scholarly journals Silencing ofEag1Gene Inhibits Osteosarcoma Proliferation and Migration by Targeting STAT3-VEGF Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Xinyu Wu ◽  
Zhida Chen ◽  
Wengrong Zeng ◽  
Yuanfu Zhong ◽  
Qingjun Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Small Interfering Rnas ◽  
Expression Levels ◽  
Cell Proliferation And Migration ◽  
Vegf Pathway ◽  
And Migration ◽  
Endothelial Growth Factor ◽  
Proliferation And Migration

So far, the role of Ether à go-go 1 (Eag1) potassium channels in migration and invasion progression of cancers remains elusive. In the present study, the effects ofEag1knockdown on osteosarcoma cell proliferation, growth, and apoptosis were examined. Then, we evaluated the effects ofEag1silencing on osteosarcoma cell migration and invasion. In addition, we detected the expression of vascular endothelial growth factor (VEGF) and signal transducer and activator of transcription 3 (STAT3) in osteosarcoma cell treated with Eag1 small interfering RNAs (siRNAs). Finally, STAT3 siRNA was employed to determine the influence of downregulation of STAT3 on cell proliferation and migration. The results showed that knockdown ofEag1significantly suppressed osteosarcoma cell proliferation and osteosarcoma xenografts growth. However,Eag1silencing had little effect on cell apoptosis. Additionally, osteosarcoma cell adhesion, migration, and invasion were also potently attenuated. Notably, the expression levels of VEGF decreased evidently upon Eag1 siRNAs treatment, paralleled with reductions in the expression levels of STAT3. Moreover, a similar pattern was observed in osteosarcoma cell proliferation and migration suppression between STAT3 siRNA and Eag1 siRNAs groups. Our data indicated that Eag1 promotes osteosarcoma proliferation and migration, at least in part, by targeting STAT3-VEGF pathway.

scholarly journals Identification of CTRP1 as a Prognostic Biomarker and Oncogene in Human Glioblastoma

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Liyan Chen ◽  
Gang Su
Keyword(s):  
Cell Proliferation ◽  
Mrna Expression ◽  
Genetic Alterations ◽  
Expression Levels ◽  
Cell Proliferation And Migration ◽  
Ccl2 Expression ◽  
Human Gbm ◽  
And Migration ◽  
Mrna Expression Levels ◽  
Proliferation And Migration

Introduction. Glioblastoma (GBM) is the most frequent and malignant type of primary brain tumors in adults. The valuable prognostic biomarkers and therapeutic targets for GBM remain to be elucidated. The association of adipokines with cancer has been well documented. The C1q/TNF-related protein 1 (CTRP1), a novel adipokine, belongs to the CTRP family.Methods. In the present study, the expression and potential roles of CTRP1 in GBM were explored based on in silico evaluation, including GEPIA, the Pathology Atlas of the Human Protein Atlas, cBioPortal, TIMER, and SurvExpress. The CCK8, transwell, and wound healing assays were used to detect cell proliferation and migration.Results. It was found that mRNA expression levels ofCTRP1were significantly upregulated in GBM tissues compared with those in nontumor tissues according to the analysis on public dataset and immunohistochemical results of GBM tissues (P<0.05). CTRP1 was mainly localized in the cytoplasm and cell membrane of GBM cells. The genetic alterations of CTRP1 occurred at a low rate in GBM (2 of 591 sequenced cases/patients, 0.33%). The mRNA expression levels ofCTRP1were positively associated with the tumor-infiltrating macrophages and CCL2 in GBM (P<0.05, respectively). The higher mRNA expression levels ofCTRP1were significantly correlated with higher risk and shorter overall survival time in GBM (P<0.05). CTRP1 knockdown significantly inhibited the proliferation and migration in human GBM cells, suggesting the inhibition of CTRP1 on human GMB progression. Moreover, CTRP1 knockdown inhibited CCL2 expression, and CCL2 overexpression reversed the inhibition of cell proliferation and migration induced by CTRP1 knockdown, suggesting that CTRP1 promoted tumor progression by regulating CCL2 expression.Conclusions. These findings suggest that CTRP1 potentially indicates poor prognosis in GBM and promotes the progression of human GBM.

scholarly journals Lobaplatin Inhibits Prostate Cancer Proliferation and Migration Through Regulation of BCL2 and BAX

Dose-Response ◽  
2019 ◽  
Vol 17 (2) ◽  
pp. 155932581985098 ◽  
Author(s):  
Hongwen Cao ◽  
Yigeng Feng ◽  
Lei Chen ◽  
Chao Yu
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Cancer Proliferation ◽  
Expression Levels ◽  
And Migration ◽  
Proliferation And Migration

Lobaplatin is a diastereometric mixture of platinum (II) complexes, which contain a 1,2-bis (aminomethyl) cyclobutane stable ligand and lactic acid. Previous studies have showed that lobaplatin plays inhibiting roles in various types of tumors. However, the role of lobaplatin in prostate cancer remains unknown. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Cell proliferation was detected by cell colony formation assay. Cell migration and invasion were determined by transwell migration and invasion assay. Cell apoptosis was detected by flow cytometry. The messenger RNA and protein expression levels were detected by quantitative real-time polymerase chain reaction and Western blot. Lobaplatin treatment inhibits cell viability, cell proliferation, cell migration, and invasion, while promotes cell apoptosis of prostate cancer cell lines DU145 and PC3. Meanwhile, lobaplatin treatment regulates apoptosis by downregulation of BCL2 expression and upregulation of BAX expression levels. Our study suggests lobaplatin inhibits prostate cancer proliferation and migration through regulation of BCL2 and BAX expression.

scholarly journals Solanine Attenuated Hepatocarcinoma Migration and Invasion Induced by Acetylcholine

2020 ◽  
Vol 19 ◽  
pp. 153473542090989
Author(s):  
Liang-Tzung Lin ◽  
Chen-Yen Choong ◽  
Chen-Jei Tai
Keyword(s):  
Cell Proliferation ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Mesenchymal Transition ◽  
Cell Proliferation And Migration ◽  
G2 Cells ◽  
And Migration ◽  
Proliferation And Migration

Aim: Evidence has provided an explanation of the correlation between the nervous system and the tumor microenvironment. Neurotransmitters may be involved in different aspects of cancer progression. The glycoalkaloid solanine has been reported to suppress neural signaling pathways and exists in numerous plants, including Solanum nigrum, which have been demonstrated to inhibit cancer cell proliferation. Methods: We evaluated the potentials of solanine on inhibiting acetylcholine-induced cell proliferation and migration in hepatocellular carcinoma cells. Results: The results indicated that solanine markedly attenuated cell proliferation and migration via inhibiting epithelial-mesenchymal transition and matrix metalloproteinases in acetylcholine-treated Hep G2 cells. In addition, exosomes derived from acetylcholine-treated Hep G2 cells were isolated, and solanine showed inhibiting effects of extrahepatic metastasis on blocking cell proliferation in exosome-treated A549 lung carcinoma cells through regulating microRNA-21 expression. Conclusion: Solanine has strong potential for application in integrative cancer therapy.

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