MicroRNA-101 reverses temozolomide resistance by inhibition of GSK3β in glioblastoma

Tian, Tian; Ma, Ming; Xia, Qi‐Dong; Qiu, Yang

doi:10.18632/oncotarget.12861

Cited by 53 publications

(34 citation statements)

References 52 publications

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“…Previously, it was reported that miR‐101 sensitized resistant GBM cells to TMZ through downregulation of GSK3 β , which is a multifunctional protein kinase that regulates various cellular pathways . Moreover, inhibition of GSK3 β could enhance TMZ effect by decreasing O 6 ‐methylguanine‐DNA methyltransferase (MGMT) expression via promoter methylation .…”

Section: Resultsmentioning

confidence: 99%

“…Previously, Tian et al. indicated that miR‐101 reversed TMZ resistance by inhibition of GSK3 β in GBM. Moreover, the suppression of GSK3 β could subsequently be decreasing MGMT expression via promoter methylation to regulate the TMZ resistance in GBM .…”

Section: Discussionmentioning

confidence: 99%

“…For example, Tian et al. reported that miR‐101 reversed TMZ resistance by inhibition of GSK3 β in GBM . Although some studies demonstrated the important roles of lncRNAs or miRNAs played in the regulation of chemoresistance, the association of specific lncRNA or miRNA with drug resistance in GBM cells is still largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA‐101 in glioblastoma

2018

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Glioblastoma (GBM) is the most common and lethal tumor of the central nervous system with highly infiltrative and resistant to chemotherapy. Temozolomide (TMZ) is widely used as the first‐line treatment for the therapy of GBM. However, a considerable percentage inherent or acquired resistance in GBM accounts for many treatment failures of the TMZ chemotherapy. Therefore, a deeper understanding of the molecular characteristics underlying TMZ resistance and the identification of novel therapeutic target is urgent. Here, we show that MALAT1 was significantly upregulated in TMZ‐resistant GBM cells. On the other hand, MALAT1 knockdown reduces TMZ resistance of GBM cells both in vitro and in vivo by inhibiting cell proliferation and promoting apoptosis. We also show that miR‐101 overexpression reduced TMZ resistance of GBM cells and played an antagonistic role compared with MALAT1. Importantly, we demonstrate that MALAT1 promoted the chemoresistance through suppressing miR‐101 signaling pathway via directly binding it in GBM cells. In conclusion, our study indicates that knockdown of MALAT1 reverses chemoresistance to TMZ via promoting miR‐101 regulatory network in GBM and thus offers a novel prognostic marker and potential target for GBM TMZ‐based chemotherapy.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA‐101 in glioblastoma

2018

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“…These results indicated that miR-101 plays key roles in BC progression. Although miR-101 has been reported to target many downstream genes, including CDK8 [10], c-FOS [11], CXCR7 [18], SOX9 [14, 19] and GSK3β [20], the potential correlation between miR-101 and Sex-determining region Y-box 2 (SOX2) in BC is still unknown and needs to be further explored.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2

Wang

Zeng

et al. 2017

Cell Physiol Biochem

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Background: Increasing evidence has demonstrated that microRNAs play a critical role in breast cancer (BC) progression. microRNA-101 (miR-101) has been considered a tumor suppressive miRNA in different cancer types. This study aimed to investigate miR-101 expression in BC tissues and to investigate its roles in BC progression that are mediated by Sex-determining region Y-box 2 (SOX2), a critical oncogene in various cancers. Methods: qRT-PCR and immunohistochemistry were performed to detect miR-101 and SOX2 expression in BC tissues and paired normal tissues or BC cell lines. MTT, transwell migration, wound healing, colony formation, flow cytometric and xenograft assays were performed to determine the influence of miR-101 and SOX2 on the malignant behaviors of BC cells in vitro and in vivo. Results: miR-101 was significantly downregulated in BC tissues and cell lines. miR-101 overexpression inhibited the malignant behaviors of BC cells, both in vitro and in vivo. miR-101 downregulation had the converse effect. A miR-101 binding site was identified by luciferase reporter assay in the 3’UTR of SOX2. SOX2 was upregulated in BC tissues and cell lines, and its upregulation was associated with lymph node metastasis, pathological grade and TNM classification. SOX2 knockdown mimicked the effects of miR-101 overexpression on the malignant behaviors of BC cells, while SOX2 overexpression mitigated the miR-101-induced inhibition of these effects. Conclusions: Our study revealed that miR-101 plays a critical role in suppressing tumor progression by directly targeting SOX2.

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“…GSK3β is also a target of miR-101b (Tian et al 2016). Treatment of thapsigargin stimulated fibroblasts with miR-101b mimic results in decreased abundance of GSK3β mRNA (Fig.…”

Section: Thapsigargin Dependent Up-regulation Of Mir-101b and Effect mentioning

confidence: 92%

Endoplasmic reticulum and the microRNA environment in the cardiovascular system

Groenendyk

Fan

Peng

et al. 2019

Can. J. Physiol. Pharmacol.

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Stress responses are important to human physiology and pathology, and the inability to adapt to cellular stress leads to cell death. To mitigate cellular stress and re-establish homeostasis, cells, including those in the cardiovascular system, activate stress coping response mechanisms. The endoplasmic reticulum, a component of the cellular reticular network in cardiac cells, mobilizes so-called endoplasmic reticulum stress coping responses, such as the unfolded protein response. MicroRNAs play an important part in the maintenance of cellular and tissue homeostasis, perform a central role in the biology of the cardiac myocyte, and are involved in pathological cardiac function and remodeling. In this paper, we review a link between endoplasmic reticulum homeostasis and microRNA with an emphasis on the impact on stress responses in the cardiovascular system.

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MicroRNA-101 reverses temozolomide resistance by inhibition of GSK3β in glioblastoma

Cited by 53 publications

References 52 publications

Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA‐101 in glioblastoma

Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA‐101 in glioblastoma

MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2

Endoplasmic reticulum and the microRNA environment in the cardiovascular system

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