O-GlcNAc Regulated Proliferation and Deterioration of the Nasal Inverted Papilloma

Abstract Background: The nasal inverted papilloma occurs mostly in the epithelium of the nasal mucosa. Histopathological manifestations of the nasal inverted papilloma are benign but it has the characteristics of aggressive growth, strong local destruction, frequent recurrence, and malignant change. Nasal inverted papilloma is a tumor with malignant biological behavior. O-GLcNAc is a posttranslational modification that is ubiquitous in cells. This seemingly simple carbohydrate modification played a key role in cell physiology and disease progression. Methods: In this study, immunohistochemical staining and western blot were used to determine the expression of O-GlcNAc in the nasal inverted papilloma; RT-qPCR was used to detect the expression of ogt. The expression levels of ogt and oga genes were detected by RT-qPCR in the SCC6 and CNE-E1 cells. An ogt and oga small-interference RNA fragment was transfected into cells to both reduce and increase the O-GlcNAc. The effect of O-GlcNAc on the proliferative ability of cells was detected by CCK8. The migration and invasion of cells was detected by wound healing assay and transwell invasion assay. Results: The expression of O-GlcNAc and ogt mRNA levels in nasal inverted papilloma were higher than that in the control group. O-GlcNAc enhanced SCC6- and CNE-E1- cell proliferative, migratory, and invasive ability. This study found that changes in the glycosylation level of O-GLcNAc affected the proliferation, invasion, and migration of the NIP.

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Human Uterine Decidual NK Cells in Women with a History of Early Pregnancy Enhance Angiogenesis and Trophoblast Invasion

BioMed Research International ◽

10.1155/2020/6247526 ◽

2020 ◽

Vol 2020 ◽

pp. 1-7 ◽

Cited By ~ 1

Author(s):

Ningyi Jia ◽

Jian Li

Keyword(s):

Early Pregnancy ◽

Mrna Level ◽

Trophoblast Invasion ◽

Migration And Invasion ◽

Enzyme Linked Immunosorbent Assay ◽

Control Group ◽

Mrna Levels ◽

History Of ◽

And Migration ◽

Primiparous Women

Objective. The present study aimed to identify changes in decidual natural killer (dNK) cells and related cytokines in women who have undergone induced abortions (IAs). The effects of dNK cells on subsequent pregnancies remain unknown. Accordingly, we sought to investigate whether a history of early pregnancy can change dNK cells and facilitate their role in the regulation of angiogenesis and trophoblast invasion. Materials and Methods. dNK cells were obtained from primiparous women who had undergone IA(s) prior to this study and primiparous women who had never been pregnant before this IA (control). Real-time polymerase chain reaction (PCR) was used to measure the mRNA levels of IFN-γ, IP-10, VEGF, and PLGF in dNK cells. The levels of these cytokines were quantified using the enzyme-linked immunosorbent assay. HUVEC and HTR-8/SVneo cells were used to evaluate the angiogenesis, migration, and invasion activities influenced by dNK cells. Results. In dNK cells, the mRNA level of IFN-γ was higher in the control group than that in the IA group. The secretion of IP-10 and VEGF was higher in the IA group compared to the control group. After coculturing with the dNK supernatant, the HTR-8/SVneo cells exhibited better invasiveness and migration in the IA group than those in the control group. Angiogenesis assay demonstrated that dNK cells from IA group might help HUVEC attain better tube formation ability. Conclusion. The findings of this study suggest that a history of early pregnancy has an impact on dNK cells. These trained dNK cells can regulate angiogenesis and trophoblast invasion and migration by promoting the production of certain cytokines.

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Gypenosides inhibits migration and invasion of human oral cancer SAS cells through the inhibition of matrix metalloproteinase-2 -9 and urokinase-plasminogen by ERK1/2 and NF-kappa B signaling pathways

Human & Experimental Toxicology ◽

10.1177/0960327110372405 ◽

2010 ◽

Vol 30 (5) ◽

pp. 406-415 ◽

Cited By ~ 36

Author(s):

Kung-Wen Lu ◽

Jung-Chou Chen ◽

Tung-Yuan Lai ◽

Jai-Sing Yang ◽

Shu-Wen Weng ◽

...

