Cyclin F and KIF20A, FOXM1 target genes, increase proliferation and invasion of ovarian cancer cells

2020 ◽  
Vol 395 (2) ◽  
pp. 112212
Author(s):  
Yingwei Li ◽  
Haiyang Guo ◽  
Zixiang Wang ◽  
Hualei Bu ◽  
Shourong Wang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Target Genes ◽  
Ovarian Cancer Cells ◽  
Cyclin F ◽  
Proliferation And Invasion

scholarly journals BCL7C suppresses ovarian cancer growth by inactivating mutant p53

2020 ◽  
Author(s):  
Canhua Huang ◽  
Qian Hao ◽  
Getao Shi ◽  
Xiang Zhou ◽  
Yu Zhang
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Target Genes ◽  
Ovarian Cancer Cells ◽  
Mutant P53 ◽  
Ovarian Carcinomas ◽  
Ovarian Tumorigenesis ◽  
P53 Target Genes ◽  
Proliferation And Invasion

Abstract B-cell CLL/lymphoma 7 protein family member C (BCL7C) located at chromosome 16p11.2 shares partial sequence homology with the other two family members, BCL7A and BCL7B. Its role in cancer remains completely unknown. Here, we report our finding of its tumor-suppressive role in ovarian cancer. Supporting this is that BCL7C is downregulated in human ovarian carcinomas, and its underexpression is associated with unfavorable prognosis of ovarian cancer as well as some other types of human cancers. Also, ectopic BCL7C restrains cell proliferation and invasion of ovarian cancer cells. Consistently, depletion of BCL7C reduces apoptosis and promotes cell proliferation and invasion of these cancer cells. Mechanistically, BCL7C suppresses mutant p53-mediated gene transcription by binding to mutant p53, while knockdown of BCL7C enhances the expression of mutant p53 target genes in ovarian cancer cells. Primary ovarian carcinomas that sustain low levels of BCL7C often show the elevated expression of mutant p53 target genes. In line with these results, BCL7C abrogates mutant p53-induced cell proliferation and invasion, but had no impact on proliferation and invasion of cancer cells with depleted p53 or harboring wild-type p53. Altogether, our results demonstrate that BCL7C can act as a tumor suppressor to prevent ovarian tumorigenesis and progression by counteracting mutant p53 activity.

scholarly journals MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Ruitao Zhang ◽  
Huirong Shi ◽  
Fang Ren ◽  
Wei Feng ◽  
Yuan Cao ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Target Genes ◽  
Erk Signaling ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Inhibition Of Proliferation ◽  
Mesenchymal Transition ◽  
Biomedical Databases

Abstract Background Downregulation of microRNA-338-3p (miR-338-3p) was detected in many malignant tumors, which indicated miR-338-3p might serve as a role of antioncogene in those cancers. The present study aimed to explore the roles of miR-338-3p in the growth and metastasis of ovarian cancer cells and elaborate the underlying possible molecular mechanism. Methods Multiply biomedical databases query and KEGG pathway enrichment assay were used to infilter possible target genes and downstream pathways regulated by miR-338-3p. Overexpression miR-338-3p lentiviral vectors were transfected into ovarian cancer OVCAR-3 and OVCAR-8 cells, cell proliferation, migration and invasion were analyzed by MTT, colony formation, transwell, Matrigel assay and xenograft mouse model. One 3′-untranslated regions (UTRs) binding target gene of miR-338-3p, MACC1 (MET transcriptional regulator MACC1), and its regulated gene MET and downstream signaling pathway activities were examined by western blot. Results Biomedical databases query indicated that miR-338-3p could target MACC1 gene and regulate Met, downstream Wnt/Catenin beta and MEK/ERK pathways. Rescue of miR-338-3p could inhibit the proliferation, migration and invasion of ovarian cancer cells, and suppress the growth and metastasis of xenograft tumor. Restoration of miR-338-3p could attenuate MACC1 and Met overexpression induced growth, epithelial to mesenchymal transition (EMT) and activities of Wnt/Catenin beta and MEK/ERK signaling in vitro and in vivo. Conclusions The present data indicated that restoration of miR-338-3p could suppress the growth and metastasis of ovarian cancer cells, which might due to the inhibition of proliferation and EMT induced by MACC1, Met and its downstream Wnt/Catenin beta and MEK/ERK signaling pathways.

scholarly journals Targeting miR-21-3p inhibits proliferation and invasion of ovarian cancer cells

Oncotarget ◽  
2016 ◽  
Vol 7 (24) ◽  
pp. 36321-36337 ◽  
Author(s):  
Perla M. Báez-Vega ◽  
Ileabett M. Echevarría Vargas ◽  
Fatma Valiyeva ◽  
Joel Encarnación-Rosado ◽  
Adriana Roman ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Proliferation And Invasion

scholarly journals Metformin Affects the Transcriptomic Profile of Chicken Ovarian Cancer Cells

Genes ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 30
Author(s):  
Lalitha Gopalan ◽  
Aswathy Sebastian ◽  
Craig A. Praul ◽  
Istvan Albert ◽  
Ramesh Ramachandran
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Pathway Analysis ◽  
Target Genes ◽  
Epithelial Mesenchymal Transition ◽  
Ovarian Cancer Cells ◽  
Metformin Treatment ◽  
Mesenchymal Transition ◽  
Sphere Formation ◽  
Upstream Regulators

