Isoflurane activates AMP-activated protein kinase to inhibit proliferation, and promote apoptosis and autophagy in cervical carcinoma both <i>in vitro</i> and <i>in vivo</i>

Wei, Hongfang; Sun, Tianze; Liu, Jie; Wang, Xiaowei; Zhao, Guangping; Shi, Jiong; Chen, Yongxue

doi:10.1080/10799893.2020.1831535

Cited by 8 publications

(11 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Isoflurane was reported to significantly inhibit the proliferation and survival of cervical cancer cells. 39 However, isoflurane was reported to accelerate cell proliferation in the study of bladder cancer cells. 40 In the present study, we revealed that isoflurane promoted PC cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Isoflurane Promotes Cell Proliferation, Invasion, and Migration by Regulating BACH1 and miR-375 in Prostate Cancer Cells In Vitro

Zheng

Chen

et al. 2022

Int J Toxicol

View full text Add to dashboard Cite

The aim of this study was to investigate the mechanism of isoflurane in proliferation, invasion, and migration in prostate cancer (PC) cells in vitro by regulating BACH1 and miR-375. The effect of different concentrations of isoflurane (0%, 0.5%, 1%, and 2%) on PC cell proliferation (PC3 and 22RV1) was measured. After PC cells and normal human prostate stromal immortalized WPMY-1 cells were treated with isoflurane, BACH1 and miR-375 expression was measured. Subsequently, PC3 and 22RV1 cells underwent gain- and loss-of-function assays with or without 4-h 2% isoflurane pretreatment. The levels of miR-375, BACH1, and PTEN were assessed. The binding of BACH1 to miR-375 promoter was detected by ChIP assay. Dual-luciferase reporter assay detected the targeting relationship of miR-375 with BACH1 and PTEN. Isoflurane promoted PC3 and 22RV1 cell proliferation. In addition, isoflurane elevated the levels of BACH1 and miR-375 in a dosage-dependent manner in PC cells. Transfection with miR-375 inhibitor or sh-BACH1 repressed PC cell proliferation, invasion, and migration, while exposure to 2% isoflurane for 4 h before transfection counteracted the inhibitory effects of sh-BACH1 or miR-375 inhibitor on PC cells. PTEN expression was suppressed after 2% isoflurane treatment, but the transfection with miR-375 inhibitor partly abrogated this suppressive effect in PC cells. Moreover, BACH1 bound to miR-375 and miR-375 negatively targeted PTEN. miR-375 mimic could partially reverse the inhibitory effects of sh-BACH1 on the proliferation, invasion, and migration of isoflurane-treated PC cells. Isoflurane facilitated PC cell proliferation, migration, and invasion by activating BACH1 to upregulate miR-375.

show abstract

Section: Discussionmentioning

confidence: 99%

Isoflurane Promotes Cell Proliferation, Invasion, and Migration by Regulating BACH1 and miR-375 in Prostate Cancer Cells In Vitro

Zheng

Chen

et al. 2022

Int J Toxicol

View full text Add to dashboard Cite

show abstract

“…Evidence has shown that anesthesia may affect apoptosis [ 75 , 76 , 86 , 87 , 139 , 140 , 141 , 142 , 143 ]. Wang et al reported that propofol inhibited migration, induced apoptosis of PC cells, and inhibited cell migration in PC cells in vitro by promoting miR-34a -dependent LOC 285194 and E-cadherin upregulation [ 75 ].…”

Section: Tumor Factors: Emt Hypoxia-inducible Factor-1α (Hif-1α) Matr...mentioning

confidence: 99%

“…Propofol also induced apoptosis and increased gemcitabine sensitivity in PC cells via the nuclear factor-κB signaling pathway [ 76 ]. Wei et al reported that isoflurane suppressed proliferation and increased apoptosis and autophagy by activating the AMPK/mTOR pathway in cervical carcinoma, both in vitro and in vivo [ 139 ]. In contrast, promotion of bladder tumor cell proliferation, invasion, and migration was reported to be induced by isoflurane instead of apoptosis inhibition [ 141 ].…”

Section: Tumor Factors: Emt Hypoxia-inducible Factor-1α (Hif-1α) Matr...mentioning

confidence: 99%

“…Zhang et al demonstrated that propofol reduced oxidative stress in the human neuroblastoma cell line [ 158 ]. With regard to VAs, Wei et al showed that oxidative stress was triggered by isoflurane, which elevated ROS levels and lowered the ratio of NAD+/NADH and ATP levels in cervical cancer cells [ 139 ]. In addition, there have been some indications in animal studies that sevoflurane may be neurotoxic in the developing brain, in part due to increased oxidative stress [ 159 , 160 , 161 ].…”

