scholarly journals Role of Differential Expression of miRNAs miR-125a, miR-200a and miR-199a in Metastatic Property of Ovarian Cancer Cell lines and Relationship between miR-199a and its Predicted Target Protein GSK3β

2020 ◽  
Author(s):  
Divya RSJB Rana ◽  
Lin Xu ◽  
Jie Zhang

AbstractOvarian cancer is a gynecological cancer of high mortality rate. Most of the ovarian cancer origin from the surface epithelium of the ovaries. Ovarian cancers gain metastatic and invasive properties from various biochemical events taking place during tumorogenesis. MicroRNAs (miRNA) are non-coding RNAs and they have an important function of inhibiting translation of specific mRNAs in the cytoplasm. Present study uses two ovarian cancer cell lines as model to study the differential expression of miR-125a, miR-200a, and miR-199a, and provides indirect proof for possible relationship between miR-199a and its predicted target gene Glycogen Synthase Kinase 3 β (GSK3β). As expected the expression of these three microRNAs are decreased in metastatic ovarian cancer cell line A2780 compared to epithelial ovarian cancer OVCAR3. Reciprocal expression pattern of miR-199a and its predicted target GSK3β was found in two different cell lines providing information on possible inhibitory role of miR-199a against GSK3β.

2010 ◽  
Vol 4 (S2) ◽  
Author(s):  
Fernanda Silva ◽  
Jacinta Serpa ◽  
Germana Domingues ◽  
Gabriela Silva ◽  
António Almeida ◽  
...  

2019 ◽  
Vol 20 (8) ◽  
pp. 2053 ◽  
Author(s):  
Świerczewska ◽  
Sterzyńska ◽  
Wojtowicz ◽  
Kaźmierczak ◽  
Iżycki ◽  
...  

Background: Ovarian cancer is the 7th most common cancer and 8th most mortal canceramong woman. The standard treatment includes cytoreduction surgery followed bychemotherapy. Unfortunately, in most cases, after treatment, cancer develops drug resistance.Decreased expression and/or activity of protein phosphatases leads to increased signaltransduction and development of drug resistance in cancer cells. Methods: Using sensitive (W1,A2780) and resistant ovarian cancer cell lines, the expression of Protein Tyrosine PhosphataseReceptor Type K (PTPRK) was performed at the mRNA (real‐time PCR analysis) and protein level(Western blot, immunofluorescence analysis). The protein expression in ovarian cancer tissues wasdetermined by immunohistochemistry. Results: The results showed a decreased level of PTPRKexpression in ovarian cancer cell lines resistant to cisplatin (CIS), paclitaxel (PAC), doxorubicin(DOX), topotecan (TOP), vincristine (VIN) and methotrexate (MTX). Additionally, the lowerPTPRK expression was observed in Aldehyde Dehydrogenase 1 Family Member A1 (ALDH1A1)positive cancer stem cells (CSCs) population, suggesting the role of PTPRK downregulation inprimary as well as acquired resistance to cytotoxic drugs. Conclusions: These results provideimportant insights into the role of PTPRK in mechanism leading to drug resistance in ovariancancer and has raised important questions about the role of imbalance in processes ofphosphorylation and dephosphorylation.


2021 ◽  
Vol 9 (3) ◽  
pp. 138-147
Author(s):  
Marta Nowacka ◽  
Barbara Ginter-Matuszewska ◽  
Monika Świerczewska ◽  
Michał Nowicki ◽  
Maciej Zabel ◽  
...  

