Propofol induces hepatocellular carcinoma cell apoptosis via regulating miR-105/JAK2/STAT3 axis

Li, Jingjin; Liu, Mengjiang; Zeng, Bin; Wang, Zhonghai

doi:10.1016/j.cyto.2021.155649

Cited by 8 publications

(3 citation statements)

References 18 publications

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“…LncRNA GAS5 contained miR-21 response elements and competed with miR-21, upregulating its target genes PDCD4 and PTEN for anticancer effects (Hu et al, 2016). Studies indicated that resveratrol (Li et al, 2014), matrine (Luo et al, 2017), oxymatrine (Huang et al, 2014), and ursolic acid (Liu et al, 2015) all reduced miR-21 expression in HCC cells, inhibiting proliferation and promoting apoptosis, suggesting their involvement in the lncRNA GAS5/miR-21/PDCD4 pathway for anti-HCC action. Sophorae Fructus flavonoids regulated the lncRNA FBXL19-AS1/miR-342-3p axis, inhibiting HCC cell proliferation and invasion (Jin et al, 2020).…”

Section: Tcm Active Compoundsmentioning

confidence: 99%

The role of competing endogenous RNA network in the development of hepatocellular carcinoma: potential therapeutic targets

Tang,

Li,

Zheng

et al. 2024

Front. Cell Dev. Biol.

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The current situation of hepatocellular carcinoma (HCC) management is challenging due to its high incidence, mortality, recurrence and metastasis. Recent advances in gene genetic and expression regulation have unveiled the significant role of non-coding RNA (ncRNA) in various cancers. This led to the formulation of the competing endogenous RNA (ceRNA) hypothesis, which posits that both coding RNA and ncRNA, containing miRNA response elements (MRE), can share the same miRNA sequence. This results in a competitive network between ncRNAs, such as lncRNA and mRNA, allowing them to regulate each other. Extensive research has highlighted the crucial role of the ceRNA network in HCC development, impacting various cellular processes including proliferation, metastasis, cell death, angiogenesis, tumor microenvironment, organismal immunity, and chemotherapy resistance. Additionally, the ceRNA network, mediated by lncRNA or circRNA, offers potential in early diagnosis and prevention of HCC. Consequently, ceRNAs are emerging as therapeutic targets for HCC. The complexity of these gene networks aligns with the multi-target approach of traditional Chinese medicine (TCM), presenting a novel perspective for TCM in combating HCC. Research is beginning to show that TCM compounds and prescriptions can affect HCC progression through the ceRNA network, inhibiting proliferation and metastasis, and inducing apoptosis. Currently, the lncRNAs TUG1, NEAT1, and CCAT1, along with their associated ceRNA networks, are among the most promising ncRNAs for HCC research. However, this field is still in its infancy, necessitating advanced technology and extensive basic research to fully understand the ceRNA network mechanisms of TCM in HCC treatment.

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Section: Tcm Active Compoundsmentioning

confidence: 99%

The role of competing endogenous RNA network in the development of hepatocellular carcinoma: potential therapeutic targets

Tang,

Li,

Zheng

et al. 2024

Front. Cell Dev. Biol.

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“…Apart from that, miR-556-3p played an essential role in propofol regulated non-coding RNA activated by DNA damage (NORAD)/miR-556-3p/migration and invasion enhancer 1 (MIEN1) axis, which involved in suppressing HCC cell proliferation and EMT progression (34). In addition, propofol increased the expression of miR-105, a potential JAK2/STAT3 signaling inhibitor, serving as a key mediator in HCC apoptosis process (35).…”

Section: Intravenous Anesthetic Agents Propofolmentioning

confidence: 99%

Long-term effect of anesthesia choice on patients with hepatocellular carcinoma undergoing open liver resection

Zhao

Sun

et al. 2023

Front. Oncol.

