MicroRNA-20a contributes to cisplatin-resistance and migration of OVCAR3 ovarian cancer cell line

Liu, Yankun; Han, Song; Li, Yuhui; Liu, Yan; Zhang, Di; Zhang, Jinghua

doi:10.3892/ol.2017.6348

Cited by 18 publications

(10 citation statements)

References 32 publications

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“…Thus, to better define, at a molecular level, the induction chemotherapy response of PR patients, we established a new approach. We evaluated in the whole cohort of patients (n = 52) all the exo-miRNAs modulated after the induction chemotherapy that have been previously reported to be associated with the response to each chemotherapeutic drug employed in the induction treatment (Table 3) [18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58]. HR-NB patients are treated with a combination of different drugs including cisplatin (CDDP), carboplatin (CBDCA), etoposide (VP-16), doxorubicin (DOXO), vincristine (VCR), and cyclophosphamide (CPM), administered in several cycles (see Material and Methods).…”

Section: Resultsmentioning

confidence: 99%

Exosomal microRNAs from Longitudinal Liquid Biopsies for the Prediction of Response to Induction Chemotherapy in High-Risk Neuroblastoma Patients: A Proof of Concept SIOPEN Study ‖

Morini

Cangelosi

Segalerba

et al. 2019

Cancers

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Despite intensive treatment, 50% of children with high-risk neuroblastoma (HR-NB) succumb to their disease. Progression through current trials evaluating the efficacy of new treatments for children with HR disease usually depends on an inadequate response to induction chemotherapy, assessed using imaging modalities. In this study, we sought to identify circulating biomarkers that might be detected in a simple blood sample to predict patient response to induction chemotherapy. Since exosomes released by tumor cells can drive tumor growth and chemoresistance, we tested the hypothesis that exosomal microRNA (exo-miRNAs) in blood might predict response to induction chemotherapy. The exo-miRNAs expression profile in plasma samples collected from children treated in HR-NBL-1/SIOPEN before and after induction chemotherapy was compared to identify a three exo-miRs signature that could discriminate between poor and good responders. Exo-miRNAs expression also provided a chemoresistance index predicting the good or poor prognosis of HR-NB patients.

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Section: Resultsmentioning

confidence: 99%

Exosomal microRNAs from Longitudinal Liquid Biopsies for the Prediction of Response to Induction Chemotherapy in High-Risk Neuroblastoma Patients: A Proof of Concept SIOPEN Study ‖

Morini

Cangelosi

Segalerba

et al. 2019

Cancers

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“…Whereas the above-mentioned micro-RNAs suppress EMT and therapy resistance, some micro-RNAs such as miR-20a, do the opposite. Indeed, miR-20a induced EMT and cisplatin resistance in OVCAR3 cells [132]. Furthermore, overexpression of miR-181a induced EMT and paclitaxel resistance in SKOV3 cells through upregulation of P-glycoprotein [133].…”

Section: Emt and Chemotherapy Resistancementioning

confidence: 99%

The Role of Epithelial-to-Mesenchymal Plasticity in Ovarian Cancer Progression and Therapy Resistance

Loret

Denys

Tummers

et al. 2019

Cancers

194

134

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Ovarian cancer is the most lethal of all gynecologic malignancies and the eighth leading cause of cancer-related deaths among women worldwide. The main reasons for this poor prognosis are late diagnosis; when the disease is already in an advanced stage, and the frequent development of resistance to current chemotherapeutic regimens. Growing evidence demonstrates that apart from its role in ovarian cancer progression, epithelial-to-mesenchymal transition (EMT) can promote chemotherapy resistance. In this review, we will highlight the contribution of EMT to the distinct steps of ovarian cancer progression. In addition, we will review the different types of ovarian cancer resistance to therapy with particular attention to EMT-mediated mechanisms such as cell fate transitions, enhancement of cancer cell survival, and upregulation of genes related to drug resistance. Preclinical studies of anti-EMT therapies have yielded promising results. However, before anti-EMT therapies can be effectively implemented in clinical trials, more research is needed to elucidate the mechanisms leading to EMT-induced therapy resistance.

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“…Overexpression of miR-20a in these cancers enhances tumor growth and metastasis [33,34]. More importantly, previous research indicates that miR-20a induces cisplatin resistance in some cancer [35,36]. However, the relationship between miR-20a and chemosensitivity to cisplatin in CRC should be explored.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of MiR-20a Enhances Sensitivity of Colorectal Cancer Cells to Cisplatin by Increasing ASK1 Expression

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Platinum-based chemotherapy is one of the most important strategies for treatment of colorectal cancer. To improve the therapeutic efficiency, adjuvant drugs were sought to sensitize colorectal cancer cells to platinum-based agents such as cisplatin. As previous research has shown that miRNAs are associated with chemosensitivity, we aimed to alter miRNA regulation in colorectal cancer cells to increase their chemosensitivity. Methods: MTT assays were performed to determine the viability of HT29, SW480, and LoVo cells. Quantitative real time polymerase chain reaction (qRT-PCR) was performed to examine the expression of miR-20a in these cell lines. Regulation of the miR-20a/ASK1 axis was confirmed by western blotting and luciferase reporter assays. After treatment with miR-20a inhibitor (anti-miR-20a) and cisplatin, production of reactive oxygen species (ROS), mitochondrial membrane potential, and apoptosis were measured by flow cytometry. Activation of ASK1, Bcl-xl, JNK, and caspase-9, -7, and -3 was detected by western blotting. Results: miR-20a was overexpressed in colorectal cancer cell lines. Furthermore, knockdown of miR-20a increased the sensitivity of colorectal cancer cells to cisplatin treatment in vitro and in vivo. We demonstrated that the ASK1 gene was the target of miR-20a, and knockdown of miR-20a increased the expression of ASK1 in colorectal cancer cells. As cisplatin treatment induced production of ROS, knockdown of miR-20a enhanced ROS signaling through promoting the phosphorylation of ASK1. Phosphorylation of JNK and the subsequent mitochondrial apoptosis were triggered by the combination of cisplatin and anti-miR-20a. Conclusions: Knockdown of miR-20a enhanced sensitivity of colorectal cancer cells to cisplatin through the ROS/ASK1/JNK pathway.

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MicroRNA-20a contributes to cisplatin-resistance and migration of OVCAR3 ovarian cancer cell line

Cited by 18 publications

References 32 publications

Exosomal microRNAs from Longitudinal Liquid Biopsies for the Prediction of Response to Induction Chemotherapy in High-Risk Neuroblastoma Patients: A Proof of Concept SIOPEN Study ‖

Exosomal microRNAs from Longitudinal Liquid Biopsies for the Prediction of Response to Induction Chemotherapy in High-Risk Neuroblastoma Patients: A Proof of Concept SIOPEN Study ‖

The Role of Epithelial-to-Mesenchymal Plasticity in Ovarian Cancer Progression and Therapy Resistance

Knockdown of MiR-20a Enhances Sensitivity of Colorectal Cancer Cells to Cisplatin by Increasing ASK1 Expression

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