Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Galectin-3 gene silencing inhibits migration and invasion of human tongue cancer cells in vitro via downregulating β-catenin.

ABSTRACT: AIM: Galectin-3 (Gal-3) is a member of the carbohydrate-binding protein family that contributes to neoplastic transformation, tumor survival, angiogenesis, and metastasis. The aim of this study is to investigate the role of Gal-3 in human tongue cancer progression. METHODS: Human tongue cancer cell lines (SCC-4 and CAL27) were transfected with a small-interfering RNA against Gal-3 (Gal-3-siRNA). The migration and invasion of the cells were examined using a scratch assay and BD BioCoat Matrigel Invasion Chamber, respectively. The mRNA and protein levels of β-catenin, Akt/pAkt, GSK-3β/pGSK-3β, MMP-9 in the cells were measured using RT-PCR and Western blotting, respectively. RESULTS: Transient silencing of Gal-3 gene for 48 h significantly suppressed the migration and invasion of both SCC-4 and CAL27 cells. Silencing of Gal-3 gene significantly decreased the protein level of β-catenin, leaving the mRNA level of β-catenin unaffected. Furthermore, silencing Gal-3 gene significantly decreased the levels of phosphorylated Akt and GSK-3β, and suppressed the mRNA and protein levels of MMP-9 in the cells. CONCLUSION: Our data suggest that Gal-3 mediates the migration and invasion of tongue cancer cells in vitro via regulating the Wnt/β-catenin signaling pathway and Akt phosphorylation.

SUBMITTER: Zhang D

PROVIDER: S-EPMC4086502 | biostudies-other | 2013 Jan

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Transient gene silencing of galectin-3 suppresses pancreatic cancer cell migration and invasion through degradation of ?-catenin.

Project description:Pancreatic cancer is a leading cause of cancer-related mortality and often has a poor prognosis because of its late diagnosis, aggressive local invasion, early metastasis and poor response to chemotherapy. The chemotherapeutic agent gemcitabine is effective for treating advanced pancreatic cancer, but its efficacy remains less than satisfactory. It is expected that further investigation of pancreatic cancer cell invasion and development of strategies to block this process should improve the disease prognosis. In this study, we tested our hypothesis that galectin-3 (gal-3), a multifunctional member of the ?-galactoside-binding protein family, may regulate pancreatic cancer cell motility and silencing of it inhibit cell motility. Previous studies demonstrated that this protein is associated with tumor cell adhesion, proliferation, differentiation, angiogenesis, apoptosis and metastasis. Here, we used gal-3 small interfering RNA (siRNA) to silence its expression in various pancreatic cancer cell lines to determine whether gal-3 regulates cell proliferation, migration and invasion in vitro. We found that silencing gal-3 reduced cellular migration and invasion, but failed to affect proliferation. In gal-3 siRNA-transfected cells, we detected a decrease in ?-catenin expression, an important signal for cancer cell invasion, which was caused by downregulation of phosphorylated Akt and GSK-3?. We also found that matrix metalloproteinase (MMP)-2 expression was reduced by gal-3 silencing. These results indicate that gal-3-mediated invasion via MMP-2 regulated by ?-catenin degradation is initiated by Akt phosphorylation in pancreatic cancer cells. Our results suggest that gal-3 can be a novel therapeutic target in pancreatic cancer.

| S-EPMC3833077 | biostudies-literature

miR-34a inhibits migration and invasion of tongue squamous cell carcinoma via targeting MMP9 and MMP14.

