Microrna-137 Downregulates Mcl1 in Ovarian Cancer Cells and Mediates Cisplatin-Induced Apoptosis

Chen, Wei; Du, Jingjie; Li, Xiaodi; Zhi, Ziming; Jiang, Siqi

doi:10.2217/pgs-2019-0122

Cited by 12 publications

(9 citation statements)

References 37 publications

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“…It has been shown that there were miR-106a and miR-137 down regulations in DDP-resistant OC cell line. They increased DDP sensitivity via MCL-1 targeting in ovarian tumor cells [ 31 , 32 ]. Neurofibromatosis type 1 (NF1) is a tumor suppressor involved in regulation of PIK3 / AKT / mTOR and MAPK signaling pathways by Ras inactivation [ 106 – 108 ].…”

Section: Main Textmentioning

confidence: 99%

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MicroRNAs as the critical regulators of Cisplatin resistance in ovarian cancer cells

Moghbeli

2021

J Ovarian Res

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Background Ovarian cancer (OC) is one of the leading causes of cancer related deaths among women. Due to the asymptomatic tumor progression and lack of efficient screening methods, majority of OC patients are diagnosed in advanced tumor stages. A combination of surgical resection and platinum based-therapy is the common treatment option for advanced OC patients. However, tumor relapse is observed in about 70% of cases due to the treatment failure. Cisplatin is widely used as an efficient first-line treatment option for OC; however cisplatin resistance is observed in a noticeable ratio of cases. Regarding, the severe cisplatin side effects, it is required to clarify the molecular biology of cisplatin resistance to improve the clinical outcomes of OC patients. Cisplatin resistance in OC is associated with abnormal drug transportation, increased detoxification, abnormal apoptosis, and abnormal DNA repair ability. MicroRNAs (miRNAs) are critical factors involved in cell proliferation, apoptosis, and chemo resistance. MiRNAs as non-invasive and more stable factors compared with mRNAs, can be introduced as efficient markers of cisplatin response in OC patients. Main body In present review, we have summarized all of the miRNAs that have been associated with cisplatin resistance in OC. We also categorized the miRNAs based on their targets to clarify their probable molecular mechanisms during cisplatin resistance in ovarian tumor cells. Conclusions It was observed that miRNAs mainly exert their role in cisplatin response through regulation of apoptosis, signaling pathways, and transcription factors in OC cells. This review highlighted the miRNAs as important regulators of cisplatin response in ovarian tumor cells. Moreover, present review paves the way of suggesting a non-invasive panel of prediction markers for cisplatin response among OC patients.

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Section: Main Textmentioning

confidence: 99%

“… Rao [ 31 ] 2013 miR-106a China MCL1 A2780 cell line Increased DDP sensitivity. Chen [ 32 ] 2020 miR-137 China MCL1 OVCAR3 cell line Increased DDP sensitivity. Su [ 33 ] 2019 miR-142-5p China MCL1 OVCAR3 and SKOV3 cell lines Increased DDP resistance.…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs as the critical regulators of Cisplatin resistance in ovarian cancer cells

Moghbeli

2021

J Ovarian Res

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“…For instance, cisplatin is a potential chemotherapeutic agent with the ability of inhibiting the proliferation and viability of various cancers [ 206 ]. In ovarian cancer, it has been reported that miR-137 reduces the expression of MCL1 to sensitize tumor cells into cisplatin-induced apoptosis [ 207 ]. In this section, we seek to understand how miR modulation on ZEB can contribute to tumor resistance.…”

