scholarly journals The Role of miRNA in Ovarian Cancer: an Overview

2022 ◽  
Author(s):  
Lihui Zhao ◽  
Xiaolei Liang ◽  
Liyan Wang ◽  
Xuehong Zhang
Keyword(s):  
Ovarian Cancer ◽  
Drug Resistance ◽  
Malignant Disease ◽  
Rna Degradation ◽  
Early Screening ◽  
Gene Expressions ◽  
Translation Inhibition ◽  
Biological Targets ◽  
Prognostic Prediction

AbstractOvarian cancer (OC) is a highly malignant disease that seriously threatens women’s health and poses challenges for clinicians. MicroRNAs (miRNAs) have recently been intensively studied in the field of oncology due to their regulatory roles in gene expressions through RNA degradation and/or translation inhibition. This review summarizes the current studies on miRNAs in OC and introduces the latest updates of miRNAs in the early screening, treatment, and prognostic prediction of OC, thereby demonstrating the clinical significance of miRNAs in OC. Further exploration on potential targets of miRNAs in OC may provide new insights on optimizing the diagnosis and treatment of OC. MiRNAs are important driving factors for the progression of OC and the dysregulation of miRNAs can serve as biomarkers in the diagnosis, treatment and prognosis of OC. Therefore, miRNAs are potential biological targets for early screening, targeted therapy, drug resistance monitoring, and prognosis improvement in malignancies such as OC.

Role of p53 in drug resistance in ovarian cancer

The Lancet ◽  
1997 ◽  
Vol 349 (9054) ◽  
pp. 744-745 ◽  
Author(s):  
Andrew N Shelling
Keyword(s):  
Ovarian Cancer ◽  
Drug Resistance

scholarly journals Crucial role of HMGA1 in the self-renewal and drug resistance of ovarian cancer stem cells

2016 ◽  
Vol 48 (8) ◽  
pp. e255-e255 ◽  
Author(s):  
Dae Kyoung Kim ◽  
Eun Jin Seo ◽  
Eun J Choi ◽  
Su In Lee ◽  
Yang Woo Kwon ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Drug Resistance ◽  
Cancer Stem Cells ◽  
Crucial Role ◽  
The Self ◽  
Ovarian Cancer Stem Cells ◽  
Self Renewal

scholarly journals The effect of iron on the expression levels of calcium related gene in cisplatin resistant epithelial ovarian cancer cells

2021 ◽  
Author(s):  
Bahire Kucukkaya ◽  
Demet Erdag ◽  
Fahri Akbas ◽  
Leman Yalcintepe
Keyword(s):  
Ovarian Cancer ◽  
Drug Resistance ◽  
Epithelial Ovarian Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Calcium Homeostasis ◽  
Ovarian Cancer Cell Line ◽  
Ovarian Cancer Cells ◽  
Gene Expressions ◽  
Iron Treatment

Aim: Anticancer drugs (chemotherapeutics) used in cancer treatment (chemotherapy) lead to drug resistance. This study was conducted to investigate the possible effect of iron on calcium homeostasis in epithelial ovarian cancer cells (MDAH-2774) and cisplatin-resistant cells of the same cell line (MDAH-2774/DDP). Methods: To develop MDAH-2774/DDP cells, MDAH-2774 (MDAH) cells were treated with cisplatin in dose increases of 5 μM between 0 μM and 70 μM. The effect of iron on the viability of MDAH and MDAH/DDP cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test at the end of 24 h incubation. Results: At increasing iron concentrations in MDAH and MDAH/DDP cells, the mRNA gene of fifteen genes [inositol 1,4,5-triphosphate receptor (IP3R)1/2/3, ryanodine receptor (RYR)1/2, sarco/endoplasmic reticulum Ca2+ ATPase (SERCA)1/2/3, Na+/Ca2+ exchange (NCX)1/2/3, and plasma membrane Ca2+ ATPase (PMCA)1/2/3/4] associated with Ca2+ differences in expression were determined by quantitative reverse transcription-polymerase chain reaction. Changes in IP3R2, RYR1, SERCA2, NCX3, PMCA1, and PMCA3 gene expressions were observed in iron treatment of MDAH/DDP cells, while changes were detected in iron treatment of MDAH cells in IP3R1/2/3, RYR1/2, SERCA1/2/3, NCX2/3, and PMCA1 expressions. Conclusions: This changes in the expression of calcium channels, pumps, and exchange proteins in the epithelial ovarian cancer cell line and in cisplatin-resistant epithelial ovarian cancer cells suggest that iron may have an important role in regulating calcium homeostasis. Due to differences in the expression of genes that play of an important role in the regulation of calcium homeostasis in the effect of iron, drug resistance can be prevented by introducing a new perspective on the use of inhibitors and activators of these genes and thus cytostatic treatment strategies.