Keyword(s):

Oral Cancer ◽

Matrix Metalloproteinase ◽

Cancer Cells ◽

Time Dependent ◽

Migration And Invasion ◽

Mrna Levels ◽

Dependent Manner ◽

Invasion And Migration ◽

Oral Cancer Cells ◽

And Migration

Gypenosides (Gyp), found in Gynostemma pentaphyllum Makino, has been used as a folk medicine in the Chinese population for centuries and is known to have diverse pharmacologic effects, including anti-proliferative and anti-cancer actions. However, the effects of Gyp on prevention from invasion and migration of oral cancer cells are still unsatisfactory. The purpose of this study was to investigate effects of Gyp treatment on migration and invasion of SAS human oral cancer cells. SAS cells were cultured in the presence of 90 and 180 μg/mL Gyp for 24 and 48 hours. Gyp induced cytotoxic effects and inhibited SAS cells migration and invasion in dose- and time-dependent response. Wound-healing assay and boyden chamber assay were carried out to investigate Gyp-inhibited migration and invasion of SAS cells. Gyp decreased the abundance of several proteins, including nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), extracellular signal-regulated kinase 1/2 (ERK1/ 2), matrix metalloproteinase-9, -2 (MMP-9, -2), sevenless homolog (SOS), Ras, urokinase-type plasminogen activator (uPA), focal adhesion kinase (FAK) and RAC-alpha serine/threonine-protein kinase (Akt), in a time-dependent manner. In addition, Gyp decreased mRNA levels of MMP-2, MMP-7, MMP-9 but did not affect FAK and Rho A mRNA levels in SAS cells. These results provide evidences for the role of Gyp as a potent anti-metastatic agent, which can markedly inhibit the metastatic and invasive capacity of oral cancer cells. The inhibition of NF-κB and MMP-2, -7 and -9 signaling may be one of the mechanisms that is present in Gyp-inhibited cancer cell invasion and migration.

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EPHA2 Promotes the Invasion and Migration of Human Tongue Squamous Cell Carcinoma Cal-27 Cells by Enhancing AKT/mTOR Signaling Pathway

BioMed Research International ◽

10.1155/2021/4219690 ◽

2021 ◽

Vol 2021 ◽

pp. 1-13

Author(s):

Fengqin Wang ◽

Hanzhong Zhang ◽

Zhigang Cheng

Keyword(s):

Cell Cycle ◽

Signaling Pathway ◽

Mtor Inhibitor ◽

Mtor Signaling ◽

Biological Behavior ◽

Migration And Invasion ◽

Mtor Signaling Pathway ◽

Akt Inhibitor ◽

Invasion And Migration ◽

And Migration

EPHA2 is a member of the ephrin receptor tyrosine kinase family and is closely related to the malignant tumor progression. The effect of EPHA2 on OSCC is not clear. This study explored the role of EPHA2 and AKT/mTOR signaling pathways in Cal-27 cell invasion and migration. The expression of EPHA2 and EPHA4 in human OSCC and normal oral tissue was detected by immunohistochemistry. EPHA2-overexpressing and EPHA2-knockdown Cal-27 cells were established, and the cells were treated with an AKT inhibitor (MK2206) and mTOR inhibitor (RAD001). The expression of EPHA2 was detected by qRT-PCR, cell proliferation was evaluated by MTT assay, cell migration and invasion were examined by scratch and Transwell assay, and cell morphology and apoptosis were assessed by Hoechst 33258 staining. Western blot was performed to detect the expression of proteins related to AKT/mTOR signaling, cell cycle, and pseudopod invasion. EPHA2 and EPHA4 were highly expressed in clinical human OSCC. Overexpression of EPHA2 promoted the proliferation, migration, and invasion of Cal-27 cells, inhibited cell cycle blockage and apoptosis, and enhanced the activity of the AKT/mTOR signaling pathway. MK2206 (AKT inhibitor) and RAD001 (mTOR inhibitor) reversed the effect of EPHA2 overexpression on the biological behavior of Cal-27 cells. EPHA2 promotes the invasion and migration of Cal-27 human OSCC cells by enhancing the AKT/mTOR signaling pathway.

