The Effects of Curcumin Combined with Cisplatin on Apoptosis, Invasion and Metastasis of Nasopharyngeal Carcinoma Cells Through TGF-β1/Smads Signaling Pathways

2020 ◽  
Vol 10 (4) ◽  
pp. 469-476 ◽  
Author(s):  
Zhengxiang He ◽  
Yuyang Chen ◽  
Suzhen Wang ◽  
Yufeng Dong ◽  
Huiguang Liu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Carcinoma Cells ◽  
Control Group ◽  
Proliferation Inhibition ◽  
Invasion And Metastasis ◽  
Migration Ability ◽  
Group 10 ◽  
Tgf Β1

Objective: To explore the influences of Curcumin combined with Cisplatin on proliferation inhibition, apoptosis, invasion and metastasis of human nasopharyngeal carcinoma cells CNE-2 in vitro , and its relationship with TGF-β 1/Smads signaling pathway. Method: The experiment included four groups: the Control group, Curcumin group (10 μmol/L), Cisplatin group (10 μmol/L), Merge group (10 mol/L Curcumin and 10 mol/L Cisplatin). The inhibition of Curcumin combined with Cisplatin on CNE-2 cell proliferation was measured by using MTT assay. Apoptosis was detected by flow cytometry and DAPI staining. The invasion and migration ability of CNE-2 cells were tested by Transwell test and scratch test. The Caspase-3 activity was detected. The expression levels of TGF-β1, Smad2, Smad3, Smad4 and Smad7 in the cells were measured by Western blot. Results: Compared with the control group, the proliferation rate of CNE-2 achieved remarkable decline in the Curcumin group, the Cisplatin group and the merge group (P < 0 05); the apoptosis rate and the Caspase-3 activity were significantly elevated (P < 0 05); the invasion and metastasis ability was obviously reduced (P < 0 05); The merge group had the most significant effect of proliferation inhibition and apoptosis promotion (P < 0 05). In addition, the Curcumin group, cisplatin group and combined group could inhibit the expression of TGF- β1, Smad2/3/4 proteins, and increase the expression of Smad7 proteins with significantly difference (P < 0 05). The regulatory effects of the merge group was the most significant (P < 0 05). Conclusion: Curcumin combined with Cisplatin has a synergistic effect, inhibiting proliferation, inducing apoptosis and inhibiting invasion and metastasis of CNE-2 cells, possibly being related with the down-regulation of TGF-β1/Smads signaling pathway.

S100A14 Induces Apoptosis and Negatively Regulates Proliferation of Nasopharyngeal Carcinoma Cells

2021 ◽  
Author(s):  
Yu Xiao ◽  
Jibo Han ◽  
Fen Li ◽  
Anyuan Zheng ◽  
Qibing Chen ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Caspase 3 ◽  
Suppressor Gene ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Control Group ◽  
Phase Arrest ◽  
M Phase ◽  
Density Values

Abstract Background: S100A14 is involved in multiple pathological processes; however, its role in nasopharyngeal carcinoma is poorly understood. Methods: S100A14 was deleted or upregulated in 6-10B cells. Results: S100A14-knockdown 6-10B cells showed significantly higher optical density values in the CCK-8 assay, smaller scratch width in the scratch experiment, and significantly more invading cells in the transwell assay compared with controls. Compared with the control group, the G2/M and S phase proportions of the S100A14-overexpression group were significantly higher, early apoptosis was observed via JC-1 fluorescence, and flow cytometry showed a significantly higher proportion of apoptotic cells. Protein expression of Bcl-2 and Bcl-xl decreased significantly, whereas that of Bax, Bad, cleaved-PARP, and cleaved-caspase-3/9 increased. Conclusions: Knockdown of S100A14 promoted proliferation, migration, and invasion of 6-10B cells, whereas its upregulation promoted caspase-dependent apoptosis and induced S and G2/M phase arrest, indicating a role of S100A14 as a tumor suppressor gene in nasopharyngeal carcinoma.

scholarly journals Influences of S100A8 and S100A9 on Proliferation of Nasopharyngeal Carcinoma Cells through PI3K/Akt Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Liting Wen ◽  
Yu Ding ◽  
Xiaodong Chen ◽  
Keyong Tian ◽  
Danfeng Li ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Carcinoma Cells ◽  
Akt Pathway ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Protein Levels ◽  
Positive Rate ◽  
Sirna Group

Objective. To investigate the effects of S100A8 and S100A9 on proliferation in nasopharyngeal carcinoma cells and the regulatory effects of PI3K/Akt signaling pathway. Methods. Nasopharyngeal carcinoma cells (CNE1) were cultured and randomly divided into three groups: control group, S100A8/S100A9 overexpression group, and siRNA S100A8/S100A9 group. CCK-8 method was used to detect the effect of S100A8 and S100A9 on the viability of nasopharyngeal carcinoma cells. The effects of S100A8 and S100A9 on the colony forming ability of nasopharyngeal carcinoma cells were detected by colony forming assay. The effects of S100A8 and S100A9 on the proliferation of nasopharyngeal carcinoma cells were detected by EdU staining. The mRNA levels of PI3K and Akt were detected by RT-PCR. The expression levels of PI3K and Akt in NPC cells were detected by Western blot. Wortmannin, an inhibitor of PI3K/Akt pathway, was used to inhibit the activation of PI3K/Akt pathway. Results. Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were increased in the overexpression group. Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were decreased in the siRNA group. After inhibiting the activation of PI3K/Akt pathway, the viability of NPC cells in the overexpression group decreased significantly at 48 h and 72 h, while that in the siRNA group increased significantly. Conclusion. SiRNA S100A8 and S100A9 could inhibit the proliferation of nasopharyngeal carcinoma cells, and the underlying mechanism may be related to the inhibition of PI3K/Akt signaling pathway.

