Antitumor activity of sevoflurane in HCC cell line is mediated by miR‐29a‐induced suppression of Dnmt3a

Guang-ming, Song; Tian, Ling; Cheng, Yi; Jin-shan, Liu; Wang, Kun; Li, Shuai; Li, Tianhua

doi:10.1002/jcb.29121

Cited by 21 publications

(20 citation statements)

References 30 publications

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“…The advanced insights into the predictive and prognostic relevance of miR-29a in HCC patients are summarized in Table 6. There are several studies reported that decreased expression levels of miR-29a act as a biomarker of HCC tissue [45,53,55,56,65,66,70,84,85]. Parpart et al have identified an inverse correlation between miR-29a and AFP where tumor miR-29a level decrease significantly as serum AFP levels increase.…”

Section: Mir-29a As a Diagnostic/prognostic Indicatormentioning

confidence: 99%

New Insights into the Role of miR-29a in Hepatocellular Carcinoma: Implications in Mechanisms and Theragnostics

Yang

Chang

et al. 2021

JPM

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Hepatocellular carcinoma (HCC) remains one of the most lethal human cancer globally. For advanced HCC, curable plan for advanced HCC is yet to be established, and the prognosis remains poor. The detail mechanisms underlying the progression of HCC tumorigenicity and the corruption of tumor microenvironment (TME) is complex and inconclusive. A growing body of studies demonstrate microRNAs (miRs) are important regulators in the tumorigenicity and TME development. Notably, mounting evidences indicate miR-29a play a crucial role in exerting hepatoprotective effect on various types of stress and involved in the progression of HCC, which elucidates their potential theragnostic implications. In this review, we reviewed the advanced insights into the detail mechanisms by which miR-29a dictates carcinogenesis, epigenetic program, and metabolic adaptation, and implicated in the sponging activity of competitive endogenous RNAs (ceRNA) and the TME components in the scenario of HCC. Furthermore, we highlighted its clinical significance in diagnosis and prognosis, as well as the emerging therapeutics centered on the activation of miR-29a.

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Section: Mir-29a As a Diagnostic/prognostic Indicatormentioning

confidence: 99%

New Insights into the Role of miR-29a in Hepatocellular Carcinoma: Implications in Mechanisms and Theragnostics

Yang

Chang

et al. 2021

JPM

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“…Another study from Sun et al (13) showed that Sevo inhibited migration and invasion of colorectal cancer cells by regulating miR-34a. Notably, Song et al (14) found that Sevo restored the expression of miR-29 and in turn miR-29a inhibition abolished the antitumor property of Sevo in HCC cells. Nonetheless, whether Sevo exerts its antitumor effect by regulating miRNA in HCC is not fully clear.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane inhibits the proliferation and invasion of hepatocellular carcinoma cells through regulating the PTEN/Akt/GSK‑3β/β‑catenin signaling pathway by downregulating miR‑25‑3p

Cao

Ding

et al. 2020

Int J Mol Med

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Sevoflurane (Sevo) is one of the most frequently used volatile anesthetic agents in surgical oncology and has various effects on tumors, including inhibiting tumor growth, recurrence, and metastases; however, the molecular mechanisms are unknown. This study tried to investigate the influence of Sevo on hepatocellular carcinoma (HCC) cells and its possible mechanisms of action. The present study found that Sevo suppressed both the proliferative and invasive capabilities of both HCCLM3 and Huh7 cells in a dose-dependent manner. Moreover, 53 differentially expressed microRNAs (miRNAs/miRs) in HCC cells that resulted from Sevo were screened out using miRNA microarray assay. In particular, miR-25-3p displayed a significant decrease in response to Sevo treatment. Further studies showed that Sevo's inhibitory actions on HCC cells were attenuated by overexpression of miR-25-3p but enhanced by its inhibitor. Phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN (PTEN), a tumor suppressor gene, was directly targeted by miR-25-3p and its expression was upregulated by Sevo. In addition, Sevo suppressed the expression of phosphorylated-protein kinase B (p-Akt) (S473), glycogen synthase kinase (GSK) 3β (p-GSK3β) (S9), β-catenin, c-Myc and matrix metalloproteinase 9; whereas these inhibitory effects were reversed by miR-25-3p overexpression. More importantly, Sevo's tumor-suppressive effects were enhanced by LY294002 (a PI3-kinase inhibitor) but weakened by insulin growth factor-1 (an agonist of the Akt signaling pathway). These data suggest that Sevo's antitumor effects on HCC could be explained, in part, by Sevo inhibiting the miR-25-3p/PTEN/Akt/GSK-3β/β-catenin signaling pathway.

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“…MiR-29a inhibited the expression of recombinant claudin 1 (CLDN1) to reduce the migration and proliferation of HCC cells [9]. After the overexpression of miR-29a in HCC cells, Dnmt3a was down-regulated to mediate epigenetic regulation of methylation [10]. These results suggested that miR-29a played an important role of antitumor activity in HCC.…”

Section: Introductionmentioning

confidence: 92%

miR-29a overexpresion induces apoptosis through targeting VEGF in hepatocellular carcinoma

Wang¹,

Wu²,

Yuan³

et al. 2020

Preprint

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Background : This study aimed to explore the role of miR-29a in hepatocellular carcinoma (HCC) cells. Further, to confirm whether miR-29a targetes vascular endothelial growth factor (VEGF) in HCC cells. Methods: Cell counting Kit-8 (CCK8) and clone formation assay were used to analyze the proliferation of HCC cells. Flow cytometry was performed to analyze the apoptosis and cell cycle of HCC cells. Western blot was used to analyze the expression of Bax, B-cell lymphoma-2 (Bcl-2), cyclin dependent kinase 4 (CDK4), CyclinD1, Retinoblastoma (Rb), p53 and myeloid cell leukemia-1 (MCL1). The targeting relations between miR-29a and VEGF was measuered by dual luciferase assay. Results : Overexpression of miR-29a could distinctly inhibit the proliferation and promote apoptosis of HCC cells. Overexpression of miR-29a obviously up-regulated the expressions of Bax and Rb, and reduced the expressions of CDK4, Bcl-2, Cyclin D1, p53, MCL1 and VEGF in HCC cells. Dual luciferase assay proved that VEGF was the target of miR-29a. Rescue experiments showed that miR-29a targeted VEGF to regulate the proliferation and apoptosis in HCC cells. Conclusions : These results indicated overexpression of miR-29a inhibited the HCC cells proliferation through targeting VEGF.

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Antitumor activity of sevoflurane in HCC cell line is mediated by miR‐29a‐induced suppression of Dnmt3a

Cited by 21 publications

References 30 publications

New Insights into the Role of miR-29a in Hepatocellular Carcinoma: Implications in Mechanisms and Theragnostics

New Insights into the Role of miR-29a in Hepatocellular Carcinoma: Implications in Mechanisms and Theragnostics

Sevoflurane inhibits the proliferation and invasion of hepatocellular carcinoma cells through regulating the PTEN/Akt/GSK‑3β/β‑catenin signaling pathway by downregulating miR‑25‑3p

miR-29a overexpresion induces apoptosis through targeting VEGF in hepatocellular carcinoma

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