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MiR-134, Mediated by IRF1, Suppresses Tumorigenesis and Progression by Targeting VEGFA and MYCN in Osteosarcoma

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520620666200402074752 ◽

2020 ◽

Vol 20 (10) ◽

pp. 1197-1208

Author(s):

Zhuo Ma ◽

Kai Li ◽

Peng Chen ◽

Qizheng Pan ◽

Xuyang Li ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Mrna Levels ◽

Invasion And Migration ◽

And Migration

Background: Osteosarcoma (OS) is a prevalent primary bone malignancy and its distal metastasis remains the main cause of mortality in OS patients. MicroRNAs (miRNAs) play critical roles during cancer metastasis. Objective: Thus, elucidating the role of miRNA dysregulation in OS metastasis may provide novel therapeutic targets. Methods: The previous study found a low miR-134 expression level in the OS specimens compared with paracancer tissues. Overexpression of miR-134 stable cell lines was established. Cell viability assay, cell invasion and migration assay and apoptosis assay were performed to evaluate the role of miR-134 in OS in vitro. Results: We found that miR-134 overexpression inhibits cell proliferation, migration and invasion, and induces cell apoptosis in both MG63 and Saos-2 cell lines. Mechanistically, miR-134 targets the 3'-UTR of VEGFA and MYCN mRNA to silence its translation, which was confirmed by luciferase-reporter assay. The real-time PCR analysis illustrated that miR-134 overexpression decreases VEGFA and MYCN mRNA levels. Additionally, the overexpression of VEGFA or MYCN can partly attenuate the effects of miR-134 on OS cell migration and viability. Furthermore, the overexpression of miR-134 dramatically inhibits tumor growth in the human OS cell line xenograft mouse model in vivo. Moreover, bioinformatic and luciferase assays indicate that the expression of miR-134 is regulated by Interferon Regulatory Factor (IRF1), which binds to its promoter and activates miR-134 expression. Conclusion: Our study demonstrates that IRF1 is a key player in the transcriptional control of miR-134, and it inhibits cell proliferation, invasion and migration in vitro and in vivo via targeting VEGFA and MYCN.

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The Mechanism of Human Umbilical Mesenchymal Stem Cells (HUMSC) on Biological Behavior of Human Papillomavirus (HPV) Cells Through Restraining the Programmed Cell Death Protein 1/Programmed Cell Death Ligand 1 (PD-1/PD-L1) Signal Pathway

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2022.2884 ◽

2022 ◽

Vol 12 (2) ◽

pp. 265-272

Author(s):

Min Wang ◽

Yanong Zhu ◽

Tongmin Li ◽

Chaofeng Xia

Keyword(s):

