Retraction: The inhibition of tumor protein p53 by microrna-151a-3p induced cell proliferation, migration and invasion in nasopharyngeal carcinoma

Abstract A close relation between microRNA-151a-3p (miR-151a-3p) and nasopharyngeal carcinoma (NPC) has been reported, however, the molecular mechanism is still unclear. The aim of the present study was to explore the mechanism in the promotion of miR-151a-3p to NPC progression. The levels of miR-151-3p in several NPC cell lines were detected in order to screen an experimental cell line. MiR-151a-3p mimic and inhibitor were constructed and transfected into 5-8F cells and cell proliferation were detected by Cell Counting Kit-8 (CCK-8). The apoptosis rate, cell migration and invasion were determined by flow cytometry, wound healing and Transwell assays. The predicted target was further verified by luciferase reporter assay. Real-time quantification-PCR and Western blot were carried out for mRNA and protein level analysis. Tumor protein p53 was co-transfected to verify the functions of miR-151a-3p. The miR-151a-3p level in NPC tissues was much higher than that in adjacent tissues. After transfecting cells with miR-151a-3p mimic, the cell proliferation and patients’ survival rate were much increased, and this was accompanied by the increase in B-cell lymphoma 2 (Bcl-2) and decreases in Bax and cleaved caspase-3 (P<0.01). Moreover, the migration rate and number of invaded cells were also remarkably increased, however, the miR-151a-3p inhibitor had opposite effects on the 5-8F cells. Noticeably, p53 was revealed as a potential target of miR-151a-3p. Co-transfection of P53 could partially reverse the promotive effects of miR-151a-3p on NPC cell progression. Our data indicated that blocking p53 expression and mediated signal pathways contribute to the positive effects of miR-151a-3p on NPC cell proliferation, migration and invasion.

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The Effect of Hispidulin, a Flavonoid from Salvia plebeia, on Human Nasopharyngeal Carcinoma CNE-2Z Cell Proliferation, Migration, Invasion, and Apoptosis

Molecules ◽

10.3390/molecules26061604 ◽

2021 ◽

Vol 26 (6) ◽

pp. 1604

Author(s):

Yiqun Dai ◽

Xiaolong Sun ◽

Bohan Li ◽

Hui Ma ◽

Pingping Wu ◽

...

Keyword(s):

Cell Proliferation ◽

Nasopharyngeal Carcinoma ◽

Migration And Invasion ◽

Dependent Manner ◽

Etoh Extract ◽

Tumor Drug Resistance ◽

Diphenyltetrazolium Bromide ◽

Scratch Wound ◽

Low Toxicity ◽

Induced Apoptosis

Nasopharyngeal carcinoma (NPC) is a common malignant head and neck tumor. Drug resistance and distant metastasis are the predominant cause of treatment failure in NPC patients. Hispidulin is a flavonoid extracted from the bioassay-guided separation of the EtOH extract of Salvia plebeia with strong anti-proliferative activity in nasopharyngeal carcinoma cells (CNE-2Z). In this study, the effects of hispidulin on proliferation, invasion, migration, and apoptosis were investigated in CNE-2Z cells. The [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT) assay and the colony formation assay revealed that hispidulin could inhibit CNE-2Z cell proliferation. Hispidulin (25, 50, 100 μM) also induced apoptosis in a dose-dependent manner in CNE-2Z cells. The expression of Akt was reduced, and the expression of the ratio of Bax/Bcl-2 was increased. In addition, scratch wound and transwell assays proved that hispidulin (6.25, 12.5, 25 μM) could inhibited the migration and invasion in CNE-2Z cells. The expressions of HIF-1α, MMP-9, and MMP-2 were decreased, while the MMPs inhibitor TIMP1 was enhanced by hispidulin. Moreover, hispidulin exhibited potent suppression tumor growth and low toxicity in CNE-2Z cancer-bearing mice at a dosage of 20 mg/kg/day. Thus, hispidulin appears to be a potentially effective agent for NPC treatment.

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FOXD3 inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma through regulation of the PI3K–Akt pathway

Biochemistry and Cell Biology ◽

10.1139/bcb-2020-0011 ◽

2020 ◽

Vol 98 (6) ◽

pp. 653-660 ◽

Cited By ~ 1

Author(s):

Xiaoxing Xie ◽

Gaoyun Xiong ◽

Wenjun Chen ◽

Hongdan Fu ◽

Mingqian Li ◽

...