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Clinical and experimental evidence suggested that anesthesia choice can influence cancer progression and patients’ outcomes by modulating tumor microenvironment and tumorigenic pathways. Curative resection is the mainstay of therapy for hepatocellular carcinoma (HCC), which is an intractable disease due to high recurrence and poor prognosis. However, different anesthetics may play different roles in alleviating surgery-induced stress response and inflammatory cytokines release that are considered to be closely associated with proliferation, invasion and metastasis of tumor cells. Propofol, sevoflurane, non-steroidal anti-inflammatory drugs and local anesthetics have shown to exert anti-tumor effect on HCC mainly through regulating microRNAs or signaling pathways, while other inhalational agents, dexmedetomidine and opioids have the potential to promote tumor growth. In terms of anesthetic methods and analgesia strategies, propofol based total intravenous anesthesia and thoracic epidural analgesia could be preferred for HCC patients undergoing open liver resection rather than inhalational anesthesia. Local anesthesia techniques have great potential to attenuate perioperative stress response, hence they may contribute to more favorable outcomes. This review summarized the relations between different anesthesia choices and HCC patients’ long-term outcomes as well as their underlying mechanisms. Due to the complexity of molecules interactions and signaling pathways, further studies are warranted to confirm these results so as to optimize anesthesia strategy for HCC patients.

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“…Animal experiments and in vitro cell experiments consistently show that propofol possesses the potential to inhibit the malignancy of primary cancer ( Sessler and Riedel, 2019 ). Several literature discussing relationships among propofol, chemotherapeutic agents, and cancer cell in vitro have focused on cell apoptosis ( Li et al, 2017 ; Li et al, 2021 ; Shen et al, 2021 ). Cell apoptosis caused by propofol and chemotherapeutic drugs has been widely reported.…”

Section: Introductionmentioning

confidence: 99%

Propofol Augments Paclitaxel-Induced Cervical Cancer Cell Ferroptosis In Vitro

et al. 2022

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Introduction: Cervical cancer is common in women. The present standardized therapies including surgery, chemotherapy, and radiotherapy are still not enough for treatment. Propofol is the most commonly used intravenous anesthetic agent for induction and maintenance of anesthesia and has been shown to exert anti-malignancy effects on cancer cells, inducing oxidative stress and apoptosis. However, the biological effects of propofol have not yet been systematically assessed. In this study, we examined the ferroptosis-related changes caused by propofol and the chemotherapeutic agent paclitaxel besides apoptosis in vitro.Methods: Cervical cancer cell lines (C-33A and HeLa) were treated with propofol alone (1, 2, 5, 10, and 20 μg/ml) or in combination with paclitaxel (0.5, 1, and 5 μg/ml). The viability was assessed using cell counting kit-8 (CCK8), apoptosis was detected by flow cytometry, morphological changes of mitochondria were examined using transmission electron microscope (TEM), cellular reactive oxygen species (ROS), and intracellular ferrous ions were determined by fluorescence microscope or confocal microscopy. The expression and cellular localization of apoptosis and ferroptosis-related molecules were detected by Western blot and multiplex immunohistochemistry (mIHC), respectively. Calcusyn software was used to determine whether propofol has a synergistic effect with paclitaxel.Results: Propofol and paclitaxel inhibited C-33A and HeLa cell viability. There were also synergistic effects when propofol and paclitaxel were used in combination at certain concentrations. In addition, propofol promoted paclitaxel-induced cervical cancer cell death via apoptosis. ROS level and Fe2+ concentrations were also influenced by different drug treatments. Furthermore, propofol, propofol injectable emulsion, and paclitaxel induced ferroptosis-related morphological changes of mitochondria in C-33A and HeLa cells. Ferroptosis-related signaling pathways including SLC7A11/GPX4, ubiquinol/CoQ10/FSP1, and YAP/ACSL4/TFRC were found to be changed under drug treatments.Conclusion: Propofol showed synergistic anticancer effects with paclitaxel in cervical cancer cells. Propofol and paclitaxel may induce ferroptosis of cervical cancer cells besides apoptosis.

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Propofol induces hepatocellular carcinoma cell apoptosis via regulating miR-105/JAK2/STAT3 axis

Cited by 8 publications

References 18 publications

The role of competing endogenous RNA network in the development of hepatocellular carcinoma: potential therapeutic targets

The role of competing endogenous RNA network in the development of hepatocellular carcinoma: potential therapeutic targets

Long-term effect of anesthesia choice on patients with hepatocellular carcinoma undergoing open liver resection

Propofol Augments Paclitaxel-Induced Cervical Cancer Cell Ferroptosis In Vitro

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