Sevoflurane inhibits migration and invasion of glioma cells via regulating miR-34a-5p/MMP-2 axis

Zhao, Hongxia; Xing, Fei; Yuan, Jingjing; Li, Zhisong; Zhang, Wei

doi:10.1016/j.lfs.2020.117897

Cited by 23 publications

(16 citation statements)

References 27 publications

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“…Our study results concur with these findings, by showing that hsa-miR-34a inhibits MMP-2 expression and thereby suppresses cell migration and invasion in BC cells. The relevant results indicate that the hsa-miR-34a/MMP-2 axis is involved in the regulation of the antitumor effect of esophageal squamous cell carcinoma and glioma (47,48). In addition, we also found that hsa-miR-34a was significantly correlated with clinical and histopathologic characteristics in human BC.…”

Section: Discussionsupporting

confidence: 56%

MicroRNA‑34a‑5p serves as a tumor suppressor by regulating the cell motility of bladder cancer cells through matrix metalloproteinase‑2 silencing

Chou¹,

Chang²,

Tsai³

et al. 2020

Oncol Rep

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Bladder cancer (BC), a common urologic cancer, is the fifth most frequently diagnosed tumor worldwide. hsa-miR-34a displays antitumor activity in several types of cancer. However, the functional mechanisms underlying hsa-miR-34a in BC remains largely unknown. We observed that hsa-mir-34a levels were significantly and negatively associated with clinical disease stage as well as regional lymph node metastasis in human BC. In a series of in vitro investigations, overexpression of hsa-miR-34a inhibited cell migration and invasion in BC cell lines 5637 and UMUC3 as detected by Transwell assays. We further found that hsa-miR-34a inhibited cell migration and invasion by silencing matrix metalloproteinase-2 (MMP-2) expression and thus interrupting MMP-2-mediated cell motility. Our analysis of BC datasets from The Cancer Genome Atlas database revealed a negative correlation between hsa-miR-34a and MMP-2. Moreover, higher MMP-2 protein expression was observed in the BC tissues when compared with that noted in the normal tissue. MMP-2 levels were also significantly associated with clinical disease stage and poor survival rate in human BC. These findings indicate that MMP-2 plays a critical role in regulating BC progression. Therefore, hsa-miR-34a is a promising treatment to target MMP-2 for the prevention and inhibition of cell migration and invasion in BC.

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Section: Discussionsupporting

confidence: 56%

MicroRNA‑34a‑5p serves as a tumor suppressor by regulating the cell motility of bladder cancer cells through matrix metalloproteinase‑2 silencing

Chou¹,

Chang²,

Tsai³

et al. 2020

Oncol Rep

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“…Previously, several studies have demonstrated that SEV treatment leads to miRNA alteration in several tumour cells. For instance, Zhao et al 38 reported that SEV dampens the MMP‐2 expression by upregulating miR‐34a‐5p, thus repressing glioma. Also, Zhang et al 39 pointed out that SEV prevents glioma cell migration and invasion by modulating miR‐146b‐5p/MMP16, bringing a novel theoretical reference for the utilization of SEV and other narcotic drugs in glioma.…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane inhibits neuroblastoma cell proliferation and invasion and induces apoptosis by miR‐144‐3p/YAP1 axis

Yang

Zhang

et al. 2021

Basic Clin Pharma Tox

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Background: Sevoflurane (SEV) is a typical volatile anaesthetic and has an antitumour activity in various cancer cells. Here, we were curious whether SEV has tumour-suppressive effects in neuroblastoma (NB).Methods: NB cell lines (K-N-SH and SK-N-AS) were treated with SEV (1%, 2% and 4%). Cell Counting Kit-8 (CCK8) and Transwell assays were conducted to examine cell proliferation and invasion, respectively. The apoptosis was verified by flow cytometry, and the yes-associated protein 1 (YAP1), Bax, Bcl2 and cleaved caspase3 levels were detected by western blotting. Quantitative real-time PCR (qRT-PCR) was conducted to monitor the miR-144-3p level in SEV-treated NB cells. The targeted relationship between miR-144-3p and YAP1 was predicted by bioinformatics and testified by the dual-luciferase reporter assay. Results: SEV mitigated NB cell proliferation and invasion and strengthened apoptosis dose-dependently. SEV upregulated miR-144-3p. Moreover, the miR-144-3p inhibitor transfection significantly reduced the tumour-suppressive effect of SEV on NB cells. Furthermore, the dual-luciferase reporter assay confirmed that miR-144-3p targeted YAP1 and overexpressing YAP1 partially weakened the inhibitive effects of miR-144-3p on NB cells. Conclusion:SEV abated NB cell proliferation and invasion and accelerated apoptosis through the miR-144-3p/YAP1 axis.

