scholarly journals Ludartin treatment exhibits promising inhibitory effect on the epithelial ovarian cancer growth and metastasis

2016 ◽  
Vol 11 (3) ◽  
pp. 646
Author(s):  
Lin Bai ◽  
Hui Wang ◽  
Luo-Ying Zhang ◽  
Ai-Hua Wang ◽  
Jie Bai
Keyword(s):  
Ovarian Cancer ◽  
Cell Viability ◽  
Video Clip ◽  
Inhibitory Effect ◽  
Carcinoma Cells ◽  
Ovarian Cancer Cells ◽  
Invasive Potential ◽  
Invasion And Migration ◽  
Migration Potential ◽  
And Migration

<p class="Abstract">In the present study, the effect of ludartin on OVCAR5 ovarian carcinoma cells was investigated. MTT cell assay was used for the analysis of cell viability and wound healing assay for migration potential. Results revealed that ludartin treatment at 10 and 30 µM doses reduced the cell viability from 94 to 38%. The invasive potential was decreased from 62 to 24% with increase in ludartin concentration from 10 to 30 µM. Western blot analysis showed that ludartin treatment reduced the expression of p-FAK in OVCAR5 cells significantly. Ludartin treatment for 48 hours also caused a significant decrease in the expression of MMP-2 and MMP-9 in OVCAR5 cells at a concentration of 30 µM. The metastatic regions were absent in the rats treated with 30 µM/kg doses of ludartin daily for 15 days.  Thus, ludartin treatment inhibits the proliferation, invasion and migration of ovarian cancer cells through down-regulation of pFAK and MMPs, therefore can be used for the treatment of ovarian cancer.</p><p><strong>Video Clip:</strong></p><p><a href="https://youtube.com/v/GMpEHXdGSeI">Cell proliferation assay:</a> 2 min 45 sec</p><p> </p>

scholarly journals A Zn(ii)–organic cage with semirigid ligand for solvent-free cyanosilylation and inhibitory effect on ovarian cancer cell migration and invasion ability via regulating mi-RNA16 expression

2020 ◽  
Vol 18 (1) ◽  
pp. 1117-1124
Author(s):  
Yan Yin ◽  
Hong Mai ◽  
Li-Ying Zhang ◽  
Yan Liao ◽  
Xu-Peng Liu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Inhibitory Effect ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Invasion And Migration ◽  
Catalytic Activities ◽  
Heterogeneous Catalytic ◽  
Relative Expression Level ◽  
Metal Organic ◽  
And Migration

Abstract[Zn6(L)4(DMF)2(H2O)4](1,4-Dioxane)2(DMF)10(H2O)4 (1, L  =  4,4′,4″-(benzene-1,3,5-triyltris(oxy))tribenzoate), the metal-organic cage, was produced via Zn(NO3)2·6H2O reacting with the H3L ligand in the mixed solvent of DMF and water. The heterogeneous catalytic activities of the complex 1 for the aldehydes cyanidation under the conditions of free solvent were studied, which indicates that the removal of coordination solvents could greatly improve the catalytic activities. Furthermore, the inhibitory effect of the compound against the ovarian cancer cells was assessed. The mi-RNA16 relative expression level was measured after exposure to the compound with real-time reverse transcription-polymerase chain reaction. The invasion and migration of cells after compound treatment were also detected by the transwell method.

scholarly journals Long non-coding RNA XIST regulates ovarian cancer progression via modulating miR-335/BCL2L2 axis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qingjuan Meng ◽  
Ningning Wang ◽  
Guanglan Duan
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna

Abstract Background X inactivation-specific transcript (XIST) is the long non-coding RNA (lncRNA) related to cancer, which is involved in the development and progression of various types of tumor. However, up to now, the exact role and molecular mechanism of XIST in the progression of ovarian cancer are not clear. We studied the function of XIST in ovarian cancer cells and clinical tumor specimens. Methods RT-qPCR was performed to detect the expression levels of miR-335 and BCL2L2 in ovarian cancer cells and tissues. MTT and transwell assays were carried out to detect cell proliferation, migration, and invasion abilities. Western blot was performed to analyze the expression level of BCL2L2. The interaction between miR-335 and XIST/BCL2L2 was confirmed using a luciferase reporter assay. Results The inhibition of XIST can inhibit the proliferation invasion and migration of human ovarian cancer cells. In addition, the miR-335/BCL2L2 axis was involved in the functions of XIST in ovarian cancer cells. These results suggested that XIST could regulate tumor proliferation and invasion and migration via modulating miR-335/BCL2L2. Conclusion XIST might be a carcinogenic lncRNA in ovarian cancer by regulating miR-335, and it can serve as a therapeutic target in human ovarian cancer.

scholarly journals circ-CSPP1 promotes proliferation, invasion and migration of ovarian cancer cells by acting as a miR-1236-3p sponge

