MicroRNA‑101 modulates cisplatin chemoresistance in liver cancer cells via the DNA‑PKcs signaling pathway

Chai, Zong‐Tao; Yin, Xiaolan; Jin, Chen; Shi, Jie; Sun, Jianzhong; Liu, Chang; Liu, Feng; Cheng, Shuqun

doi:10.3892/ol.2019.10674

Cited by 9 publications

(9 citation statements)

References 34 publications

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“…MiR-101 overexpression augments cytotoxicity and reduces chemoresistance to chemotherapeutic reagent cisplatin (CDDP) in liver cancer cell line HepG2 cells through inhibiting the DNA-PKcs/Akt/NF-κB signaling pathway. 30 Circular RNA circVAPA is upregulated and exerts oncogenic properties by sponging miR-101 in colorectal cancer. 31 MiR-101 has been reported to inhibit Nrf2 expression from impeding breast cancer cell proliferation and enhancing their sensitivity to oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

MiR-101 Protects Against the Cerebral I/R Injury Through Regulating JAK2/STAT3 Signaling Pathway

Guo

Shen

Yong

2021

NDT

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Background: Ischemic stroke is a devastating disease with very limited therapeutics. Although miR-101 has been reported to play crucial roles in various human diseases, its role in ischemic stroke remains unclear. Methods: Ischemia-reperfusion (I/R) injury neuronal cells and rat model with I/R injury were constructed. Viability and apoptosis of I/R model cells with miR-101 overexpression or downregulation were evaluated. Potential targets of miR-101 were predicted using miRNA database microRNA.org and confirmed using luciferase reporter assays. Meanwhile, JAK2 and p-STAT3 protein levels were evaluated by Western blot. In addition, rescue experiments (silencing of JAK2) were applied to determine the role of miR-101 in cerebral I/R injury. Results: MiR-101 was significantly downregulated in OGD/R-induced neuronal cells and brain tissues with I/R injury. MiR-101 overexpression (miR-101 mimics) significantly promoted viability and inhibited apoptosis of OGD/R-induced neuronal cells in vitro and efficiently protected rats from ischemic brain injury in vivo. By contrast, miR-101 inhibitor exacerbated growth defect, apoptosis, and ischemic brain injury. Luciferase reporter assay indicated that JAK2 was a direct target of mIR-101, and JAK2 silencing effectively reversed the miR-101 inhibitor-induced neuronal cell apoptosis in vitro and reduced cerebral infarction volume in vivo. Conclusion:Our study demonstrated that miR-101 efficiently protected neuronal cells from apoptosis and ischemic brain injury through regulating the JAK2/STAT3 signaling pathway, suggesting that miR-101 might be a potential target for treatment of ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

MiR-101 Protects Against the Cerebral I/R Injury Through Regulating JAK2/STAT3 Signaling Pathway

Guo

Shen

Yong

2021

NDT

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“…The NF-κB pathway is involved in the regulation of the inflammatory and immune responses (58) and miR-101 regulates the NF-κB pathway in several diseases. For example, miR-101 attenuates cisplatin chemoresistance by reducing NF-κB signaling in hepatocarcinoma (59) and miR-101 silencing facilitates the pathogenesis of neuropathic pain by promoting NF-κB activity (60). In the present study, the expression of NF-κB-related proteins in SLE PBMCs was markedly decreased following miR-101-3p overexpression, indicating that miR-101-3p may be involved in the development of SLE via its inhibition of the NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

miR‑101‑3p negatively regulates inflammation in systemic lupus erythematosus via MAPK1 targeting and inhibition of the NF‑κB pathway

