&lt;p&gt;Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis&lt;/p&gt;

Wang, Dongmei; Yang, Tao; Liu, Junqi; Liu, Yafei; Xing, Na; He, Jun; Yang, Jianjun; Ai, Yanqiu

doi:10.2147/ott.s232601

Cited by 26 publications

(20 citation statements)

References 34 publications

(30 reference statements)

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“…In line with these findings, the present study further demonstrated that propofol decreased ROS in tumors via regulation of DMT1. Previous published works demonstrating the antitumor effect of propofol in glioma were mainly based on in vitro studies, illustrated that propofol suppresses proliferation and invasion of glioma cells by upregulating microRNA-218 expression, inhibiting Wnt signaling or blocking the PI3K/Akt pathway through miR-206/ROCK1 axis (32)(33)(34). The present study revealed propofol anti-tumor effect from the perspective of oxidative stress inhibition in glioma cells through regulating DMT1 expression by modifying CPARs.…”

Section: Discussionsupporting

confidence: 54%

Antioxidant Effect of Propofol in Gliomas and Its Association With Divalent Metal Transporter 1

et al. 2020

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BackgroundOxidative stress enhances tumor invasion and metastasis in brain cancer. The activation of divalent metal transporter 1 (DMT1), which is regulated by glutamate receptors, can result in the increase of oxidative stress and risk of cancer development. Propofol, an anesthetic with antioxidant capacity, has been shown to decrease oxidative stress in several different types of cancer. However, the underlying mechanism remains unclear. Therefore, the present study aimed to elucidate the mechanism underlying the suppression of oxidative stress in glioma cells by propofol. It was hypothesized that propofol may inhibit oxidative stress in gliomas via suppressing Ca2+-permeable α-amino-3-hydroxyl-5-methylisoxazole-4-propionic acid (AMPA) receptor (CPAR)-DMT1 signaling.MethodsMale Wistar rats with C6 gliomas, which were established by intracranial injection of C6 glioma cells, were either treated with propofol or not for 6 h before being sacrificed. The levels of AMPA receptor subunit GluR2 and DMT1 protein expression were assessed using western blotting. The association between CPARs and DMT1 was confirmed in vitro using the AMPA receptor activator (R, S)-AMPA. Glutathione and reactive oxygen species assay kits were used to evaluate tumor oxidative stress. The effect of propofol on glioma proliferation was evaluated by determining tumor weight, cell cycles and a growth curve.ResultsPropofol infusion at either 20 or 40 mg/kg-1/h-1 increased GluR2 levels and downregulated DMT1 expression as well as glutathione content markedly in the periphery compared with that in the glioma core. The in vitro results revealed that (R, S)-AMPA increased DMT1 expression and reactive oxygen species levels, which were partly reversed by propofol treatment.ConclusionPropofol regulated DMT1 expression by modulating CPARs, resulting in the inhibition of tumor oxidative stress and glioma growth. The present study provides evidence for optimizing the selection of anesthetic drugs in perioperative management and prognosis of patients with glioma.

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Section: Discussionsupporting

confidence: 54%

Antioxidant Effect of Propofol in Gliomas and Its Association With Divalent Metal Transporter 1

et al. 2020

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“…glioma through the inactivation of the PI3K/AKT pathway. 40 However, there are little researches on the interaction between Tim-1 and the PI3K/AKT axis in glioma, which proved the novelty of our study to some degree.…”

Section: Discussionmentioning

confidence: 68%

<p>Knockdown of T Cell Immunoglobulin and Mucin 1 (Tim-1) Suppresses Glioma Progression Through Inhibition of the Cytokine-PI3K/AKT Pathway</p>