Ovarian cancer is the most lethal gynecological malignancy in women. Metformin intake is associated with a reduced incidence of ovarian cancer and increased overall survival rate. We determined the effect of metformin on sphere formation, extracellular matrix invasion, and transcriptome profile of ovarian cancer cells (COVCAR) isolated from ascites of chickens that naturally developed ovarian cancer. We found that metformin treatment significantly decreased sphere formation and invasiveness of COVCAR cells. RNA-Seq data analysis revealed 0, 4, 365 differentially expressed genes in cells treated with 0.5, 1, 2 mM metformin, respectively compared to controls. Transcriptomic and ingenuity pathway analysis (IPA) revealed significant downregulation of MMP7, AICDA, GDPD2, APOC3, APOA1 and predicted inhibition of upstream regulators NFKB, STAT3, TP53 that are involved in epithelial–mesenchymal transition, DNA repair, and lipid metabolism. The analysis revealed significant upregulation of RASD2, IHH, CRABP-1 and predicted activation of upstream regulators VEGF and E2F1 that are associated with angiogenesis and cell cycle. Causal network analysis revealed novel pathways suggesting predicted inhibition of ovarian cancer through master regulator ASCL1 and dataset genes DCX, SEMA6B, HEY2, and KCNIP2. In summary, advanced pathway analysis in IPA revealed novel target genes, upstream regulators, and pathways affected by metformin treatment of COVCAR cells.

scholarly journals Cyclooxygenase 2 Promotes Proliferation and Invasion in Ovarian Cancer Cells via the PGE2/NF-κB Pathway

2019 ◽  
Vol 28 (1_suppl) ◽  
pp. 1S-13S ◽  
Author(s):  
Xiao Zhang ◽  
Keqin Yan ◽  
Lin Deng ◽  
Jing Liang ◽  
Haiyan Liang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Prostaglandin E2 ◽  
Cancer Cells ◽  
Nuclear Factor Kappa B ◽  
Cyclooxygenase 2 ◽  
High Expression ◽  
Ovarian Cancer Cells ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Proliferation And Invasion

Ovarian cancer is the leading cause of death among gynecological malignancies. Cyclooxygenase 2 is widely expressed in various cancer cells and participates in the occurrence and development of tumors by regulating a variety of downstream signaling pathways. However, the function and molecular mechanisms of cyclooxygenase 2 remain unclear in ovarian cancer. Here, we demonstrated that cyclooxygenase 2 was highly expressed in ovarian cancer and the expression level was highly correlated with ovarian tumor grades. Further, ovarian cancer cells with high expression of cyclooxygenase 2 exhibit enhanced proliferation and invasion abilities. Specifically, cyclooxygenase 2 promoted the release of prostaglandin E2 upregulated the phosphorylation levels of phospho-nuclear factor-kappa B p65. Celecoxib, AH6809, and BAY11-7082 all can inhibit the promoting effect of cyclooxygenase 2 on SKOV3 and OVCAR3 cell proliferation and invasion. Besides, celecoxib inhibited SKOV3 cell growth in the xenograft tumor model. These data suggest that high expression of cyclooxygenase 2 promotes the proliferation and invasion of ovarian cancer cells through the prostaglandin E2/nuclear factor-kappa B signaling pathway. Cyclooxygenase 2 may be a potential therapeutic target for the treatment of ovarian cancer.

scholarly journals EMP1 Promotes the Proliferation and Invasion of Ovarian Cancer Cells Through Activating the MAPK Pathway

2020 ◽  
Vol Volume 13 ◽  
pp. 2047-2055 ◽  
Author(s):  
Yang Liu ◽  
Yiling Ding ◽  
Yanting Nie ◽  
Mengyuan Yang
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Mapk Pathway ◽  
Ovarian Cancer Cells ◽  
Proliferation And Invasion

scholarly journals MiRNA-802 suppresses proliferation and migration of epithelial ovarian cancer cells by targeting YWHAZ

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Bo Yang ◽  
Li Sun ◽  
Lei Liang
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Target Genes ◽  
Gene Prediction ◽  
Biological Effects ◽  
Expression Level ◽  
Ovarian Cancer Cells ◽  
And Migration

Abstract Background The imbalance of expression of microRNA-802 may have a significant place in tumor progression. However, the bio-function of epithelial ovarian cancer cells remains unclear. Therefore, we setup this study to explore the pathogenesis of epithelial ovarian cancer based on microRNA-802. Methods RT-qPCR analysis was used to measure the expression level of microRNA802 and YWHAZ in epithelial ovarian cancer. CCK-8, colony formation, flow cytometry and transwell assay were used to detect the effects of microRNA-802 on cell proliferation, apoptosis, invasion and migration. Target gene prediction and screening, luciferase reporting experiments were applied to validate the downstream target genes of microRNA-802. The effects of microRNA-802 on the expression of YWHAZ and its biological effects were measured by Western blotting and RT-qPCR. Results Compared with normal cell lines and tissues, the expression level of microRNA-802 was obviously down-regulated in cancer related cell lines and tissues. Overexpression of microRNA-802 could obviously inhibit the invasion and proliferation and induce apoptosis. In addition, YWHAZ was the binding target protein of miR-802 for epithelial ovarian cancer cells. YWHAZ was obviously up-regulated in human epithelial ovarian cancer cells, and YWHAZ was negatively correlated with the expression of miR-802. YWHAZ can partly eliminate the inhibitory effect caused by overexpression of miR-802 on growth and metastasis of epithelial ovarian cancer cells. Conclusion miR-802 can regulate the occurrence and development of epithelial ovarian cancer by targeting YWHAZ.

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