Cell Death ◽

Test Group ◽

Signal Pathway ◽

Biological Behavior ◽

Control Group ◽

Migration Ability ◽

Blank Group ◽

Invasion And Migration ◽

And Migration

Biological behavior of HPV cell was observed by HUMSC through restraining PD-1/PD-L1 signal pathway. And HUMSC was adopted as target cell for the treatment on HPV. The rat HPV model was established and divided into three groups including blank group, control group and test group according to different reagents being injected into rats. Use HE staining method to observe the cancerous transformation of tumor tissue sections. The gene presentation of PD-1/PD-L1 and lymphocyte was detected with Western blot. The invasion and migration condition of cancer cells was observed from experiment in vitro. The quantity of cancer cells in test group was the least. And invasion and migration ability in test group was the weakest. The control group was the second. The number of tumor cells in the blank group was the largest. Strongest ability to invade and migrate. The presentation of PD-L1 was restrained partly by HUMSC. The increasing of immune-associated cells could be prompted by HUMSC. The quantity of CD3+, CD4+ and CD8+ in PB was the most in test group. The expression of blank groups is the lowest than others restrained by HUMSC. And quantity of abundant immune cells including CD3+, CD4+ and CD8+ could be activated partly through activating immune action of body. And monitoring function of immune system on HPV cells could be increased effectively. The invasion and migration ability in vitro of HPV could be reduced partly.

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The Correlations between CXCL12, CXCR4, EAAT1 and GS in Malignant Pleural Mesothelioma, and CXCL12 Regulates Cell Invasion and Migration via CXCR4/EAAT1/GS Pathway

10.20944/preprints202009.0380.v1 ◽

2020 ◽

Author(s):

Shuo Li ◽

Tong Li ◽

Qiang Lin ◽

Debing Shi ◽

Haishi Zheng ◽

...

Keyword(s):

Malignant Pleural Mesothelioma ◽

Cell Invasion ◽

Mrna Level ◽

Migration And Invasion ◽

Pleural Mesothelioma ◽

Mrna Levels ◽

Cxcr4 Antagonist ◽

Invasion And Migration ◽

Normal Tissues ◽

And Migration

Purpose: To elucidate the mechanism of CXCR4/EAAT1/GS pathway in CXCL12 regulating invasion and migration in malignant pleural mesothelioma (MPM). Methods: Immunohistochemistry for CXCL12, CXCR4, EAAT1 and GS stainings and correlation analysis between them were conducted in MPM and normal tissues. Western blot and real-time PCR were performed to examine the CXCR4, EAAT1 and GS expression in H2052 cells. Wound healing and transwell assay were applied to determine the cell migration and invasion. MTT was utilized to assess cell viability. Results: CXCL12, CXCR4, EAAT1 and GS were highly expressed in MPM tissues and correlated with each other. CXCL12 upregulated both in protein and mRNA levels of CXCR4, EAAT1 and GS in H2052 cells. The EAAT1 and GS expression upregulated or not by CXCL12 were decreased by CXCR4 and EAAT1 knockdown. CXCR4 antagonist AMD3100 and EAAT1 antagonist TFB-TBOA also resulted in the same effects as CXCR4 and EAAT1 knockdown, respectively. CXCL12 promoted cell invasion and migration and increased the Matrix metalloproteinase 9 (MMP9) mRNA level. CXCR4 and EAAT1 knockdown suppressed all these functions. Furthermore, CXCL12 promoted H2052 cells growth in nude mice, both AMD3100 and TFB-TBOA inhibited this promotion. Conclusions: CXCL12 regulated the invasion and migration through CXCR4/EAAT1/GS pathway in H2052 cells.

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ANXA2 Silencing Inhibits Proliferation, Invasion, and Migration in Gastric Cancer Cells

Journal of Oncology ◽

10.1155/2019/4035460 ◽

2019 ◽

Vol 2019 ◽

pp. 1-13 ◽

Cited By ~ 3

Author(s):

