Sevoflurane and thiopental preconditioning attenuates the migration and activity of MMP-2 in U87MG glioma cells

Hurmath, Fathima Kamaluddin; Mittal, Mohit; Ramaswamy, Palaniswamy; Rao, Gautam; Nanjaiah, Nandakumar Dalavaikodihalli

doi:10.1016/j.neuint.2016.02.003

Cited by 34 publications

(34 citation statements)

References 68 publications

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“…Enrichment analysis suggested that DEGs function differed between different glioma grades. DEGs in GBM tissue compared to non-tumor tissue were mainly involved in the regulation of the extracellular matrix (ECM) (Table 2), an environment that is essential to tumor development and maintenance [24, 25]. …”

Section: Resultsmentioning

confidence: 99%

COL3A1 and SNAP91: novel glioblastoma markers with diagnostic and prognostic value

et al. 2016

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Although patients with glioblastoma (GBM) have grave prognosis, significant variability in patient outcome is observed. This study aims to identify novel targets for GBM diagnosis and therapy. Microarray data (GSE4290, GSE7696, and GSE4412) obtained from the Gene Expression Omnibus was used to identify the differentially expressed genes (DEGs) by significant analysis of microarray (SAM). Intersection of the identified DEGs for each profile revealed 46 DEGs in GBM. A subset of common DEGs were validated by real-time reverse transcription quantitative PCR (qPCR). The prognostic value of some of the markers was also studied. We determined that RRM2 and COL3A1 were increased and directly correlated with glioma grade, while SH3GL2 and SNAP91 were decreased in GBM and inversely correlated with glioma grade. Kaplan-Meir analysis of GSE7696 revealed that COL3A1 and SNAP91 correlated with survival, suggesting that COL3A1 and SNAP91 may be suitable biomarkers for diagnostic or therapeutic strategies for GBM.

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Section: Resultsmentioning

confidence: 99%

COL3A1 and SNAP91: novel glioblastoma markers with diagnostic and prognostic value

et al. 2016

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“…Inhibits proliferation and induce apoptosis [28] Upregulates miRNA-203 Inhibits breast cancer cells proliferation [30] Downregulates MMP-2, MMP-9, fascin, and ezrin Inhibits the invasion and migration of human lung cancer cells [31] Downregulates MMP-2 Inhibits migration of glioma cells [32] Downregulates HIF-1α Inhibits hypoxia-induced growth and metastasis of lung cancer cells [33] Upregulates miR-637 and downregulates Akt1…”

Section: The Biological Function Of Sevoflurane In Suppressing Oncogementioning

confidence: 99%

<p>The Role of Inhaled Anesthetics in Tumorigenesis and Tumor Immunity</p>

Xu¹,

Jiang²,

Xie³

et al. 2020

CMAR

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Inhaled anesthetics are widely used for induction and maintenance of anesthesia during surgery, including isoflurane, sevoflurane, desflurane, haloflurane, nitrous oxide (N 2 O), enflurane and xenon. Nowadays, it is controversial whether inhaled anesthetics may influence the tumor progression, which urges us to describe the roles of different inhaled anesthetics in human cancers. In the review, the relationships among the diverse inhaled anesthetics and patient outcomes, immune response and cancer cell biology were discussed. Moreover, the mechanisms of various inhaled anesthetics in the promotion or inhibition of carcinogenesis were also reviewed. In summary, we concluded that several inhaled anesthetics have different immune functions, clinical outcomes and cancer cell biology, which could contribute to opening new avenues for selecting suitable inhaled anesthetics in cancer surgery.

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“…The incidence of glioma is also relatively high, presenting in 5.26 per 100 000 individuals. [3][4][5] Tramadol, a non-opioid central analgesic, attenuates the sensitivity of glioblastoma to the chemotherapy drug temozolomide through the suppression of Cx43-mediated gap junction intercellular communication. The median overall survival rates for low-grade gliomas (WHO grade II), anaplastic gliomas (WHO grade III) and glioblastomas (GBM, WHO IV) are 78.1, 37.6 and 14.4 months, respectively.…”

Section: Introductionmentioning

confidence: 99%

“…The median overall survival rates for low-grade gliomas (WHO grade II), anaplastic gliomas (WHO grade III) and glioblastomas (GBM, WHO IV) are 78.1, 37.6 and 14.4 months, respectively. [5][6][7][8] These varying effects may be due to different specific biological effects. An increasing number of studies indicate that many anaesthetics and analgesics used during or after the surgical excision exert significant effects on various hallmarks of tumours.…”

Section: Introductionmentioning

confidence: 99%

“…An increasing number of studies indicate that many anaesthetics and analgesics used during or after the surgical excision exert significant effects on various hallmarks of tumours. [3][4][5] Tramadol, a non-opioid central analgesic, attenuates the sensitivity of glioblastoma to the chemotherapy drug temozolomide through the suppression of Cx43-mediated gap junction intercellular communication. 3 In contrast, research has suggested that these types of drugs, such as propofol, lidocaine, sevoflurane and thiopental, may suppress the proliferation and invasion of glioma cells and, therefore, be beneficial in the control of cancer progression.…”

Section: Introductionmentioning

confidence: 99%

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Effects of dexmedetomidine on glioma cells in the presence or absence of cisplatin

Yang

Chen

Yan

et al. 2019

J of Cellular Biochemistry

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With the extensive use of dexmedetomidine (Dex) in the surgical resection of tumours for its potent sedative and analgesic properties, its effects on various properties of tumours have received increased attention. The study described herein aimed to investigate the effects of Dex on glioma cells in the presence or absence of cisplatin (DDP). Glioma U251 and U87MG cells were treated with different doses (1‐50 nM) of Dex for 12 hours, then recultured in a Dex‐free medium. In addition, Dex was added to U251 and U87MG cells 12 hours before or simultaneously with a 12‐hour DDP treatment. Treatment with Dex increased the viability of both cell lines; this effect continued for at least 24 hours after Dex was removed. A cell invasion assay indicated that Dex inhibited cell invasion at 50 nM, but not at 10 nM. Western blot analysis showed that Dex increased the expression of phosphorylated extracellular‐signal‐regulated kinase 1/2, phosphoitide 3‐kinase and p‐AKT, but decreased ROCK protein levels at a dose of 50 nM. Intracellular Ca 2+ concentration was decreased by Dex in a dose‐dependent manner. DDP toxicity was attenuated by 10 nM Dex added either before or with DDP treatment. However, pretreatment with 50 nM Dex instead enhanced the toxicity of DDP. Single‐dose treatment with Dex did not significantly change glioma volume in nude mice, but changed the expression of Ki67 and matrix metalloproteinase‐3 in the tumour. In conclusion, this study provides evidence of the regulatory effects of Dex on proliferation, invasion and chemosensitivity of glioma cells, and outlines potential mechanisms for these effects.

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Sevoflurane and thiopental preconditioning attenuates the migration and activity of MMP-2 in U87MG glioma cells

Cited by 34 publications

References 68 publications

COL3A1 and SNAP91: novel glioblastoma markers with diagnostic and prognostic value

COL3A1 and SNAP91: novel glioblastoma markers with diagnostic and prognostic value

<p>The Role of Inhaled Anesthetics in Tumorigenesis and Tumor Immunity</p>

Effects of dexmedetomidine on glioma cells in the presence or absence of cisplatin

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