scholarly journals Long non-coding (lnc)RNA profiling and the role of a key regulator lnc-PNRC2-1 in the transforming growth factor-β1-induced epithelial–mesenchymal transition of CNE1 nasopharyngeal carcinoma cells

2021 ◽  
Vol 49 (3) ◽  
pp. 030006052199651
Author(s):  
Jie Yang ◽  
Enzi Feng ◽  
Yanxin Ren ◽  
Shun Qiu ◽  
Liufang Zhao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Nasopharyngeal Carcinoma ◽  
Rna Sequencing ◽  
Western Blotting ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Emt Markers ◽  
Tgf Β1

Objectives To identify key long non-coding (lnc)RNAs responsible for the epithelial–mesenchymal transition (EMT) of CNE1 nasopharyngeal carcinoma cells and to investigate possible regulatory mechanisms in EMT. Methods CNE1 cells were divided into transforming growth factor (TGF)-β1-induced EMT and control groups. The mRNA and protein expression of EMT markers was determined by real-time quantitative PCR and western blotting. Differentially expressed genes (DEGs) between the two groups were identified by RNA sequencing analysis, and DEG functions were analyzed by gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses. EMT marker expression was re-evaluated by western blotting after knockdown of a selected lncRNA. Results TGF-β1-induced EMT was characterized by decreased E-cadherin and increased vimentin, N-cadherin, and Twist expression at both mRNA and protein levels. Sixty lncRNA genes were clustered in a heatmap, and mRNA expression of 14 dysregulated lncRNAs was consistent with RNA sequencing. Knockdown of lnc-PNRC2-1 increased expression of its antisense gene MYOM3 and reduced expression of EMT markers, resembling treatment with the TGF-β1 receptor inhibitor LY2109761. Conclusion Various lncRNAs participated indirectly in the TGF-β1-induced EMT of CNE1 cells. Lnc-PNRC2-1 may be a key regulator of this and is a potential target to alleviate CNE1 cell EMT.

scholarly journals miR-206 regulates a metabolic switch in nasopharyngeal carcinoma by suppressing HK2 expression

2020 ◽  
Author(s):  
Chunying Luo ◽  
Min Liu ◽  
Jianwei Zhang ◽  
Guoqiang Su ◽  
Zhonghua Wei
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Warburg Effect ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Metabolic Shift ◽  
Invasion And Metastasis ◽  
Metabolic Switch ◽  
And Function ◽  
The Relationship

Abstract Background: Many studies have shown that microRNAs play key functions in nasopharyngeal carcinoma proliferation, invasion and metastasis. However, whether the dysregulated level of miRNAs contributes to the metabolic shift in nasopharyngeal carcinoma is not completely understood.Objectives: This study was conducted to explore the expression and function of miR-206 in nasopharyngeal carcinoma.Methods: miR-206 expression level was examined by real-time PCR. miR-206 inhibitor, mimics, and scrambled control were transiently transfected into nasopharyngeal carcinoma cells and their effects on colony formation, glucose uptake, and lactate secretion were observed in vitro. Moreover, the relationship between the levels of miR-206 and HK2 was examined by luciferase reporter and assay western blot.Results: In our study, we reported downregulation of miR-206 expression leads to metabolic change in nasopharyngeal carcinoma cells. miR-206 controls this function by enhancing HK2 expression. The enhancement of aerobic metabolism activity induced by miR-206 leads to the rapid proliferation of nasopharyngeal carcinoma cells.Conclusions: Our data demonstrated that miR-206 was involved in the regulation of Warburg effect in nasopharyngeal carcinoma by suppressing HK2 expression.

Effect of SRY-Related High Mobility Group Box 9 on Extracellular Signal-Regulated Kinase/p38 Signaling Pathway in Glioma

2021 ◽  
Vol 11 (1) ◽  
pp. 171-175
Author(s):  
Tianlong Quan ◽  
Chunhua Zhang ◽  
Xin Song ◽  
Lu Wang
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Invasion ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
High Mobility ◽  
Negative Control ◽  
Glioma Cell Line ◽  
High Mobility Group ◽  
Control Group

As a common malignant tumor in neurosurgery, glioma is characterized as high incidence rate, easy to invade, metastasize and recurrent. It is difficult to treat and has a poor prognosis. The gliomas pathogenesis is complex and has not been fully resolved. Therefore, finding effective molecular targets for glioma is beneficial to improve therapeutic effect. The SRY-related high mobility group box 9 (SOX9) gene involves in mammalian development and is significantly increased in glioma. However, SOX9’s role in gliomas is unclear. The glioma cell line U87 was assigned into control group, scramble group that was transfected with siRNA negative control, and SOX9 siRNA group that was transfected with SOX9 siRNA followed by analysis of SOX9 mRNA and protein level by qPCR and Western blot, cell proliferation by MTT assay, cell apoptosis by Caspase 3 activity assay, cell invasion by Transwell assay, and MMP-9 level by ELISA. SOX9 siRNA transfection significantly downregulated SOX9 mRNA and protein expressions, inhibited U87 cell proliferation, enhanced Caspase 3 activity, suppressed cell invasion of U87, decreased the secretion of MMP-9 in the supernatant, and reduced ERK1/2 and P38 phosphorylation levels (P < 0.05). SOX9 can regulate the progression of glioma by regulating ERK/P38 signaling pathway, promoting cell apoptosis, inhibiting cell proliferation, and restraining cell invasion.

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.

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