Anti-tumor effects of differentiation-inducing factor-1 in malignant melanoma: GSK-3-mediated inhibition of cell proliferation and GSK-3-independent suppression of cell migration and invasion

2017 ◽  
Vol 138 ◽  
pp. 31-48 ◽  
Author(s):  
Masaki Arioka ◽  
Fumi Takahashi-Yanaga ◽  
Momoko Kubo ◽  
Kazunobu Igawa ◽  
Katsuhiko Tomooka ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Malignant Melanoma ◽  
Migration And Invasion ◽  
Cell Migration And Invasion

scholarly journals Study of LBHD1 Expression with Invasion and Migration of Bladder Cancer

2019 ◽  
Vol 14 (1) ◽  
pp. 440-447
Author(s):  
Chunhui Dong ◽  
Yihui Liu ◽  
Guiping Yu ◽  
Xu Li ◽  
Ling Chen
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Tumor Antigens ◽  
Urinary Bladder Cancer ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Invasion And Migration ◽  
Bladder Cancer Cells

AbstractLBHD1 (C11ORF48) is one of the ten potential tumor antigens identified by immunoscreening the urinary bladder cancer cDNA library in our previous study. We suspect that its expression is associated with human bladder cancer. However, the exact correlation remains unclear. To address the potential functional relationship between LBHD1 and bladder cancer, we examined the LBHD1 expression at the mRNA and protein level in 5 different bladder cancer cell lines: J82, T24, 253J, 5637, and BLZ-211. LBHD1 high and low expressing cells were used to investigate the migration, invasion, and proliferation of bladder cancer cells following transfection of LBHD1 with siRNA and plasmids, respectively. Our experiment showed that the degree of gene expression was positively related to the migration and invasion of the cancer cells while it had little effect on cell proliferation. Knocking down LBHD1 expression with LBHD1 siRNA significantly attenuated cell migration and invasion in cultured bladder cancer cells, and overexpressing LBHD1 with LBHD1 cDNA plasmids exacerbated cell migration and invasion. Nevertheless, a difference in cell proliferation after transfection of LBHD1 siRNA and LBHD1 cDNA plasmids was not found. Our findings suggest that LBHD1 might play a role in cell migration and invasion.

scholarly journals ANLN Promotes Cell Migration and Invasion Through RhoA-ROCK Signaling in Cervical Cancer

2021 ◽  
Author(s):  
Congzhe Hou ◽  
Zhen Liang ◽  
Yongxia Yang ◽  
Yunhai Yu ◽  
Tingting Liang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Stress Fiber ◽  
Actin Binding ◽  
Migration And Invasion ◽  
Actin Stress Fiber ◽  
Western Blots ◽  
Expression Levels ◽  
Cell Migration And Invasion

IntroductionAnillin actin binding protein (ANLN) is involved in various human cancers. It is often upregulated in various cancers, including cervical cancer (CC). however, the exact role of ANLN in the modulation of CC and the underlying molecular mechanism remain unknown. In this study, we aimed to investigate the effects of ANLN on the proliferation, migration, and invasion of CC cells, as well as determine the molecular mechanisms underlying these effects.Material and methodsANLN expression levels were analyzed in normal cervical and CC specimens using public databases and tissue samples. The prognosis was determined using TCGA database. Cell proliferation, migration and invasion were measured by Edu assay, wound-healing assay and transwell assay, respectively. Immunofluorescence was used to examined the influence actin stress fiber integrity caused by ANLN inhibition. Western blots were used to measure the protein expression.ResultsANLN expression levels in CC were higher than those in normal tissues, and ANLN overexpression was highly correlated with poor prognosis. ANLN knockdown inhibited CC cell proliferation, migration, and invasion in vitro, while ANLN overexpression exerted an inverse biological phenotype. Immunofluorescence showed that ANLN inhibition could influence actin stress fiber integrity. ANLN expression was positively correlated with ROCK1 and ROCK2 expression in CC. Overexpression of ANLN activated RhoA and upregulated ROCK1 and ROCK2. Furthermore, ROCK1 and ROCK2 expression levels were also impeded by Y27632, which is a specific inhibitor of RhoA. They also weakened the migration and invasion ability in ANLN overexpression HeLa cells.ConclusionsANLN promotes cell migration and invasion through RhoA-ROCK signaling in CC.

scholarly journals Acetyl-CoA Synthetase 2 Promotes Cell Migration and Invasion of Renal Cell Carcinoma by Upregulating Lysosomal-Associated Membrane Protein 1 Expression