Non-coding RNAs in Lung Cancer Chemoresistance

2020 ◽  
Vol 20 (13) ◽  
pp. 1023-1032 ◽  
Author(s):  
Priya Mondal ◽  
Jagadish Natesh ◽  
Mohammad Amjad Kamal ◽  
Syed Musthapa Meeran
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Kinase Inhibitors ◽  
Treatment Options ◽  
Acquired Resistance ◽  
Gene Expressions ◽  
Intrinsic Factors ◽  
Non Coding Rnas ◽  
Altered Gene

Background: Lung cancer is the leading cause of cancer-associated death worldwide with limited treatment options. The major available treatment options are surgery, radiotherapy, chemotherapy and combinations of these treatments. In chemotherapy, tyrosine kinase inhibitors and taxol are the first lines of chemotherapeutics used for the treatment of lung cancer. Often drug resistance in the clinical settings hinders the efficiency of the treatment and intrigues the tumor relapse. Drug-resistance is triggered either by intrinsic factors or due to the prolonged cycles of chemotherapy as an acquired-resistance. There is an emerging role of non-coding RNAs (ncRNAs), including notorious microRNAs (miRNAs), proposed to be actively involved in the regulations of various tumor-suppressor genes and oncogenes. Result: The altered gene expression by miRNA is largely mediated either by the degradation or by interfering with the translation of targeted mRNA. Unlike miRNA, other type of ncRNAs, such as long non-coding RNAs (lncRNAs), can target the transcriptional activator or the repressor, RNA polymerase, and even DNA-duplex to regulate the gene expressions. Many studies have confirmed the crucial role of ncRNAs in lung adenocarcinoma progression and importantly, in the acquisition of chemoresistance. Recently, ncRNAs have become early biomarkers and therapeutic targets for lung cancer. Conclusion: Targeting ncRNAs could be an effective approach for the development of novel therapeutics against lung cancer and to overcome the chemoresistance.

Drug resistance in ovarian cancer — the role of p53

1998 ◽  
Vol 4 (2) ◽  
pp. 97-102 ◽  
Author(s):  
Russel Petty ◽  
Alan Evans ◽  
Iain Duncan ◽  
Christian Kurbacher ◽  
Ian Cree
Keyword(s):  
Ovarian Cancer ◽  
Drug Resistance

scholarly journals Special Agents Hunting Down Women Silent Killer: The Emerging Role of the p38αKinase

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Valentina Grossi ◽  
Cristiano Simone
Keyword(s):  
Ovarian Cancer ◽  
Drug Resistance ◽  
Metabolic Reprogramming ◽  
Proliferating Cells ◽  
Improve Patient Survival ◽  
High Incidence ◽  
Current Therapies ◽  
Therapy Success ◽  
Improve Patient

Ovarian cancer is sensitive to chemotherapy with platinum compounds; however, the therapy success rate is significantly lowered by a high incidence of recurrence and by the acquisition of drug resistance. These negative outcomes mainly depend on altered apoptotic and drug resistance pathways, determining the need for the design of new therapeutic strategies to improve patient survival. This challenge has become even more critical because it has been recognized that hindering uncontrolled cell growth is not sufficient as the only curative approach. In fact, while current therapies are mostly conceived to impair survival of highly proliferating cells, several lines of research are now focusing on cancer-specific features to specifically target malignant cells with the aim of avoiding drug resistance and reducing adverse effects. Recently, great interest has been generated by the identification of metabolic reprogramming mechanisms occurring in cancer cells, such as the increase in glycolysis levels. In this light, pharmacologic manipulation of relevant pathways involved in cancer-specific metabolism and drug resistance could prove an effective approach to treat ovarian cancer patients.

Role of the colony-stimulating factor (CSF)/CSF-1 receptor axis in cancer

2016 ◽  
Vol 44 (2) ◽  
pp. 333-341 ◽  
Author(s):  
Daniela Achkova ◽  
John Maher
Keyword(s):  
Ovarian Cancer ◽  
Malignant Disease ◽  
Large Body ◽  
Colony Stimulating Factor ◽  
Autocrine Growth ◽  
Receptor System ◽  
Therapeutic Targeting ◽  
Tumour Formation ◽  
Stimulating Factor

Cancer cells employ a variety of mechanisms to evade apoptosis and senescence. Pre-eminent among these is the aberrant co-expression of growth factors and their ligands, forming an autocrine growth loop that promotes tumour formation and progression. One growth loop whose transforming potential has been repeatedly demonstrated is the CSF-1/CSF-1R axis. Expression of CSF-1 and/or CSF-1R has been documented in a number of human malignancies, including breast, prostate and ovarian cancer and classical Hodgkin's lymphoma (cHL). This review summarizes the large body of work undertaken to study the role of this cytokine receptor system in malignant transformation. These studies have attributed a key role to the CSF-1/CSF-1R axis in supporting tumour cell survival, proliferation and enhanced motility. Moreover, increasing evidence implicates paracrine interactions between CSF-1 and its receptor in defining a tumour-permissive and immunosuppressive tumour-associated stroma. Against this background, we briefly consider the prospects for therapeutic targeting of this system in malignant disease.

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