<i>Retracted</i>:Propofol exerts anticancer activity on hepatocellular carcinoma cells by raising lncRNA DGCR5

Sun, Yan; Sun, Hai

doi:10.1002/jcp.29202

Cited by 13 publications

(12 citation statements)

References 37 publications

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“…These aforementioned findings indicated that propofol may not serve an anticancer role in all types of neoplasms. The cell type, propofol concentration and duration of stimulation in the present study were consistent with those implemented in previous studies ( 37 , 38 ). There are several possible explanations for the observed differences between the current results and previous findings.…”

Section: Discussionsupporting

confidence: 91%

Effects of propofol on the proliferation and migration of liver cancer cells

Cai

et al. 2021

Exp Ther Med

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Liver cancer is a malignant cancer with worldwide prevalence. It has been reported that cancer cells are usually exposed to a hypoxic microenvironment, which is associated with a poor prognosis in patients with cancer. Propofol is an intravenous anesthetic that is widely used in cancer surgery. The present study aimed to determine the effects of propofol stimulation on the viability, proliferation and migration of liver cancer cells under normoxia and cobalt chloride (CoCl 2 )-induced hypoxia. Under normoxia, HepG2 and HCCLM3 cells were randomly divided into six groups as follows: i) Control group; ii) 10 µM propofol group; iii) 25 µM propofol group; iv) 50 µM propofol group; v) 100 µM propofol group; and vi) DMSO group. Cell viability and proliferation were analyzed using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays, respectively, following 24 or 48 h of propofol treatment. In addition, wound healing and Transwell migration assays were used to determine the changes in cell migration. Under CoCl 2 -induced hypoxia, the protein levels of hypoxia inducible factor-1α (HIF-1α) of HepG2 cells were analyzed using western blotting. Subsequently, CCK-8 and wound healing assays were used to determine the effect of propofol on cell viability and migration. The results of the present study revealed that propofol stimulation had no significant effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxia. The protein levels of HIF-1α were significantly upregulated following the treatment with 200 µM CoCl 2 for 12 h. However, no significant differences were found in the viability and migration of HepG2 cells following the stimulation with propofol in the presence of CoCl 2 . In conclusion, the findings of the present study revealed that propofol exerted no effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxic and hypoxic conditions.

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Section: Discussionsupporting

confidence: 91%

Effects of propofol on the proliferation and migration of liver cancer cells

Cai

et al. 2021

Exp Ther Med

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“…For example, Sun et al confirmed that propofol inhibited the development of hepatocellular carcinoma via increasing the level of lncRNA DGCR5. 27 Chen et al revealed that propofol reduced the level of lncRNA ANRIL to repress the proliferation and mobility of thyroid cancer cells. 28 In this study, we found that TMPO-AS1 was highly expressed in EC cells, and TMPO-AS1 expression was downregulated due to the treatment of propofol.…”

Section: Discussionmentioning

confidence: 99%

Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis

Gao

Guo

et al. 2020

Thoracic Cancer

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Background Propofol has been reported to be related to the migration, invasion, and epithelial‐mesenchymal transition (EMT) of esophageal cancer (EC) cells. However, the detailed mechanism has not yet been fully reported. The purpose of this research was to elucidate the function of long non‐coding RNA TMPO antisense RNA 1 (lncRNA TMPO‐AS1) and microRNA‐498 (miR‐498) in propofol‐regulated EC. Methods Transwell assay was performed to assess cell migratory and invasive abilities. Western blot assay was employed to determine the levels of EMT markers and hypoxia inducible factor‐1 (HIF‐1α). Quantitative real‐time polymerase chain reaction (qRT‐PCR) was carried out to detect the levels of TMPO‐AS1 and miR‐498. Moreover, the interaction between TMPO‐AS1 and miR‐498 was predicted by starBase, and then confirmed by the dual‐luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results Propofol suppressed hypoxia‐induced EC cell migration, invasion, and EMT. Both TMPO‐AS1 overexpression and miR‐498 knockdown weakened the effect of propofol on hypoxia‐induced EC cell progression. Interestingly, TMPO‐AS1 targeted miR‐498 and suppressed miR‐498 expression. TMPO‐AS1 regulated EC cell progression via downregulating miR‐498 expression. Conclusions Collectively, our findings demonstrated that propofol inhibited hypoxia‐induced EC cell mobility through modulation of the TMPO‐AS1/miR‐498 axis, providing a theoretical basis for the treatment of EC.

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“…Similarly, LINC00460 has also been confirmed to promote the progression of multiple cancers through different target genes [32][33][34]. The last lncRNA, DGCR5, is slightly different because when it is highly expressed it exerts anticancer activity in various cancers, including gastric cancer, hepatocellular carcinoma, cervical cancer, and bladder cancer, suggesting a good prognosis [35][36][37][38]. Interestingly, DGCR5 promotes LUAD progression by inhibiting hsa-mir-22-3p [39], which means higher expression DGCR5 implies a worse prognosis for LUAD patients and this finding was consistent with our current survival analysis results.…”

Section: Discussionmentioning

confidence: 99%

A signature related to lung adenocarcinoma prognosis: A study based on TCGA database

Wang¹,

Zhang²,

Zhang³

et al. 2020

Preprint

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Background: The intrinsic molecular subtypes of lung adenocarcinoma (LUAD) impact clinical treatment decision-making, but the molecular mechanisms are still unclear. Therefore, we aimed to identify sensitive biomarkers to evaluate LUAD patient prognosis. Methods: Differentially expressed RNAs from LUAD patients were obtained from The Cancer Genome Atlas (TCGA) database and they were used to construct a competitive endogenous RNA (ceRNA) network. Based on the examination of clinical data, long noncoding RNAs (lncRNAs) and mRNAs in the network were selected by univariate and multivariate Cox regression analysis. Finally, functional enrichment analysis was used to reveal prognostic signatures based on the classification into high and low-risk groups, survival analysis, and an independence test. Results: The ceRNA network consisted of 21 mRNAs, 53 lncRNAs, and 8 miRNAs that were selected from the differentially expressed RNAs identified. Next, based on univariate and multivariate Cox regression analysis, a prognostic signature, including two mRNAs (HOXA10 and CBX2) and four lncRNAs (LINC00460, LINC00330, DGCR5, and C14orf132) was constructed. Eventually, survival analysis showed that significant differences in survival rates between high and low-risk groups and the area under the curve (AUC) for three‐year survival was 0.714. Compared with clinical risk factors, including age, pathological stage, and TNM stage, our risk score had a higher prognostic value. Conclusion: By screening from a ceRNA network, we constructed a signature, including two mRNAs (HOXA10 and CBX2) and four lncRNAs (LINC00460, LINC00330, DGCR5, and C14orf132), that can be utilized as a prognostic biomarker in LUAD. This signature may provide options for clinical treatment.

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Retracted:Propofol exerts anticancer activity on hepatocellular carcinoma cells by raising lncRNA DGCR5

Cited by 13 publications

References 37 publications

Effects of propofol on the proliferation and migration of liver cancer cells

Effects of propofol on the proliferation and migration of liver cancer cells

Propofol suppresses hypoxia‐induced esophageal cancer cell migration, invasion, and EMT through regulating lncRNA TMPO‐AS1/miR‐498 axis

A signature related to lung adenocarcinoma prognosis: A study based on TCGA database

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