2018 ◽  
Vol 45 (3) ◽  
pp. 984-992 ◽  
Author(s):  
Lv Yao ◽  
Xiaoqiang Guo ◽  
Yaoting Gui
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Lipid Metabolism ◽  
Western Blotting ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Acetyl Coa ◽  
Cell Migration And Invasion ◽  
Qrt Pcr

Background/Aims: Reprogramming energy metabolism is an emerging hallmark of many cancers, and this alteration is especially evident in renal cell carcinomas (RCCs). However, few studies have been conducted on lipid metabolism. This study investigated the function and mechanism of lipid metabolism-related acetyl-CoA synthetase 2 (ACSS2) in RCC development, cell migration and invasion. Methods: Quantitative real-time PCR (qRT-PCR) was used to determine the expression of ACSS2 in cancer tissue and adjacent tissue. The inhibition of ACSS2 expression was achieved by RNA interference, which was confirmed by qRT-PCR and Western blotting. Cell proliferation and apoptosis were detected by a CCK8 assay and a flow cytometry analysis, respectively. Cell migration and invasion were determined by the scratch and transwell assays. Following the knockdown of ACSS2 expression, the expression of the autophagy-related factor LAMP1 was measured by qRT-PCR and Western blotting. Results: Compared to adjacent tissues, ACSS2 expression was upregulated in RCC cancer tissues and positively correlated with metastasis. Inhibition of ACSS2 had no effect on RCC cell proliferation or apoptosis. However, decreased ACSS2 expression was found to inhibit RCC cell migration and invasion. ACSS2 was determined to promote the expression of LAMP1, which can also promote cell migration. This pathway may be considered a potential mechanism through which ACSS2 participates in RCC development. Conclusion: These data suggest that ACSS2 is an important factor for promoting RCC development and is essential for cell migration and invasion, which it promotes by increasing the expression of LAMP1. Taken together, these findings reveal a potential target for the diagnosis and treatment of RCC.

MiR-375 Enriched in Bone Marrow Mesenchymal Stem Cells (BMSC) Exosomes Inhibits Prostate Cancer Cell Migration and Invasion by Down-Regulating Trefoil Factor 3 (TFF3)

2021 ◽  
Vol 11 (12) ◽  
pp. 2407-2414
Author(s):  
Qihong Liang ◽  
Wei Zhong
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Clinical Samples ◽  
Cell Migration And Invasion ◽  
Marrow Mesenchymal Stem Cells ◽  
Proliferation And Metastasis

To study the effect and mechanism of miR-375 enriched in BMSC exosomes on prostate cancer (PC) cells. Bioinformatics assessed the potential regulatory miRNA of TFF3 and miR-375 level in breast cancer cells and breast cancer clinical samples was detected by PCR. Dual luciferase assay validated the relationship between TFF3 and miR-375. miR-375 mimics or sh-TFF3 was transfected into PC cells, followed by measuring miR-375 and TFF3 by PCR and Western-blot. Cell proliferation, invasion, migration and apoptosis by Edu staining, transwell and flow cytometry. The BMSC exosomes were then isolated and co-cultured with PC cells to detect cell proliferation and invasion. PC cells and tissues showed the expression of miR-375 was decreased, indicated that miR-375 specifically inhibited TFF3 level. miR-375 was enriched in MSC-derived exosomes and could be transferred to PC cells. miR-375 mimics, exosome miR-375 or silenced TFF3 inhibited TFF3 level, up-regulated PCNA, MMP-2/9 expression, thereby inhibiting cell proliferation and metastasis, and promoting cell apoptosis. miR-375 is enriched in BMSC exosomes and inhibits PC cell migration and invasion by reducing TFF3.

scholarly journals Broussoflavonol B from Broussonetia kazinoki Siebold Exerts Anti-Pancreatic Cancer Activity through Downregulating FoxM1

Molecules ◽  
2020 ◽  
Vol 25 (10) ◽  
pp. 2328
Author(s):  
Ji Hye Jeong ◽  
Jae-Ha Ryu
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cellular Proliferation ◽  
Cyclin B1 ◽  
Human Pancreatic Cancer ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Cancer Activity