Section: Tumor Factors: Emt Hypoxia-inducible Factor-1α (Hif-1α) Matr...mentioning

confidence: 99%

See 1 more Smart Citation

Pancreatic Cancer and Microenvironments: Implications of Anesthesia

Lai

Kuo

Huang

et al. 2022

Cancers

View full text Add to dashboard Cite

Pancreatic malignancy is a lethal neoplasm, as well as one of the leading causes of cancer-associated mortality, having a 5-year overall survival rate of less than 10%. The average life expectancy of patients with advanced pancreatic cancer does not exceed six months. Although surgical excision is a favorable modality for long-term survival of pancreatic neoplasm, metastasis is initially identified in nearly 80% of the patients by the time of diagnosis, making the development of therapeutic policy for pancreatic cancer extremely daunting. Emerging evidence shows that pancreatic neoplastic cells interact intimately with a complicated microenvironment that can foster drug resistance, metastasis, or relapse in pancreatic cancer. As a result, the necessity of gaining further insight should be focused on the pancreatic microenvironment contributing to cancer progression. Numerous evidence reveals that perioperative factors, including surgical manipulation and anesthetics (e.g., propofol, volatile anesthetics, local anesthetics, epidural anesthesia/analgesia, midazolam), analgesics (e.g., opioids, non-steroidal anti-inflammatory drugs, tramadol), and anesthetic adjuvants (such as ketamine and dexmedetomidine), might alter the tumor microenvironment and cancer progression by affecting perioperative inflammatory or immune responses during cancer surgery. Therefore, the anesthesiologist plays an important role in perioperative management and may affect surgical outcomes. However, the literature on the impact of anesthesia on the pancreatic cancer microenvironment and progression is limited. This review summarizes the current knowledge of the implications of anesthesia in the pancreatic microenvironment and provides future anesthetic strategies for improving pancreatic cancer survival rates.

show abstract

“…The xenograft model also requires quality control because many cell lines have unknown sources or poorly documented receptor expression, and regulatory safeguards are needed to protect researchers from the high communicability risk from handling human cancer tissue [ 16 , 18 ]. Despite these shortcomings, xenograft models have been used extensively to identify potential molecular mechanisms underlying the observed anti-tumour effects of propofol and local anaesthetics as well as pro- and anti-tumour effects following exposure to inhalational anaesthetics [ 19 , 20 , 21 , 22 , 23 ].…”

Section: Xenograft Modelmentioning

confidence: 99%

Investigating the Influence of Anaesthesiology for Cancer Resection Surgery on Oncologic Outcomes: The Role of Experimental In Vivo Models

2022

View full text Add to dashboard Cite

The incidence and societal burden of cancer is increasing globally. Surgery is indicated in the majority of solid tumours, and recent research in the emerging field of onco-anaesthesiology suggests that anaesthetic-analgesic interventions in the perioperative period could potentially influence long-term oncologic outcomes. While prospective, randomised controlled clinical trials are the only research method that can conclusively prove a causal relationship between anaesthetic technique and cancer recurrence, live animal (in vivo) experimental models may more realistically test the biological plausibility of these hypotheses and the mechanisms underpinning them, than limited in vitro modelling. This review outlines the advantages and limitations of available animal models of cancer and how they might be used in perioperative cancer metastasis modelling, including spontaneous or induced tumours, allograft, xenograft, and transgenic tumour models.

show abstract

Isoflurane activates AMP-activated protein kinase to inhibit proliferation, and promote apoptosis and autophagy in cervical carcinoma both in vitro and in vivo

Cited by 8 publications

References 36 publications

Isoflurane Promotes Cell Proliferation, Invasion, and Migration by Regulating BACH1 and miR-375 in Prostate Cancer Cells In Vitro

Isoflurane Promotes Cell Proliferation, Invasion, and Migration by Regulating BACH1 and miR-375 in Prostate Cancer Cells In Vitro

Pancreatic Cancer and Microenvironments: Implications of Anesthesia

Investigating the Influence of Anaesthesiology for Cancer Resection Surgery on Oncologic Outcomes: The Role of Experimental In Vivo Models

Contact Info

Product

Resources

About