Rui Xie ◽

Jia Liu ◽

Xuefeng Yu ◽

Chunfeng Li ◽

Yufeng Wang ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Cell Lines ◽

Biological Behavior ◽

Migration And Invasion ◽

Gastric Cancer Cells ◽

Ags Cells ◽

Invasion And Migration ◽

Ags Cell Line ◽

And Migration

Annexin A2 (ANXA2) has been well known to associate with the progress of malignant tumor. However, the biological behavior of ANXA2 in gastric cancer (GC) remains unclear. We made a hypothesis in transcriptome level from TCGA datasets. Then, we used immunohistochemical staining to quantify the expression level of ANXA2 protein in GC tissues compared with adjacent tissues. Quantitative real-time PCR and western blot were used for analyzing ANXA2 expression in human GC (SGC-7901, MKN-45, BGC-823, and AGS) cell lines. We investigated the effect of a lentivirus-mediated knock-down of ANXA2 on the proliferation, invasion and migration of gastric cancer AGS cells. Cell proliferation was examined by MTT and colony formation tests. Cell apoptosis and cycle were measured by flow cytometry. Migration and invasion were detected by transwell assay. We found that high expression of ANXA2 can increase the mobility of cancer cells from TCGA datasets. ANXA2 was upregulated in GC tissues compared with adjacent tissues. AGS cell line displayed significantly higher expression of ANXA2 among the four GC cell lines. In addition, ANXA2 silencing led to a weakened ability of proliferation, invasion, and migration in GC cells; targeting of ANXA2 may be a potential therapeutic strategy for GC patients.

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miR-21 down-regulation promotes apoptosis and inhibits invasion and migration abilities of OVCAR3 cells

Clinical & Investigative Medicine ◽

10.25011/cim.v34i5.15671 ◽

2011 ◽

Vol 34 (5) ◽

pp. 281 ◽

Cited By ~ 21

Author(s):

Yanhui Lou ◽

Zhumei Cui ◽

Fuling Wang ◽

Xingsheng Yang ◽

Jinhua Qian

Keyword(s):

Cell Proliferation ◽

Migration And Invasion ◽

Control Group ◽

Control Groups ◽

Down Regulation ◽

Transfected Cells ◽

Invasion And Migration ◽

Scratch Wound ◽

Scratch Wound Assay ◽

And Migration

Purpose: To investigate the influence of miR-21 down-regulation on cell proliferation, apoptosis, invasion and migration of ovarian papillary adenocarcinoma cell lines (OVCAR3). Methods: Short-hairpin RNA (shRNA), specifically targeting miR-21, was constructed and transfected into OVCAR3 cells using the pSIREN-RetroQ linear vector (pSIREN-miR-21). The expression of miR-21 was detected with stem-loop real-time RT-PCR in OVCAR3 cells. Cell proliferation and apoptosis were monitored using the MTT assay and flow cytometry, respectively. Cell migration and invasion were assessed using the transwell migration and scratch-wound assay, respectively. Western-bloting was used for PDCD4 protein expression. Results: pSIREN-miR-21 suppressed miR-21 expression in OVCAR3 cells. miR-21 expression levels in pSIREN-miR-21 cells was 0.3 ± 0.1, which was significantly lower when compared with pSIREN-miR-21-Neg and control groups (P < 0.01). Cell inhibition rate in the pSIREN-miR-21 group was higher than the control group (29.4% vs 9.0%, P < 0.01), as was the percentage of apoptotic and necrotic cells. By transwell migration assay, the number of cells migrating in the pSIREN-miR-21 group was significantly lower than in the control group. In addition, fewer cells were observed in the wounded area of the pSIREN-miR-21 group following the scratch-wound assay. PDCD4 expression was increased in OVCAR-3 cells transfected by pSIREN-miR-21 compared with vector-control transfected cells. Moreover, the optical density of the transfected cells was significantly lower than the two control groups.

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Long Non−Coding RNA H19 Regulates Glioma Cell Growth and Metastasis via miR-200a-Mediated CDK6 and ZEB1 Expression

Frontiers in Oncology ◽

10.3389/fonc.2021.757650 ◽

2021 ◽

Vol 11 ◽

Author(s):

Xuezhu Chen ◽

Yuhong Li ◽

Chenghai Zuo ◽

Kaiyuan Zhang ◽

Xuejiao Lei ◽

...

