A novel 2,6-diisopropylphenyl–docosahexaenoamide conjugate induces apoptosis in T cell acute lymphoblastic leukemia cell lines

Altenburg, Jeffrey D.; Harvey, Kevin; McCray, Sharon; Xu, Zhidong; Siddiqui, Rafat A.

doi:10.1016/j.bbrc.2011.06.172

Cited by 28 publications

(21 citation statements)

References 21 publications

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“…Recently, increasing evidence indicates a possible correlation between propofol and cancers. Propofol has the ability to inhibit the adhesion, proliferation, and invasion, and induce apoptosis of cancer cells (Mammoto et al, 2002;Miao et al, 2010;Altenburg et al, 2011;Zhang et al, 2013b). Therefore, propofol might be a better agent than other anesthetics for cancer surgery (Inada et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

Zt¹,

Hy²,

Fang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Propofol is one of the extensively and commonly used intravenous anesthetic agents. The current study aimed to evaluate the effects of propofol on the behavior of human gastric cancer cells and the molecular mechanisms of this activity. The effects of propofol on SGC7901 and AGS cell proliferation, apoptosis, and invasion were detected by MTT assay, flow cytometric analysis, and matrigel invasion assay. Real-time polymerase chain reaction (PCR) was used to assess microRNA (miR)-221 expression. miR-221 mimics were transfected into SGC7901 and AGS cells to assess the role of miR-221 in propofol-induced anti-tumor activity. Propofol significantly inhibited cell proliferation and invasion and promoted apoptosis of SGC7901 and AGS cells. Propofol also efficiently reduced miR-221 expression. Moreover, transfection of miR-221 mimics reversed the effects of propofol on the biological behavior of gastric cancer cells. Propofol can effectively inhibit proliferation and invasion and induce apoptosis of gastric cancer cells through, at least partly, downregulation of miR-221 expression.

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Section: Introductionmentioning

confidence: 99%

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

Zt¹,

Hy²,

Fang³

et al. 2015

Genet. Mol. Res.

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show abstract

“…Increasing evidence has shown that propofol can effectively modulate the behavior of numerous human cancer cell types in vitro and in vivo (8)(9)(10). For example, propofol can effectively inhibit cell proliferation and invasion of cervical cancer, pancreatic cancer (11), gastric cancer (12) and colon carcinoma (10).…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have confirmed that propofol also has an antitumor effect (8)(9)(10)(11)(12). Clinically relevant concentrations of propofol have the ability to inhibit cell proliferation, motility and invasion, and induce apoptosis of many cancer cells, such as HeLa, HT1080, HOS and RPMI-7951 (9).…”

Section: Introductionmentioning

confidence: 96%

Propofol inhibits hepatocellular carcinoma growth and invasion through the HMGA2-mediated Wnt/β-catenin pathway

Zou

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Propofol is a commonly used intravenous anesthetic in tumor surgery. Recently, studies have confirmed that propofol has an antitumor effect on hepatocellular carcinoma (HCC); however, the molecular mechanism underlying this effect has not been elucidated until now. The present study aimed to investigate the mechanism of propofol on HepG2 cell proliferation, apoptosis and invasion, focusing on High Mobility Group AT-Hook 2 (HMGA2)-mediated Wnt/β-catenin pathway. The HepG2 cells were treated with various concentrations of propofol for 24 h, the relative protein levels of HMGA2, Wnt3a, β-catenin, Snail Family Zinc Finger 1 and c-myc were determined by western blot analysis. HMGA2-pcDNA3.1 plasmid was transfected into the HepG2 cells to overexpress HMGA2. Cell proliferation, apoptosis and invasion were examined by MTT assays, flow cytometry and Transwell-matrigel invasion assays, respectively. The results showed that propofol suppressed HMGA2 expression and Wnt/β-catenin signaling in a dose-dependent manner. Propofol was able to inhibit cell proliferation and invasion, and induce cell apoptosis of HepG2 cells; however, these effects were attenuated by HMGA2 overexpression. The suppressed Wnt/β-catenin signaling in HepG2 cells by treatment with propofol was also reversed by HMGA2 overexpression. In conclusion, this study provided a novel mechanism underlying the anti-tumor function of propofol on HCC. To the best of our knowledge, the present study is the first to demonstrate that propofol could downregulate the expression of HMGA2, which inhibited the Wnt/β-catenin pathway, thus leading to the inhibition of cell proliferation and invasion, as well as the apoptosis of HepG2 cells.

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“…There is increasing evidence to suggest a correlation between propofol and cancer inhibition. Propofol has the ability to inhibit the adhesion, proliferation, and invasion of cancer cells, and induce their apoptosis (Mammoto et al, 2002;Miao et al, 2010;Altenburg et al, 2011;Zhang et al, 2013b). Therefore, propofol might be a better agent than other anesthetics for cancer surgery (Inada et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Propofol suppresses proliferation and invasion of pancreatic cancer cells by upregulating microRNA-133a expression

Zt¹,

Hy²,

Zheng³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Propofol is a commonly used intravenous anesthetic. We evaluated its effects on the behavior of human pancreatic cancer cells and the underlying molecular mechanisms. The effects of propofol on Panc-1 cell proliferation, apoptosis, and invasion were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, caspase-3 activity measurement, and Matrigel invasion assay. Quantitative polymerase chain reaction (qPCR) was used to assess microRNA-133a (miR-133a) expression. Anti-miR-133a was transfected into Panc-1 cells to assess the role of miR-133a in propofolinduced antitumor activity. Propofol significantly inhibited Panc-1 cell proliferation and invasion, and promoted apoptosis. Propofol also efficiently elevated miR-133a expression. Moreover, transfection of anti-miR-133a reversed the effects of propofol on the biological 7530 Z.T. Wang et al. ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 7529-7537 (2015) behavior of Panc-1 cells. Propofol can effectively inhibit proliferation and invasion, and induce apoptosis of pancreatic cancer cells, at least partly through the upregulation of miR-133a expression.

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A novel 2,6-diisopropylphenyl–docosahexaenoamide conjugate induces apoptosis in T cell acute lymphoblastic leukemia cell lines

Cited by 28 publications

References 21 publications

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

Propofol inhibits hepatocellular carcinoma growth and invasion through the HMGA2-mediated Wnt/β-catenin pathway

Propofol suppresses proliferation and invasion of pancreatic cancer cells by upregulating microRNA-133a expression

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