2019 ◽  
Vol 114 ◽  
pp. 108832 ◽  
Author(s):  
Qian-hui Li ◽  
Yao Liu ◽  
Shuo Chen ◽  
Zhi-hong Zong ◽  
Yu-ping Du ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

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

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.

scholarly journals WISP2 promotes cell proliferation via targeting ERK and YAP in ovarian cancer cells

2020 ◽  
Author(s):  
Zi-Qing Shi ◽  
Zi-Yan Chen ◽  
Yao Han ◽  
Heng-Yan Zhu ◽  
Meng-Dan Lyu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Inhibitory Effect ◽  
Ovarian Cancer Cells ◽  
Extracellular Signal ◽  
And Migration

Abstract Background: Wnt-inducible signaling pathway protein 2 (WISP2) is a wnt1-induced signaling pathway protein 2. Although studies indicate that WISP2 may promote the development of various tumors, its role in ovarian cancer remains unclear. The objective of the current study was to analyze the effects of WISP2 on the proliferation and migration of ovarian cancer cells in vitro and in vivo.Results: Immunohistochemistry and western blotting indicated that WISP2 was highly expressed in various ovarian cancer tissues and cell lines，but weakly expressed in normal ovary tissue. WISP2 deletion inhibited cell growth, clone formation, and migration of ovarian cancer cells while promoting cell apoptosis and affecting the cell cycle. This growth inhibitory effect caused by WISP2 loss is due to the inhibition of phosphorylated extracellular signal-related kinase (p-ERK)1/2, as well as CCAAT/enhancer-binding protein α (CEBPα) and CEPBβ. In addition, WISP2 deletion also activated the Yes-associated protein (YAP).Conclusion: WISP2 deletion inhibits ovarian cancer cell proliferation by affecting ERK signaling pathways.

scholarly journals WISP2 promotes cell proliferation via targeting ERK and YAP in ovarian cancer cells

2020 ◽  
Author(s):  
Zi-Qing Shi ◽  
Zi-Yan Chen ◽  
Yao Han ◽  
Heng-Yan Zhu ◽  
Meng-Dan Lyu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Inhibitory Effect ◽  
Ovarian Cancer Cells ◽  
Growth Inhibitory ◽  
Extracellular Signal ◽  
And Migration

Abstract Background Wnt inducible signaling protein 2 (WISP2) is a wnt1-induced signaling pathway protein 2. Although studies indicate that WISP2 may promote the development of various tumors, its role in ovarian cancer remains unclear. The objective of the current study was to analyze the effects of WISP2 on proliferation and migration of ovarian cancer cells in vitro and in vivo . Results Immunohistochemistry and western blot results indicated that WISP2 was highly expressed in various ovarian tissues and cell lines. WISP2 deletion inhibited cell growth, clone formation, and migration of ovarian cancer cells. WISP2 deletion promoted cell apoptosis and affected the cell cycle. This growth inhibitory effect caused by WISP2 loss is due to the inhibition of extracellular signal-related kinase (p-ERK)1/2, as well as CEBPα and CEBPβ. In addition, WISP2 deletion also activated the Yes-associated protein (YAP). Conclusion WISP2 deletion inhibits ovarian cancer cell proliferation by affecting ERK signaling pathways.

scholarly journals LncRNA DLGAP1-AS2 Suppresses the Maturation of miR-16 to Suppress Cell Invasion and Migration of Ovarian Cancer Cells

2021 ◽  
Author(s):  
Jie Luo ◽  
Yuqiang Zhang ◽  
Ting Zheng ◽  
Yongping Jing ◽  
Rongyu Cao ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Invasion ◽  
Precursor Cell ◽  
Ovarian Cancer Cells ◽  
Inhibitory Effects ◽  
Invasion And Migration ◽  
Tumor Tissues ◽  
And Migration ◽  
Migration Analysis

Abstract Background: This study aimed to explore the role of lncRNA DLGAP1-AS2 in ovarian cancer (OC). Methods: Expression of DLGAP1-AS2, mature miR-16 and miR-16 precursor in paired OC tissues and non-tumor tissues collected from 62 OC patients was determined by RT-qPCR. Correlations were analyzed by Pearson’s correlation coefficient. Overexpression of DLGAP1-AS2 was achieved in OC cell line UWB1.289 to explore the effects of DLGAP1-AS2 overexpression on the expression of mature miR-16 and miR-16 precursor by RT-qPCR. Transwell assays were performed to analyze the role of DLGAP1-AS2 and miR-16 in regulating the invasion and migration of UWB1.289 cells.Results: DLGAP1-AS2 was upregulated in OC and inversely correlated with mature miR-16, but not miR-16 precursor. In OC cells, DLGAP1-AS2 overexpression resulted in downregulated mature miR-16, but failed to significantly affect the expression of miR-16 precursor. Cell invasion and migration analysis showed that DLGAP1-AS2 overexpression reduced the inhibitory effects of miR-16 overexpression on cell invasion and migration.Conclusions: DLGAP1-AS2 may suppress the maturation of miR-16 to suppress cell invasion and migration of OC cells.

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