Abstract Resistance to chemotherapy is the main obstacle in contemporary ovarian cancer treatment. The aim of this study was the evaluation of expression of HERC5, IFIH1, SAMD4, MCTP1 and SEMA3A mRNA and assessment their role in resistance to cisplatin, paclitaxel, doxorubicin and topotecan in seven ovarian cancer cell lines. MTT assay was used in resistance assessment. Quantitative polymerase chain reaction was performed to measure the expression levels of the genes. We observed different levels of resistance among cell lines. The resistance was not related to the expression of drug transporters genes. The expression of HERC5 and IFIH1 genes was upregulated, and the expression of SEMA3A gene was downregulated. Expression of SAMD4 was upregulated in PEA1, PEA2, and PEO23 cell lines, and expression of MCTP1 was downregulated in A2780, PEA2, and PEO23 cell lines. Upregulation of HERC5, IFIH1, and SAMD4 and downregulation of SEMA3A and MCTP1 in TOP-resistant ovarian cancer cell lines may suggest some role of those genes in topotecan resistance development.


2021 ◽  
Author(s):  
Suiying Liang ◽  
Yueyang Liu ◽  
Jianhui He ◽  
Tian Gao ◽  
Lanying Li ◽  
...  

Abstract Purpose: Ovarian cancer is the most lethal malignancy with depressive 5-year survival rate, mainly due to patients with advanced stages experience tumor recurrence and resistance to the current chemotherapeutic agents. Thus, discovering the underlying molecular mechanisms involved in chemo-resistance is crucial for management of treatment to improve therapeutic outcomes. Methods: The protein and mRNA expression of FAM46A in ovarian cancer cell lines and patient tissues were determined using Real-time PCR and Western blot and IHC respectively. Functional assays, such as MTT, FACS assay used to determine the oncogenic role of FAM46A in human ovarian cancer progression. Furthermore, western blotting and luciferase assay were used to determine the mechanism of FAM46A promotes chemoresistance in ovarian cancer cells. Results: In the current study, we found overexpression of FAM46A expression in ovarian cancer patients demonstrated an aggressive phenotype and poor prognosis. Furthermore, FAM46A overexpression in ovarian cancer cells demonstrated higher CDDP resistance ability; however, inhibition of FAM46A sensitized ovarian cancer cell lines to CDDP cytotoxicity both in vitro and in vivo. Mechanically, upregulation of FAM46A activated transforming growth factor-β (TGF-β)/Smad signaling and upregulated the levels of nuclear Smad2. Conclusions: Taken together, our results highlight the important oncogenic role of FAM46A in ovarian cancer progression and might provide a potential clinical target for patients with chemoresistant ovarian cancer.


2014 ◽  
Vol 50 ◽  
pp. S193
Author(s):  
G. Hamilton ◽  
L. Klameth ◽  
B. Rath ◽  
E. Obermayr ◽  
R. Zeillinger ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Samar Masoumi Moghaddam ◽  
Afshin Amini ◽  
Ai-Qun Wei ◽  
Mohammad Hossein Pourgholami ◽  
David Lawson Morris

Sprouty (Spry) proteins, modulators of receptor tyrosine kinase signaling pathways, have been shown to be deregulated in a variety of pathological conditions including cancer. In the present study we investigated the expression of Spry1 and Spry2 isoforms in a panel of human ovarian cancer cell lines in vitro. Our western blot analysis showed nonuniform patterns of Spry expression in the cancer cells, none of which conformed to the pattern observed in the normal ovarian epithelial cells employed as the control. Among the seven cancer cell lines studied, Spry1 was expressed lower in four cell lines and higher in one as compared with the control. As for Spry2, four cell lines showed lower and two exhibited higher expression. Results from RT-PCR assay raised the possibility that Spry protein levels may not necessarily correspond with its expression at mRNA level. Our immunostaining study revealed that Spry2 was predominantly distributed within the whole cytoplasm in vesicular structures whereas Spry1 was found in both the cytoplasm and nucleus. This might provide clues to further investigation of Spry mode of action and/or function. Collectively, our study unveiled the differential expression of Spry1 and Spry2 proteins in various ovarian cancer cell lines.


2020 ◽  
Vol 31 (19) ◽  
pp. 195101 ◽  
Author(s):  
Mohammad A Obeid ◽  
Siti Aisya S Gany ◽  
Alexander I Gray ◽  
Louise Young ◽  
John O Igoli ◽  
...  

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