Project description:BackgroundmiR-34a is an important tumor suppressor gene in various cancer types. But little is known about the dysregulation of miR-34a in tongue squamous cell carcinoma (TSCC). In this study, we investigate the expression and potential role of miR-34a in TSCC.MethodsWe evaluated miR-34a expression and its relationship with clinicopathological characters in 75 pairs of TSCC samples, and confirmed the role of miR-34a for predicting lymph node metastases from a further 15 pairs of paraffin-embedded TSCC specimens with stringent clinicopathological recruitment criteria using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The effects of miR-34a on cell proliferation, migration and invasion were examined in TSCC cell lines using Cell Counting Kit-8 assay, wound healing assay and transwell assay, respectively. The effects of miR-34a on the expression of matrix metalloproteinase (MMP) 9 and 14 were detected by luciferase reporter assays and Western blot analysis. The expression of miR-34a, MMP9 and MMP14 were also confirmed in TSCC samples by in situ hybridization and immunohistochemistry.ResultsmiR-34a expression in tumor tissues from TSCC patients with positive lymph node metastases was significantly lower than that with negative lymph node metastases. Overexpression of miR-34a significantly suppressed migration and invasion in TSCC cells and simultaneously inhibited the expression of MMP9 and MMP14 through targeting the coding region and the 3'untranslated region, respectively. Moreover, miR-34a expression in TSCC was inversely correlated with protein expression of MMP9 and MMP14 in the TSCC samples.ConclusionsmiR-34a plays an important role in lymph node metastases of TSCC through targeting MMP9 and MMP14 and may have potential applications in prognosis prediction and gene therapy for lymph node metastases of TSCC patients.

| S-EPMC4182478 | biostudies-literature

Ubiquitin carboxyl-terminal hydrolase isozyme L5 inhibits human glioma cell migration and invasion via downregulating SNRPF.

Project description:Ubiquitin C-terminal Hydrolase-L5 (UCH-L5/UCH37), a member of the deubiquitinases (DUBs), suppresses protein degeneration via removing ubiquitin from the distal subunit of the polyubiquitin chain. The activity of UCH-L5 is enhanced when UCH-L5 combines with proteasome 19S regulatory subunit by Rpn13/Admr1 receptor and inhibited when UCH-L5 interacts with NFRKB. But the role of UCH-L5 in gliomas remains unknown. In this study, analysis of 19 frozen and 51 paraffin-embedded clinic pathological cases showed that UCH-L5 expression in glioma tissues was lower than normal brain tissues. In vitro, we found that UCH-L5 could inhibit migration and invasion of U87MG and U251 cells. It has been reported that the expression of SNRPN, SNRPF, and CKLF was abnormal in gliomas or other tumors. We also found that SNRPF-siRNA, SNRPN-siRNA and CKLF-siRNA could inhibit migration and invasion of U87MG cells. And knockdown of UCH-L5 expression improved both mRNA expression and protein level of SNRPF. The relationship between UCH-L5 and SNRPF was further confirmed in 293T cells. Our study showed that UCH-L5 could inhibit migration and invasion of glioma cells via down regulating expression of SNRPF. And the above findings suggest that UCH-L5 may inhibit occurrence and metastasis of gliomas.

| S-EPMC5768352 | biostudies-literature

Let-7i-3p inhibits the cell cycle, proliferation, invasion, and migration of colorectal cancer cells via downregulating CCND1.

Project description:Dysregulated microRNAs are closely related to the malignant progression of colorectal cancer (CRC). Although abnormal let-7i-3p expression has been reported in various human cancers, its biological role and potential mechanism in CRC remain unclear. Therefore, the purpose of this study was to investigate the expression and regulation of let-7i-3p in CRC. Here, we demonstrated that let-7i-3p expression was significantly downregulated in three CRC cell lines while CyclinD1 (CCND1) was upregulated compared with the normal colon epithelial FHC cells. Moreover, bioinformatics and luciferase reporter assays revealed that CCND1 was a direct functional target of let-7i-3p. In addition, let-7i-3p overexpression or CCND1 silencing inhibited cell cycle, proliferation, invasion, and migration and diminished the activation of p-ERK in HCT116 cells. However, exogenously expressing CCND1 alleviated these effects. Taken together, our findings may provide new insight into the pathogenesis of CRC and let-7i-3p/CCND1 might function as new therapeutic targets for CRC.

| S-EPMC9175015 | biostudies-literature

CD63 inhibits the cell migration and invasion ability of tongue squamous cell carcinoma.