Keyword(s):

Cell Growth ◽

Target Genes ◽

Glioma Cells ◽

Biological Behavior ◽

Migration And Invasion ◽

Promote Cell Proliferation ◽

Invasion And Migration ◽

Non Coding Rna ◽

Underlying Mechanisms ◽

And Migration

Long non-coding RNAs (lncRNAs) serve essential roles on various biological functions. Previous studies have indicated that lncRNAs are involved in the occurrence, growth and infiltration of brain tumors. LncRNA H19 is key regulator in the pathogenesis of gliomas, but the underlying mechanisms of H19-regulated tumor progression remain unknown. Therefore, we investigated the effects and mechanism of action of lncRNA H19 on the homeostasis of glioma cells. As a novel oncogenic factor, up-regulation of H19 was able to promote the proliferation of glioma cells by targeting miR-200a. Furthermore, elevated miR-200a levels could reverse H19-induced cell growth and metastasis. Overexpression of miR-200a could significantly suppress the proliferation, migration and invasion of glioma cells. These biological behavior changes in glioma cells were dependent on the binding to potential target genes including CDK6 and ZEB1. CDK6 could promote cell proliferation and its expression was remarkably increased in glioma. In addition, up-regulation of miR-200a lead to reduction of CDK6 expression and inhibit the proliferation of glioma cells. ZEB1 could be a putative target gene of miR-200a in glioma cells. Thus, miR-200a might suppress cell invasion and migration through down-regulating ZEB1. Moreover, overexpression of miR-200a resulted in down-regulation of ZEB1 and further inhibited malignant phenotype of glioma cells. In summary, our findings suggested that the expression of H19 was elevated in glioma, which could promote the growth, invasion and migration of tumor cells via H19/miR-200a/CDK6/ZEB1 axis. This novel signaling pathway may be a promising candidate for the diagnosis and targeted treatment of glioma.

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Effects and Mechanisms of Anlotinib and Dihydroartemisinin Combination Therapy in Ameliorating Malignant Biological Behavior of Gastric Cancer Cells

Current Pharmaceutical Biotechnology ◽

10.2174/1389201021666200623132803 ◽

2020 ◽

Vol 21 ◽

Author(s):

Qiong Luo ◽

Suyun Zhang ◽

Donghuan Zhang ◽

Rui Feng ◽

Nan Li ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Molecular Mechanisms ◽

Chorioallantoic Membrane ◽

Cell Counting ◽

Biological Behavior ◽

Gastric Cancer Cells ◽

Invasion And Migration ◽

Apoptosis Related Protein ◽

And Migration

Background: Gastric cancer(GC) is currently one of the major malignancies that threatens human lives and health. Anlotinib is a novel small-molecule that inhibits angiogenesis to exert anti-tumor effects. However, the function in gastric cancer is incompletely understood. Objective: The aim of the present study was to investigate the anti-tumor effects and molecular mechanisms of anlotinib combined with dihydroartemisinin (DHA) in SGC7901 gastric cancer cells. Method: Different concentrations of anlotinib and DHA were used to treat SGC7901 gastric cancer cells, after which cell proliferation was measured. Drug interactions of anlotinib and DHA were analyzed by the Chou-Talalay method with CompuSyn software. proliferation, apoptosis, invasion, migration, and angiogenesis were measured using the cell counting kit-8 (CCK8) assay, flow cytometry, Transwell invasion assays, scratch assays, and chicken chorioallantoic membrane (CAM) assays. proliferation-associated protein (Ki67), apoptosis-related protein (Bcl-2), and vascular endothelial growth factor A (VEGF-A) were quantified by Western bloting. Results: The combination of 2.5 μmol/L of anlotinib and 5 of μmol/L DHA was highly synergistic in inhibiting cell growth, significantly increased the apoptosis rate and suppressed obviously the invasion and migration capability and angiogenesis of gastric cancer cells. In addition, the expression levels of Ki67, Bcl-2, and VEGF-A, as well as angiogenesis, were significantly decreased in the Combination of drugs compared with in control and either drug alone. Conclusion: The combination of anlotinib and DHA showed synergistic antitumor activity, suggesting their potential in treating patients with gastric cancer.

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