Keyword(s):

Cell Proliferation ◽

Nasopharyngeal Carcinoma ◽

Cell Apoptosis ◽

Inhibitory Effect ◽

Akt Pathway ◽

Migration And Invasion ◽

Inhibitory Effects ◽

Protein Levels ◽

Flow Cytometric ◽

Phosphoinositide 3 Kinase

FOXD3 has been found previously to positively regulate miR-26b, a tumor inhibitor of nasopharyngeal carcinoma (NPC). However, FOXD3’s precise function and associated mechanism of action in NPC have not yet been investigated. In this study, the expression of FOXD3 mRNA and protein was evaluated using RT-qPCR, western blotting, and immunohistochemistry. Protein levels involved in the phosphoinositide 3-kinase – protein kinase B (PI3K–Akt) pathway were assessed by western blot, and cell proliferation was determined by MTT and colony forming assays. Additionally, cell apoptosis was assessed by flow cytometric assay. Finally, the migration and invasion capabilities of the NPC cells were determined using wound healing and Transwell assays. We found that FOXD3 levels were relatively low in NPC tissue and cells, while an increase caused the inhibition of the PI3K–Akt pathway. Functional experiments found that overexpression of FOXD3 suppressed cell proliferation, migration, and invasion and enhanced cell apoptosis in NPC C6661 cells. IGF-1, an activator of the PI3K–Akt pathway, reversed the inhibitory effect of FOXD3. Furthermore, we found upregulation of the PI3K–Akt pathway and upregulation of the inhibitory effects of FOXD3 on C6661 cellular activities. In conclusion, FOXD3 negatively affected the PI3K–Akt pathway to restrain the processes involved in C6661 cell pathology. These findings further exposed the function and downstream axis of FOXD3 in NPC and displayed a promising new target for NPC therapy.

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MicroRNA-144 promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma through repression of PTEN

Carcinogenesis ◽

10.1093/carcin/bgs346 ◽

2012 ◽

Vol 34 (2) ◽

pp. 454-463 ◽

Cited By ~ 127

Author(s):

Li-Yi Zhang ◽

Victor Ho-Fun Lee ◽

Alissa Michelle Go Wong ◽

Dora Lai-Wan Kwong ◽

Ying-Hui Zhu ◽

...

Keyword(s):

Cell Proliferation ◽

Nasopharyngeal Carcinoma ◽

Migration And Invasion

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Downregulation of SHCBP1 Inhibits Proliferation, Migration, and Invasion in Human Nasopharyngeal Carcinoma Cells

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2021/8262502 ◽

2021 ◽

Vol 2021 ◽

pp. 1-9

Author(s):

Tian Zhang ◽

Xingchen He ◽

Guodong Yu ◽

Zhixu He

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Nasopharyngeal Carcinoma ◽

Cell Lines ◽

Sh2 Domain ◽

Migration And Invasion ◽

Migration Assay ◽

Normal Tissues ◽

Delay Cell

Background. SHC SH2 domain-binding protein 1 (SHCBP1), one of the members of Src homolog and collagen homolog (Shc) family, has been reported to be overexpressed in several malignant cancers and involved in tumor progression. However, the expression of SHCBP1 in nasopharyngeal carcinoma (NPC) remains unclear, and its clinical significance remains to be further elucidated. Methods. The expression of SHCBP1 mRNA in 35 pair samples of NPC and adjacent normal tissues of NPC was detected by RT-qPCR. The expression level of SHCBP1 protein and mRNA in the selected cells was detected by western blot and RT-qPCR, respectively. The effects of SHCBP1 on NPC in vitro were observed by MTT method, colony formation assay, apoptosis assay, cell cycle assay, wound healing assay, transwell migration assay, and transwell invasion assay. Results. SHCBP1 was highly expressed in clinical tissues and NPC cell lines, and SHCBP1 knockdown significantly inhibited NPC cell proliferation. Overexpression of SHCBP1 promoted NPC cell proliferation, migration, and invasion in NPC cell lines. Silencing SHCBP1 expression can delay cell cycle and inhibit cell apoptosis. Conclusion. Our results suggest that SHCBP1 may promote proliferation and metastasis of NPC cells, which represents that SHCBP1 may act as a new indicator for predicting the prognosis of NPC and a new target for clinical treatment.