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“…Multiple studies suggested Sev could inhibit glioma cell migration and invasion by interacting with miRNAs, like miR-34a-5p, miR-146b-5p and miR-637 [ 4 , 34 , 35 ]. Additionally, Sev could repress cell proliferation and increase apoptosis of glioma cells [ 5 , 31 , 36 ].…”

Section: Discussionmentioning

confidence: 99%

“…Sevoflurane (Sev) is a widely used anesthetic gas by interacting with γ-aminobutyric acid [ 3 ]. Multiple reports suggest Sev has an anti-glioma activity by decreasing cell proliferation, migration and invasion [ 4–6 ]. However, the mechanism underlying Sev in glioma treatment remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane inhibits progression of glioma via regulating the HMMR antisense RNA 1/microRNA-7/cyclin dependent kinase 4 axis

Bao¹,

Peng²,

Shen

et al. 2021

Bioengineered

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Sevoflurane (Sev) is a volatile anesthetic that can inhibit tumor malignancy. Glioma is a main brain problem, but the mechanism of Sev in glioma progression is largely unclear. This study aims to explore a potential regulatory network of long noncoding RNA (lncRNA)/microRNA (miRNA)/mRNA associated with the function of Sev in glioma progression. LncRNA HMMR antisense RNA 1 (HMMR-AS1), miR-7 and cyclin-dependent kinase 4 (CDK4) abundances were examined via quantitative reverse transcription polymerase chain reaction and western blot. Cell viability, invasion, and colony formation ability were analyzed via cell counting kit-8, transwell analysis, and colony formation. The target association was analyzed via dual-luciferase reporter analysis and RNA pull-down. The in vivo function of Sev was investigated by xenograft model. HMMR-AS1 abundance was increased in glioma tissues and cells, and reduced via Sev. Sev constrained cell viability, invasion, and colony formation ability via decreasing HMMR-AS1 in glioma cells. miR-7 expression was decreased in glioma, and was targeted via HMMR-AS1. HMMR-AS1 silence restrained cell viability, invasion, and colony formation ability by up-regulating miR-7 in glioma cells. Sev increases miR-7 abundance via decreasing HMMR-AS1. CDK4 was targeted via miR-7, and highly expressed in glioma. miR-7 overexpression inhibited cell viability, invasion, and colony formation ability via reducing CDK4 in glioma cells. CDK4 expression was reduced by Sev via HMMR-AS1/miR-7 axis. Sev suppressed cell growth in glioma by regulating HMMR-AS1. Sev represses glioma cell progression by regulating HMMR-AS1/miR-7/CDK4 axis.

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Sevoflurane inhibits migration and invasion of glioma cells via regulating miR-34a-5p/MMP-2 axis

Cited by 23 publications

References 27 publications

MicroRNA‑34a‑5p serves as a tumor suppressor by regulating the cell motility of bladder cancer cells through matrix metalloproteinase‑2 silencing

MicroRNA‑34a‑5p serves as a tumor suppressor by regulating the cell motility of bladder cancer cells through matrix metalloproteinase‑2 silencing

Sevoflurane inhibits neuroblastoma cell proliferation and invasion and induces apoptosis by miR‐144‐3p/YAP1 axis

Sevoflurane inhibits progression of glioma via regulating the HMMR antisense RNA 1/microRNA-7/cyclin dependent kinase 4 axis

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