mediated NF-κB Pathway in the Development of Gestational Diabetes Mellitus

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Hui Qiu ◽  
Xuemin Liu ◽  
Shenshen Yao ◽  
Jiaren Zhou ◽  
Xue Zhang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Pregnant Women ◽  
Western Blotting ◽  
Transport Process ◽  
Inflammatory Factors ◽  
Rt Pcr ◽  
Expression Levels ◽  
Antagonist Group

Objectives. To observe the role of miR-518d in pregnant women with gestational diabetes mellitus (GDM) and its adjusting effects on PPARα and to explore the regulatory mechanisms of the NF-κB pathway in the development and progression of GDM. Methods. Placenta tissues and peripheral plasma were obtained from pregnant women with normal pregnancy and GDM, respectively, followed by the detections of miR-518d contents by RT-PCR and the expression levels of inflammatory factors using ELISA. Human placenta trophoblast cells (HTR8/SVneo) were cultured under the conditions of physiological glucose (PG group) and high glucose level (HG group). Cells in the HG group were transfected with miR-518d control, mimics, and inhibitors and were separately administered with a PPARα-specific antagonist (GW6471) and PPARα siRNA, and cells were divided into the following groups: HG+miR-518d control group (HGNC group), HG+miR-518d mimic group (HGM group), HG+miR-518d inhibitor group (HGI group), HGI+PPARα antagonist group, and HGI+PPARα siRNA group. The relative expression levels of miR-518d, PPARα, and its downstream genes and NF-κB signalling pathway-related genes were detected by RT-PCR and Western blotting. The contents of inflammatory factors were examined by Western blotting. A dual-luciferase report assay was performed to validate the correlations between miR-518d and PPARα. In this study, mouse GDM models were established to further prove the previous hypothesis with an in vivo experiment. A total of 40 C57BL/6J mice were randomly divided into the following groups: normal diet group (ControlMs), GDM group (GDMMs group), GDM+miR-518d antagomir group, and GDM+miR-518d antagomir+PPARα antagonist group. The mouse model of GDM was established by feeding with combined high-sugar and high-saturated fat diet and injecting streptozotocin (STZ) after 15-day feeding. Female and male mice were cocaged in the number ratio of 2 : 1, and the evidence of vaginal suppository detected in female mice was marked as D0 of pregnancy. The contents of total cholesterol (CH), triglyceride (TG), fast glucose, and insulin (INS) were examined using ELISA, followed by the evaluation of insulin resistance (IR). The related expression levels were also detected with the above methods shown in the previous cell culture. Results. miR-518d has a high expression level in placentas with GDM. As the target gene of miR-518d, PPARα was downregulated with the increased levels of miR-518d. When GDM occurs, inflammatory responses were elevated, stimulating the nuclear transport process of NF-κB. Activated NF-κB triggered the phosphorylation of IKKβ and IκBα. Conclusions. High expression of miR-518d was observed in the development of GDM. In this study, we validated that miR-518d negatively regulates the expression of PPARα and triggers the nuclear transport process of NF-κB and phosphorylation of pathway-associated proteins leading to an inflammatory response and the development of GDM.

Effects of Hydrogen-rich Water on the PI3K/AKT Signaling Pathway in Rats with Myocardial Ischemia-reperfusion Injury

2020 ◽  
Vol 20 (5) ◽  
pp. 396-406 ◽  
Author(s):  
Liangtong Li ◽  
Xiangzi Li ◽  
Zhe Zhang ◽  
Li Liu ◽  
Tongtong Liu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Expression Levels ◽  
Water Group

Background: The effects of hydrogen-rich water on PI3K/AKT-mediated apoptosis were studied in rats subjected to myocardial ischemia-reperfusion injury (MIRI). Methdos: Sixty rats were divided randomly into a hydrogen-rich water group and a control group. The hearts were removed and fixed in a Langendorff device. Hearts from the control group were perfused with K-R solution, and hearts from the hydrogen-rich water group was perfused with K-R solution + hydrogen-rich water. The two treatment groups were then divided randomly into pre-ischemic period, ischemic period and reperfusion period groups(10 rats per group), which were subjected to reverse perfusion for 10 min, normal treatment for 20 min, and reperfusion for 20 min, respectively. The mRNA and protein expression levels of PI3K, AKT, p-AKT, FoxO1, Bim and Caspase-3 in each group were detected by RT-qPCR, immunohistochemistry (IHC) and Western blotting. Caspase-3 activity was detected by spectrophotometry. Results: Among the hydrogen-rich water group, the PI3K/AKT signaling pathway was significantly activated, and FoxO1, Bim, and Caspase-3 mRNA and protein levels were significantly decreased in ischemia-reperfusion subgroup compared with the preischemic and ischemic subgroups. In the ischemia-reperfusion hydrogen-rich water group, PI3K, AKT and p-AKT mRNA and protein expression levels were increased while the FoxO1, Bim and Caspase-3 expression levels were significantly decreased compared with those in the corresponding control group (p<0.05). Conclusion: Hydrogen-rich water can activate the PI3K/AKT signaling pathway, alleviate ischemia-reperfusion injury in isolated rat hearts, and inhibit cardiomyocyte apoptosis.