Project description:The present study evaluated the expression and potential role of CD63 in the migration and invasion of tongue squamous cell carcinoma (TSCC) cells. Immunohistochemistry (IHC) was used to investigate the association between the expression level of CD63 protein and the histological differentiation of samples from 40 patients with TSCC and four normal tongue tissue specimens. RNA interference (RNAi) and gene transfection technology were used to alter the expression of CD63 in TCA8113 cells. The stable silencing and overexpression of CD63 in the TCA8113 cell line was used to assess the impact of the CD63 expression level on the migratory and invasive abilities of TCA8113 cells in a wound healing assay and a Transwell invasion assay. The effect of CD63 on the expression of matrix metalloproteinase (MMP)-2 and -9 were evaluated by western blot analysis. The results of IHC revealed a positive association between the CD63 expression level and the histopathological differentiation of TSCC and a negative association between the CD63 expression level and lymph node metastasis in TSCC. Western blotting revealed that the expressions of MMP-2 and MMP-9 were clearly upregulated in CD63-silenced TCA8113 cells but reduced in CD63-overexpressing TCA8113 cells, compared with the control. The wound-healing speed and the number of cells invading Matrigel-coated filters were negatively associated with the CD63 expression level. In summary, the results of the present study revealed that CD63 may be an inhibitor of TSCC malignancy and lymph node metastasis and may have applications in the prediction of prognosis and gene therapy for patients of TSCC.

| S-EPMC5958804 | biostudies-literature

KLF2 Inhibits the Migration and Invasion of Prostate Cancer Cells by Downregulating MMP2.

Project description:KLF2, a member of the Kruppel-like factor (KLF) family, is thought to be a tumor suppressor in many kinds of malignant tumors. Its functions in prostate cancer (PCa) are unknown. This study aimed to explore the role of KLF2 in the migration and invasion of PCa cells. The expression of KLF2 was measured by immunohistochemistry in PCa tissues and in paired non-tumor tissues. KLF2 and MMP2 expression in cells was measured by Western blot and RT-qPCR. Adenoviruses and siRNAs were used in cell function tests to investigate the role of KLF2 in regulating MMP2. Interactions between KLF2 and MMP2 were analyzed by a luciferase activity assay. The present study, for the first time, identified that KLF2 was downregulated both in PCa clinical tissue samples and in cancer cell lines. The overexpression of KLF2 inhibited the migration and invasion of PCa cells via the suppression of MMP2.This study demonstrates that KLF2 might act as a tumor suppressor gene in PCa and that the pharmaceutical upregulation of KLF2 may be a potential approach for treatment.

| S-EPMC6775556 | biostudies-literature

NT157 Inhibits HCC Migration via Downregulating the STAT3/Jab1 Signaling Pathway.

Project description:PurposeThe high fatality-to-case ratio of hepatocellular carcinoma is directly related to metastasis. The signal transducer and activator of transcription-3 is a key mediator of the cytokine and growth factor signaling pathways and drives the transcription of genes responsible for cancer-associated phenotypes. However, so far, no specific inhibitor for signal transducer and activator of transcription-3 has been used in clinical practice. Therefore, targeting the signal transducer and activator of transcription-3 for cancer therapy is highly desired to improve outcomes in patients with hepatocellular carcinoma.Experimental designUsing the small-molecule inhibitor NT157, the effect of signal transducer and activator of transcription-3 inhibition on cell migration was tested in hepatocellular carcinoma cell lines and a lung metastasis model of the disease.ResultsNT157 significantly inhibited the migration of hepatocellular carcinoma cell lines in vitro and lung metastasis of hepatocellular carcinoma in vivo. Mechanistically, it inhibited the phospho-signal transducer and activator of transcription-3 in a dose- and time-dependent manner. Furthermore, NT157 treatment suppressed the c-Jun activation domain-binding protein-1 levels in the nucleus but no significant decrease was observed in its expression in the cytoplasm. Finally, high mRNA expression levels of signal transducer and activator of transcription-3 and c-Jun activation domain-binding protein-1 in hepatocellular carcinoma were associated with significantly low survival rates.ConclusionNT157 inhibits hepatocellular carcinoma migration and metastasis by downregulating the signal transducer and activator of transcription-3/c-Jun activation domain-binding protein-1 signaling pathway and targeting it may serve as a novel therapeutic strategy for the clinical management of hepatocellular carcinoma in the future.

| S-EPMC8274079 | biostudies-literature

GATA1 gene silencing inhibits invasion, proliferation and migration of cholangiocarcinoma stem cells via disrupting the PI3K/AKT pathway.