Pancreatic cancer has a high mortality rate due to poor rates of early diagnosis. One tumor suppressor gene in particular, p53, is frequently mutated in pancreatic cancer, and mutations in p53 can inactivate normal wild type p53 activity and increase expression of transcription factor forkhead box M1 (FoxM1). Overexpression of FoxM1 accelerates cellular proliferation and cancer progression. Therefore, inhibition of FoxM1 represents a therapeutic strategy for treating pancreatic cancer. Broussoflavonol B (BF-B), isolated from the stem bark of Broussonetia kazinoki Siebold has previously been shown to inhibit the growth of breast cancer cells. This study aimed to investigate whether BF-B exhibits anti-pancreatic cancer activity and if so, identify the underlying mechanism. BF-B reduced cell proliferation, induced cell cycle arrest, and inhibited cell migration and invasion of human pancreatic cancer PANC-1 cells (p53 mutated). Interestingly, BF-B down-regulated FoxM1 expression at both the mRNA and protein level. It also suppressed the expression of FoxM1 downstream target genes, such as cyclin D1, cyclin B1, and survivin. Cell cycle analysis showed that BF-B induced the arrest of G0/G1 phase. BF-B reduced the phosphorylation of extracellular signal-regulated kinase ½ (ERK½) and expression of ERK½ downstream effector c-Myc, which regulates cell proliferation. Furthermore, BF-B inhibited cell migration and invasion, which are downstream functional properties of FoxM1. These results suggested that BF-B could repress pancreatic cancer cell proliferation by inactivation of the ERK/c-Myc/FoxM1 signaling pathway. Broussoflavonol B from Broussonetia kazinoki Siebold may represent a novel chemo-therapeutic agent for pancreatic cancer.

scholarly journals Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Shihua Ding ◽  
Shaohui Tang ◽  
Min Wang ◽  
Donghai Wu ◽  
Haijian Guo
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Sw620 Cells ◽  
Role Of It

Background and Aims. Acyl-CoA synthetase 5 (ACS5) has been reported to be associated with the development of various cancers, but the role of it in colorectal cancer (CRC) is not well understood. The present study aimed to explore the potential role of ACS5 in the development and progression of CRC. Methods. ACS5 expression in CRC tissues and CRC cell lines was examined, and its clinical significance was analyzed. The role of ACS5 in cell proliferation, apoptosis, and invasion was examined in vitro. Results. We found that ACS5 expression was upregulated in CRC cells and CRC tissues and that high ACS5 expression was more frequent in CRC patients with excess muscular layer and with poor tumor differentiation. Furthermore, knockdown of ACS5 in HT29 and SW480 cells significantly dampened cell proliferation, induced cell apoptosis, and reduced cell migration and invasion. In contrast, the ectopic overexpression of ACS5 in LOVO and SW620 cells remarkably promoted cell proliferation, inhibited cell apoptosis, and enhanced cell migration and invasion. Enhanced cell growth and invasion ability mediated by the gain of ACS5 expression were associated with downregulation of caspase-3 and E-cadherin and upregulation of survivin and CD44. Conclusions. Our data demonstrate that ACS5 can promote the growth and invasion of CRC cells and provide a potential target for CRC gene therapy.

scholarly journals Inhibition of Proliferation, Migration, and Invasion by Knockdown of Pyruvate Kinase-M2 (PKM2) in Ovarian Cancer SKOV3 and OVCAR3 Cells

2016 ◽  
Vol 24 (6) ◽  
pp. 463-475 ◽  
Author(s):  
Yi Miao ◽  
Meng Lu ◽  
Qin Yan ◽  
Shuangdi Li ◽  
Youji Feng
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Pyruvate Kinase ◽  
Biological Behavior ◽  
Phase Cell ◽  
Migration And Invasion ◽  
Cell Cycle Distribution ◽  
Inhibition Of Proliferation ◽  
Cell Migration And Invasion

Pyruvate kinase (PK) is a key enzyme in the process of glycolysis, catalyzing phosphoenolpyruvate (PEP) into pyruvate. Currently, PK isozyme type M2 (PKM2), one subtype of PK, has been proposed as a new tumor marker with high expression in various tumor tissues. Here we aimed to explore the effects of siRNA-PKM2 on ovarian carcinoma (OC) cell lines SKOV3 and OVCAR3, in which PKM2 was notably expressed. PKM2 gene interference lentivirus vectors were built by miRNA transfection assay. siRNA-PKM2-transfected SKOV3 and OVCAR3 cells were evaluated for cell proliferation, cell cycle distribution, cell apoptosis, cell migration, and invasion in this study. In addition, the expression levels of several tumor-related genes were measured using real-time PCR and Western blot. Results showed that siRNA-PKM2 markedly inhibited cell proliferation, induced apoptosis, and caused cell cycle arrest at the G0/G1 phase. Cell migration and invasion were significantly suppressed by siRNA-PKM2. Furthermore, the tumor-related genes caspase 7, Bad, and E-cadherin were upregulated, while MMP2, HIF1α, VEGF, and MMP9 were depressed by siRNA-PKM2. The function of siRNA-PKM2 on the biological behavior of OC cells indicated that PKM2 may also be a target for treatment of OC.