Section: Micrornas Zeb and Their Role In Tumor Resistancementioning

confidence: 99%

MicroRNAs and Their Influence on the ZEB Family: Mechanistic Aspects and Therapeutic Applications in Cancer Therapy

et al. 2020

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Molecular signaling pathways involved in cancer have been intensively studied due to their crucial role in cancer cell growth and dissemination. Among them, zinc finger E-box binding homeobox-1 (ZEB1) and -2 (ZEB2) are molecules that play vital roles in signaling pathways to ensure the survival of tumor cells, particularly through enhancing cell proliferation, promoting cell migration and invasion, and triggering drug resistance. Importantly, ZEB proteins are regulated by microRNAs (miRs). In this review, we demonstrate the impact that miRs have on cancer therapy, through their targeting of ZEB proteins. MiRs are able to act as onco-suppressor factors and inhibit the malignancy of tumor cells through ZEB1/2 down-regulation. This can lead to an inhibition of epithelial-mesenchymal transition (EMT) mechanism, therefore reducing metastasis. Additionally, miRs are able to inhibit ZEB1/2-mediated drug resistance and immunosuppression. Additionally, we explore the upstream modulators of miRs such as long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), as these regulators can influence the inhibitory effect of miRs on ZEB proteins and cancer progression.

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“…miR-137 was selected for further analyses due to it ranking high among all predicted targets for NCK1-AS1, being negatively correlated with NCK1-AS1 expression, and previously being reported to serve a tumor suppressive role in several cancers. [18][19][20][21][22] The interactions of NCK1-AS1 and miR-137 were validated by luciferase activity reporter assay and RIP Correlation of NCK1-AS1 and NUP43 in GC tissues was analyzed at ENCORI. (I) Levels of NUP43 in GC cells and normal cells were measured using RT-qPCR.…”

Section: Dovepressmentioning

confidence: 99%

<p>Long Non-Coding RNA NCK1-AS1 Serves an Oncogenic Role in Gastric Cancer by Regulating miR-137/NUP43 Axis</p>

Li¹,

Duan²,

Shi³

et al. 2020

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Introduction: Long non-coding RNA (lncRNA) NCK1-AS1 could regulate multiple cancer progression. However, little is known regarding the roles and acting mechanisms of NCK-AS1 in gastric cancer (GC) progression. This work was aimed to explore the relationship between NCK1-AS1 and GC progression to illustrate the mechanisms of NCK1-AS1. Methods: NCK1-AS1 expression level in GC tissues and cells was measured with a quantitative real-time PCR method. In vitro experiments including cell counting kit-8 assay, colony formation assay, wound-healing assay, and transwell invasion assay were employed to detect biological roles of NCK1-AS1 in GC progression. In vivo experiments were performed to analyze the roles of NCK1-AS1 on GC malignant phenotype. Moreover, mechanisms behind the biological roles of NCK1-AS1 in GC were investigated using bioinformatic analysis, luciferase activity reporter assay, RNA immunoprecipitation assay, and rescue experiments. Results: NCK1-AS1 was found to have elevated expression in GC tissues and cells in comparison with normal counterparts. Loss-of-function experiments showed knockdown of NCK1-AS1 refrained GC cell proliferation, colony formation, migration, and invasion in vitro. Animal experiments showed silence of NCK1-AS1 suppresses tumor growth in vivo. Functionally, NCK1-AS1 serves as a sponge for microRNA-137 (miR-137) to upregulate nucleoporin 43 (NUP43) expression in GC. Rescue experiments proved the carcinogenic role of NCK1-AS1/miR-137/NUP43 axis in GC progression. Discussion: In conclusion, the NCK1-AS1/miR-137/NUP43 axis was identified that could contribute to GC malignancy behaviors.

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Microrna-137 Downregulates Mcl1 in Ovarian Cancer Cells and Mediates Cisplatin-Induced Apoptosis

Cited by 12 publications

References 37 publications

MicroRNAs as the critical regulators of Cisplatin resistance in ovarian cancer cells

MicroRNAs as the critical regulators of Cisplatin resistance in ovarian cancer cells

MicroRNAs and Their Influence on the ZEB Family: Mechanistic Aspects and Therapeutic Applications in Cancer Therapy

<p>Long Non-Coding RNA NCK1-AS1 Serves an Oncogenic Role in Gastric Cancer by Regulating miR-137/NUP43 Axis</p>

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