Project description:Background/aims: Intrahepatic cholangiocarcinoma (CCA) is the second most prevalent type primary liver malignancy, accompanied by an increasing global incidence and mortality rate. Research has documented the contribution of the GATA binding protein-1 (GATA1) in the progression of liver cancer. Here, we aim to investigate the role of GATA1 in CCA stem cells via the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway. Methods: Initially, microarray-based gene expression profiling was employed to identify the differentially expressed genes associated with CCA. Subsequently, an investigation was conducted to explore the potential biological significance behind the silencing of GATA1 and the regulatory mechanism between GATA1 and PI3K/AKT pathway. CCA cell lines QBC-939 and RBE were selected and treated with siRNA against GATA1 or/and a PI3K/AKT pathway inhibitor LY294002. In vivo experiment was also conducted to confirm in vitro findings. Results: GATA1 exhibited higher expression in CCA samples and was predicted to affect the progression of CCA through blockade of the PI3K/AKT pathway. siRNA-mediated downregulation of GATA1 and LY294002 treatment resulted in reduced proliferation, migration and invasion abilities of CCA stem cells, together with impeded tumor growth, and led to increased cell apoptosis and primary cilium expression. Additionally, the siRNA-mediated GATA1 downregulation had an inhibitory effect on the PI3K/AKT pathway. LY294002 was manifested to enhance the inhibitory effects of GATA1 inhibition on CCA progression. These in vitro findings were reproduced in vivo on siRNA against GATA1 or LY294002 injected nude mice. Conclusion: Altogether, the present study highlighted that downregulation of GATA1 via blockade of the PI3K/AKT pathway could inhibit the CCA stem cell proliferation, migration and invasion, and tumor growth, and promote cell apoptosis, primary cilium expression.

| S-EPMC6620705 | biostudies-literature

Ailanthone Inhibits Proliferation, Migration and Invasion of Osteosarcoma Cells by Downregulating the Serine Biosynthetic Pathway

Project description:Osteosarcoma (OS) is a life-threatening disease affecting mainly children and adolescents, it is urgently needed to find novel anticancer agents against it. In the present study, we demonstrated that Ailanthone (AIL), a major component of the Chinese medicine Ailanthus altissima, significantly suppressed cell growth, inhibited cell migration and invasion, induced cell cycle arrest instead of apoptosis in OS cells. Mechanistically, combined transcriptomics, proteomics and metabolomics analyses revealed that AIL induced widespread changes in metabolic programs in OS cells, while the serine biosynthetic pathway was the most significantly affected pathway. The results were verified by reverse test. Metabolic reprogramming is an essential hallmark of malignancy including OS. Our findings suggest that AIL holds a great potential to be an OS treatment strategy through mediating metabolic reprogramming.

2022-01-01 | GSE190238 | GEO

Overexpression of lncRNA NLIPMT Inhibits Colorectal Cancer Cell Migration and Invasion by Downregulating TGF-?1.

Project description:Background:NLIPMT, as a tumor suppressive lncRNA, has only been investigated in breast cancer, while its roles in other types of cancer remain unknown. This study aimed to explore the role of NLIPMT in colorectal cancer (CRC). Methods:Expression levels of NLIPMT and TGF-?1 in two types of CRC tissue (Non-tumor tissues and tumor tissues) were measured and compared by qRT-PCR and paired t-test, respectively. Correlations between the expression of NLIPMT and TGF-?1 were analyzed by performing linear regression. The effects of transfections on cell invasion and migration were evaluated by Transwell assays. Results:We found that NLIPMT was downregulated, while TGF-?1 was upregulated in CRC. In CRC tumor, a negative correlation was found between the expression of NLIPMT and TGF-?1. In CRC cells, overexpression of NLIPMT resulted in downregulation, while silencing of NLIPMT resulted in upregulation of TGF-?1. Analysis of cell invasion and migration showed that overexpression of NLIPMT suppressed the tumor cell invasion and migration. In contrast, overexpression of TGF-?1 could promote CRC cell invasion and migration and also reduce the role of NLIPMT. Through the overall survival evaluation, NLIPMT-high groups of CRC represented better survival rate compared to that of the NLIPMT-low group patients. Conclusion:The expression of lncRNA NLIPMT was negatively correlated with TGF-?1 in CRC. Overexpression of NLIPMT inhibited the colorectal cancer cell migration and invasion by downregulating TGF-?1. Furthermore, the expression of NLIPMT in CRC patients predicted better prognosis, which suggested that NLIPMT could be considered as a novel diagnosis biomarker.

| S-EPMC7381797 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data