scholarly journals SPAG5 Is Involved in Human Gliomagenesis Through the Regulation of Cell Proliferation and Apoptosis

2021 ◽  
Vol 11 ◽  
Author(s):  
Chunhong Wang ◽  
Haiyang Su ◽  
Rui Cheng ◽  
Hongming Ji
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Colony Formation ◽  
Glioma Cells ◽  
Clinical Intervention ◽  
Primary Brain Tumor ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Proliferation And Apoptosis

BackgroundGlioma is the most frequent malignant primary brain tumor in adults.ObjectiveTo explore the role of sperm-associated antigen 5 (SPAG5) in glioma.MethodsThe association between SPAG5 expression and clinical features was investigated based on The Cancer Genome Atlas (TCGA) datasets. The function of SPAG5 in glioma was analyzed using U87 and U251 cells. Knockdown glioma cells were constructed by shRNA interference. qRT-PCR and Western blotting were used to measure the expression of SPAG5 and Cadherin 2 (CDH2). Cell proliferation and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, caspase 3/7 assay, and high-content screening (HCS) proliferation analysis and colony formation assay. Transwell assays and wound-healing assays were used to investigate cell migration and invasion.ResultsThe increased expression of SPAG5 was correlated with poor outcomes in glioma patients. Knocking down SPAG5 could inhibit the proliferation and colony formation and promoted the apoptosis of glioma cells. Knocking down SPAG5 could also inhibit cell migration and invasion and the expression of CDH2. Overexpression of CDH2 with SPAG5 depletion could restore the proliferation and inhibit the apoptosis of glioma cells, which also promoted cell migration and invasion.ConclusionsSPAG5 is a promising prognostic factor and potential therapeutic target for clinical intervention in glioma.

scholarly journals Effect of p21-activated kinase 1 inhibition on proliferation, migration and invasion of glioma

2020 ◽  
Author(s):  
Qinghao Yi ◽  
Tianze Chen ◽  
Kunlin Zhou ◽  
Qiang Ma ◽  
Zhiyuan Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Tumor Formation ◽  
Migration And Invasion ◽  
Cell Cycle Distribution ◽  
Cell Migration And Invasion ◽  
Protein Levels ◽  
Orthotopic Xenograft ◽  
Glioma Model ◽  
High Level

Abstract Background: Abnormally expressed the p21-activated kinases (PAKs) are implicated in the development and treatment of glioma. Previous study has reported that PAK1 is expressed in glioma. However, the role and mechanism of PAK1 in glioma progression remain unclear.Methods: Western blotting was employed to detect the expression of PAK1 in human glioma tissues. CCK-8, EdU and colony formation assay were applied to evaluate the effect of PAK1 inhibition on cell proliferation of glioma. The flow cytometry was utilized to examine the cell cycle distribution and apoptotic rate of glioma. Wound healing and transwell assay were exploited to investigate the effect of PAK1 inhibition on cell migration and invasion of glioma. The orthotopic xenograft glioma model was established to probe the effect of PAK1 silencing on tumor formation of U87 cell. Results: It was showed that PAK1 was significantly upregulated in glioma tissues. Besides, high level of PAK1 was found to be associated with poor prognosis in glioma patients in TCGA database. PAK1 inhibition restrained cell proliferation, arrested cells at G1 phase, and induced cell apoptosis of glioma. PAK1 inhibition suppressed glioma cell migration and invasion. Moreover, knockdown of PAK1 dramatically decreased the protein expressions including MDM2, p38, p-p38, CyclinD1, CDK4, Bcl-2, MMP2, MMP9, Cofilin, while increased the protein levels of p53, Bax, p21 and Cleaved Caspase-3. Finally, orthotopic xenograft glioma model confirmed that silencing of PAK1 repressed the tumor formation of U87 cell transplantation.Conclusion: Our study described that PAK1 inhibition impedes proliferation, migration and invasion of glioma cells and thus probably as a novel target for glioma therapy.

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