Zhou

Fei

Han

et al. 2020

OTT

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Background: Glioma is formed by abnormal proliferation of glial cells in the brain. T cell immunoglobulin and mucin 1 (Tim-1) is linked to cancer development. This study aimed to assess Tim-1 functions in biological behaviors. Methods: The glioma tissues and paracancerous tissues were collected. The pathological morphology of glioma and positive expression of Tim-1 were evaluated. The sh-Tim-1 lentivirus vector was infected into U251 and U87 cells to evaluate glioma cell malignant behaviors. The differentially expressed terms in glioma cells were analyzed by Agilent microarray analysis, and enrichment analyses were performed. Levels of cytokines (TGF-β1, IL-6, IL-4 and IL-10) and the PI3K/AKT pathway were measured. U87 cells with sh-Tim-1 were transplanted into nude mice, and the volume and weight of tumors were measured. Results: Tim-1 levels in glioma tissues and cells were higher than those in glial tissues and cells. Tim-1 knockdown prevented glioma cell proliferation, invasion and migration, and reduced TGF-β1, IL-6, IL-4 and IL-10 levels of glioma. Co-treatment of PI3K/AKT pathway activator and knockdown Tim-1 partially reversed these outcomes. After Tim-1 knockdown, tumor volume and weight and Ki67-positive rate of nude mice were diminished. Conclusion: Tim-1 knockdown inhibited biological behaviors of glioma cells through the PI3K/AKT pathway, which may provide a novel therapy for glioma.

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“…mTOR is a serine/threonine protein kinase and a downstream effector of PI3K/AKT. P-PI3K p85 (Tyr607), p-AKT (Ser473), and p-mTOR (Ser2448) have been shown to be related to the biological behavior of tumor cells [ 43 – 45 ]. Therefore, the PI3K/AKT/mTOR signaling pathway, one of the most important intracellular signaling pathways, affects the state of downstream effector molecules in many ways.…”

Section: Discussionmentioning

confidence: 99%

Morphine promotes the malignant biological behavior of non-small cell lung cancer cells through the MOR/Src/mTOR pathway

Liu

Yang

et al. 2021

Cancer Cell Int

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Background Morphine, a µ-opioid receptor (MOR) agonist, has been shown to be related to the activity of cancer cells, and a higher morphine dosage reduces the survival time of patients with lung cancer. However, the effect of morphine on the malignant behavior of lung cancer cells remains unclear. The aim of this study was to investigate the specific molecular mechanism by which morphine regulates the malignant biological behavior of non-small cell lung cancer. Methods Immunofluorescence staining and Western blot analyses were performed to detect MOR expression. H460 non-small cell lung cancer cells were used in this study, and cell proliferation, the cell cycle and apoptosis were evaluated using Cell Counting Kit-8 (CCK-8) and flow cytometry assays, respectively. Cell migration and invasion were detected using wound healing and Transwell assays. The effect of morphine on lung cancer development in vivo was examined by performing a xenograft tumor assay following morphine treatment. Results Morphine promoted the growth of H460 cells both in vivo and in vitro. Morphine enhanced cell migration and invasion, modified cell cycle progression through the S/G2 transition and exerted an antiapoptotic effect on H460 cells. Additionally, morphine increased Rous sarcoma oncogene cellular homolog (Src) phosphorylation and activated the phosphoinositide 3 kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. Treatment with the MOR antagonist methylnaltrexone (MNTX) and the Src inhibitor protein phosphatase 1 (PP1) reduced the phosphorylation induced by morphine. Furthermore, MNTX, PP1, and the PI3K/AKT inhibitor deguelin reversed the antiapoptotic effect of morphine on lung cancer cells. Conclusion Morphine promotes the malignant biological behavior of H460 cells by activating the MOR and Src/mTOR signaling pathways.

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<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

Cited by 26 publications

References 34 publications

Antioxidant Effect of Propofol in Gliomas and Its Association With Divalent Metal Transporter 1

Antioxidant Effect of Propofol in Gliomas and Its Association With Divalent Metal Transporter 1

<p>Knockdown of T Cell Immunoglobulin and Mucin 1 (Tim-1) Suppresses Glioma Progression Through Inhibition of the Cytokine-PI3K/AKT Pathway</p>

Morphine promotes the malignant biological behavior of non-small cell lung cancer cells through the MOR/Src/mTOR pathway

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