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SOX10 induces epithelial–mesenchymal transition and contributes to nasopharyngeal carcinoma progression

Biochemistry and Cell Biology ◽

10.1139/bcb-2017-0160 ◽

2018 ◽

Vol 96 (3) ◽

pp. 326-331 ◽

Cited By ~ 4

Author(s):

Ping He ◽

Xiaojie Jin

Keyword(s):

Cell Proliferation ◽

Nasopharyngeal Carcinoma ◽

Cell Lines ◽

Molecular Mechanisms ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Mesenchymal Transition

Objective: The aim of this study was to investigate the role of SOX10 in nasopharyngeal carcinoma (NPC) and the underlying molecular mechanisms. Methods: The expression of SOX10 was initially assessed in human NPC tissues and a series of NPC cell lines through quantitative real-time PCR (qRT-PCR) and Western blot. Then, cell proliferation, cycle, migration, and the invasiveness of NPC cells with knockdown of SOX10 were examined by MTT, flow cytometry, and Transwell migration and invasion assays, respectively. Finally, nude mice tumorigenicity experiments were performed to evaluate the effects of SOX10 on NPC growth and metastasis in vivo. Results: SOX10 was significantly increased in NPC tissues and cell lines. In-vitro experiments revealed that loss of SOX10 obviously inhibited cell proliferation, migration, and invasiveness, as well as the epithelial–mesenchymal transition (EMT) process in NPC cells. In-vivo experiments further demonstrated that disrupted SOX10 expression restrained NPC growth and metastasis, especially in lung and liver. Conclusion: Taken together, our data confirmed the role of SOX10 as an oncogene in NPC progression, and revealed that SOX10 may serve as a novel biomarker for diagnosis of NPC, as well as a potential therapeutic target against this disease.

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Enhanced expression of SETDB1 possesses prognostic value and promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma

Oncology Reports ◽

10.3892/or.2018.6490 ◽

2018 ◽

Cited By ~ 1

Author(s):

Jing Huang ◽

Weiyuan Huang ◽

Mei Liu ◽

Jianping Zhu ◽

Danxian Jiang ◽

...

Keyword(s):

Cell Proliferation ◽

Nasopharyngeal Carcinoma ◽

Prognostic Value ◽

Migration And Invasion ◽

Enhanced Expression

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MicroRNA-320a inhibits cell proliferation, migration and invasion by targeting BMI-1 in nasopharyngeal carcinoma

FEBS Letters ◽

10.1016/j.febslet.2014.08.021 ◽

2014 ◽

Vol 588 (20) ◽

pp. 3732-3738 ◽

Cited By ~ 43

Author(s):

Xiaoming Qi ◽

Jianqiang Li ◽

Changbo Zhou ◽

Chunlei Lv ◽

Min Tian

Keyword(s):

Cell Proliferation ◽

Nasopharyngeal Carcinoma ◽

Migration And Invasion

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Indole-thiazolidinone conjugate inhibits nasopharyngeal carcinoma cell migration and invasion by targeting NF κB pathway

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v18i3.11 ◽

2021 ◽

Vol 18 (3) ◽

pp. 519-525

Author(s):

Guoping Zhang ◽

Sheng Zhang

Keyword(s):

Cell Proliferation ◽

Nasopharyngeal Carcinoma ◽

Matrix Metalloproteinase ◽

Carcinoma Cells ◽

Matrix Metalloproteinase 2 ◽

Migration And Invasion ◽

Nuclear Fraction ◽

Invasion And Migration ◽

Migration Potential ◽

And Migration

Purpose: To investigate the effect of indole-thiazolidinone on metastasis in HK1 nasopharyngeal carcinoma cells. Methods: HK1 cell proliferation was determined colorimetrically using 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. Invasion and migration of HK1 cells were assessed using Matrigel™ chamber coated invasion and wound healing assays, respectively. Results: Indole-thiazolidinone suppressed proliferation of HK1 and NPC 039 NPC cell lines at 72 h. The degree of proliferation of HK1 cells on treatment with 0.25, 0.5, 1.0, 1.5, 2.0, 2.5 and 3.0 μM indolethiazolidinone was 99, 87, 71, 64, 49, 38 and 31 %, respectively. In HK1 cell cultures, migration potential was reduced to 58.32, 47.54, 28.91 and 17.65 %, on exposure to 1.5, 2.0, 2.5 and 3.0 μM indole-thiazolidinone, respectively. Incubation with 1.5, 2.0, 2.5 and 3.0 μM indole-thiazolidinone resulted in cell invasion values of 63.41, 49.37, 35.12 and 19.67 %, respectively. There was a marked decrease in the expressions of matrix metalloproteinase 2 and matrix metalloproteinase 9 in HK1 cells on treatment with indole-thiazolidinone (p < 0.05). In addition, indole-thiazolidinone treatment resulted in decrease in p65 and p50 in nuclear fraction. Treatment of HK1 and NPC 039 cells with indolethiazolidinone and henenalin synergistically decreased cell proliferation. Indole-thiazolidinone treatment caused significant decrease in tumor growth in mice (p < 0.05). Conclusion: Indole-thiazolidinone inhibits proliferation and metastasis in nasopharyngeal carcinoma cells. Therefore, it has potential for development as a therapeutic management of nasopharyngeal carcinoma in humans.

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