Zhao

Wang

et al. 2021

Mol Med Rep

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Systemic lupus erythematosus (SLE) is an autoimmune disease often used as a model in genomics research. The downregulation of microRNA-101-3p (miR-101-3p) participates in the progression of SLE, although the underlying mechanisms remain to be elucidated. The present study aimed to evaluate the specific roles of miR-101-3p in the SLE inflammatory response and its potential mechanisms. Reverse transcription-quantitative (RT-q) PCR was used to profile miR-101-3p expression in the peripheral blood mononuclear cells (PBMCs) from 40 female patients with SLE and 20 female healthy volunteers. The interactions between miR-101-3p and MAPK1 were identified and evaluated using dual-luciferase reporter and RNA pull-down assays. The levels of IL-10 and IFN-γ were evaluated by enzyme-linked immunosorbent assay. The expression of NF-κB p65 and phosphorylated IκBα were evaluated using western blotting. miR-101-3p expression was demonstrated to be downregulated in SLE PBMCs. miR-101-3p negatively regulated IL-10 and IFN-γ expression in SLE samples and was demonstrated to target MAPK1. Increases in MAPK1 expression eliminated miR-101-3p inhibition of IL-10 and IFN-γ. MAPK1 activated the NF-κB pathway in SLE PBMCs and this activation was inhibited when miR-101-3p was overexpressed. In addition, treatment with BAY11-7085 (NF-κB activator) was demonstrated to reverse the inhibitory effects of miR-101-3p expression on both IL-10 and IFN-γ in SLE PBMCs. BAY11-7082 also markedly reduced MAPK1-induced increases in IL-10 and IFN-γ in SLE PBMCs. miR-101-3p overexpression attenuated the inflammatory response in SLE PBMCs by inhibiting the expression of MAPK1 and blocking the NF-κB pathway. The results revealed a novel regulatory mechanism in SLE inflammation and offer a new direction for the development of SLE treatments.

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“…19 Chai et al reported that overexpression of miR-101 enhanced the sensitivity of liver cancer cells to cisplatin via inhibiting the activation of DNA-PKcs signaling pathway. 20 Sun et al indicated that inhibition of miR-4262 reduced PTX resistance in lung cancer cells. 21 In addition, evidences have been shown that miR-153 functioned as a tumor suppressor in several cancers including lung cancer, acute lymphoblastic leukemia and breast cancer.…”

Section: Discussionmentioning

confidence: 99%

<p>MiR-153-5p Enhances the Sensitivity of Triple-Negative Breast Cancer Cells to Paclitaxel by Inducing G2M Phase Arrest</p>

Wang¹,

Wu²,

Zhang³

et al. 2020

OTT

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Background: Paclitaxel (PTX) resistance is a main obstacle for the treatment of triplenegative breast cancers (TNBC). Evidences have shown that miR-153-5p could induce the apoptosis of breast cancer cells. Thus, this study aimed to investigate the effect of miR-153-5p on PTX-resistance TNBC cells. Methods: Cell Counting Kit-8, flow cytometry and wound healing assays were used to detect the viability, apoptosis and migration of MDA-MB-231/PTX cells, respectively. The luciferase reporter assay was used to explore the potential binding targets of miR-153-5p. The expressions of CDK1, cyclin B1 and p-Akt in MDA-MB-231/PTX cells were detected with Western blot. In vivo animal study was performed finally. Results: In this study, the inhibitory effects of PTX on the proliferation and migration of MDA-MB-231/PTX cells were significantly enhanced following transfection with miR-153-5p. In addition, overexpression of miR-153-5p markedly enhanced the pro-apoptotic effect of PTX on MDA-MB-231/PTX cells. Luciferase reporter assay validated that cyclin-dependent kinase 1 (CDK1) was a potential binding target of miR-153-5p. Moreover, overexpression of miR-153-5p prominently increased PTX-induced cell cycle arrest at G2/M phase in MDA-MB-231/PTX cells via downregulation of CDK1, cyclin B1 and p-Akt. In vivo experiments confirmed that overexpression of miR-153-5p notably enhanced PTX sensitivity in MDA-MB-231/PTX xenograft model. Conclusion: We found that overexpression of miR-153-5p could reverse PTX resistance in PTX-resistant TNBC cells via inducing G2/M phase arrest, indicating that miR-153-5p may be a promising agent for patients with PTX-resistant TNBC.

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MicroRNA‑101 modulates cisplatin chemoresistance in liver cancer cells via the DNA‑PKcs signaling pathway

Cited by 9 publications

References 34 publications

MiR-101 Protects Against the Cerebral I/R Injury Through Regulating JAK2/STAT3 Signaling Pathway

MiR-101 Protects Against the Cerebral I/R Injury Through Regulating JAK2/STAT3 Signaling Pathway

miR‑101‑3p negatively regulates inflammation in systemic lupus erythematosus via MAPK1 targeting and inhibition of the NF‑κB pathway

<p>MiR-153-5p Enhances the Sensitivity of Triple-Negative Breast Cancer Cells to Paclitaxel by Inducing G2M Phase Arrest</p>

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