scholarly journals Liraglutide Promotes Osteoblastic Differentiation in MC3T3-E1 Cells by ERK5 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yue Sun ◽  
Yuzhen Liang ◽  
Zhengming Li ◽  
Ning Xia
Keyword(s):  
Signaling Pathway ◽  
Osteoblastic Differentiation ◽  
Control Group ◽  
Activity Levels ◽  
Expression Levels ◽  
Protein Levels ◽  
Proliferation And Differentiation ◽  
Glucagon Like Peptide 1 ◽  
Differentiation And Proliferation

Liraglutide is a glucagon-like peptide-1 analogue widely used in the treatment of type 2 diabetes mellitus. However, the effects of liraglutide on osteoblast proliferation and differentiation in MC3T3-E1 cells have not been fully elucidated. In the present study, the promoting effects of liraglutide were investigated in MC3T3-E1 cells. The results indicated that cell viability was affected following the treatment of the cells with different concentrations of liraglutide (0, 10, 100, and 1000 nM) at different time periods of culture (24, 48, and 72 h). Moreover, the activity levels of alkaline phosphatase and the number of mineralized nodules in MC3T3-E1 cells were significantly increased following treatment with 100 nM liraglutide. The mRNA and protein levels of Col-1, OPG, and OCN in MC3T3-E1 cells were also markedly increased following 100 nM liraglutide treatment compared with those of the control group. The expression levels of the ERK5 signaling pathway key proteins (MEK5, p-ERK5, ERK5, and NUR77) were increased following liraglutide treatment in MC3T3-E1 cells, and the gene expression levels of the ERK5 signaling pathway were also elevated. Moreover, the ERK5 inhibitor XMD8-92 significantly decreased the expression levels of p-ERK5 and NUR77 as well as the proliferation of osteoblasts. However, these changes could be rescued by liraglutide to some extent. Therefore, these results revealed that liraglutide may promote osteoblastic differentiation and proliferation in MC3T3-E1 cells via the activation of the ERK5 signaling pathway.

scholarly journals Inhibition of PTEN Gene Expression by Small Interfering RNA on PI3K/Akt/FoxO3a Signaling Pathway in Human Nasopharyngeal Carcinoma

2020 ◽  
Vol 19 ◽  
pp. 153303382091795
Author(s):  
Liang Zhong Yao ◽  
Yan Li Zhu ◽  
Jun Jie Liu
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Signaling Pathway ◽  
Messenger Rna ◽  
Small Interfering Rna ◽  
Quantitative Polymerase Chain Reaction ◽  
Pten Gene ◽  
Control Group ◽  
Expression Levels ◽  
Human Nasopharyngeal Carcinoma ◽  
Interfering Rna

The objective of this article is to study the effect of inhibiting phosphatase and tensin homolog deleted chromatosome 10 gene on phosphoinositide 3-kinase/protein kinase B ( Akt)/Forkhead homeobox O3a signaling pathway in human nasopharyngeal carcinoma HK-1 cells. Nasopharyngeal carcinoma HK-1 cell lines were divided into PTEN gene interference group (siPTEN), nonspecific small interfering RNA group (siNC), empty vector group (Vector), and no transfection control group (Normal). The mRNA and protein expression levels of PTEN, PI3K, p-Akt, and FoxO3a were detected by real-time fluorescence quantitative polymerase chain reaction and Western blot. Immunofluorescence was used to detect the subcellular localization of PTEN, PI3K, p-Akt, and FoxO3a in HK-1 cells. The proliferation of HK-1 cells was detected by MTT assay, and the apoptosis of HK-1 cells was detected by flow cytometry. Compared with the siNC group, the expression levels of PTEN, FoxO3a messenger RNA, and protein in the siPTEN group were significantly decreased ( P < .05), while the expression levels of PI3K, p-Akt messenger RNA, and protein were significantly increased ( P < .05). The growth rate of HK-1 cells in the siPTEN group was significantly higher than the siNC group ( P < .05), while the apoptosis rate was significantly lower than that of the siNC group ( P < .05). Small interfering RNA can inhibit the expression of PTEN in HK-1 cells, and PTEN can participate in the development of NPC by affecting PI3K/Akt/FoxO3a signaling pathway.

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