Evaluation of anti-tumorigenic activity of BP3B against colon cancer with patient-derived tumor xenograft model

Kim, Hye-Youn; Kim, Jinhee; Thi, Huyen Trang Ha; Bang, Ok‐Sun; Lee, Won Suk

doi:10.1186/s12906-016-1447-8

Cited by 11 publications

(15 citation statements)

References 36 publications

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“…A few articles were published per year before 2013, two articles were published in 2010 [18,19], one article in 2011 [20], two articles in 2012 [21,22], and two articles in 2013 [23,24]. On the other hand, more than 10 articles were published each year after 2014, 15 articles were published in 2014 [25,26,27,28,29,30,31,32,33,34,35,36,37,38,39], 14 articles in 2015 [10,40,41,42,43,44,45,46,47,48,49,50,51,52], 14 articles in 2016 [53,54,55,56,57,58,59,60,61,62,63,64,65,66], 23 articles in 2017 [67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,…”

Section: Resultsmentioning

confidence: 99%

Systematic Review of Patient-Derived Xenograft Models for Preclinical Studies of Anti-Cancer Drugs in Solid Tumors

Koga

Ochiai

2019

Cells

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Patient-derived xenograft (PDX) models are used as powerful tools for understanding cancer biology in PDX clinical trials and co-clinical trials. In this systematic review, we focus on PDX clinical trials or co-clinical trials for drug development in solid tumors and summarize the utility of PDX models in the development of anti-cancer drugs, as well as the challenges involved in this approach, following the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines. Recently, the assessment of drug efficacy by PDX clinical and co-clinical trials has become an important method. PDX clinical trials can be used for the development of anti-cancer drugs before clinical trials, with their efficacy assessed by the modified response evaluation criteria in solid tumors (mRECIST). A few dozen cases of PDX models have completed enrollment, and the efficacy of the drugs is assessed by 1 × 1 × 1 or 3 × 1 × 1 approaches in the PDX clinical trials. Furthermore, co-clinical trials can be used for personalized care or precision medicine with the evaluation of a new drug or a novel combination. Several PDX models from patients in clinical trials have been used to assess the efficacy of individual drugs or drug combinations in co-clinical trials.

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Section: Resultsmentioning

confidence: 99%

Systematic Review of Patient-Derived Xenograft Models for Preclinical Studies of Anti-Cancer Drugs in Solid Tumors

Koga

Ochiai

2019

Cells

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“…The secondary antibody was followed added with using HRP-Polymer anti-Mouse/Rabbit IHC Kit (Maixin Biotech, China) for 1 h at room temperature. Then, samples were developed with diaminobezidine (Vector Laboratories) reagent and counterstained with hematoxylin and mounted with permount [ 21 ].…”

Section: Methodsmentioning

confidence: 99%

“…ImageJ software was used to quantify the MVD based on CD31 staining. The percentage of positively stained area was calculated by using a color deconvolution for separating the staining components (diaminobezidine and hematoxylin) in at least six fields per each sections [ 21 ]. The results were presented as percentage of treated group compared to control one.…”

Section: Methodsmentioning

confidence: 99%

Hsp90β promoted endothelial cell-dependent tumor angiogenesis in hepatocellular carcinoma

et al. 2017

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BackgroundVascular endothelial growth factor receptors (VEGFRs) are the major receptors involved in endothelial cell-dependent tumor angiogenesis. There are studies account for the effects of Hsp90 on angiogenesis, but the role and mechanism of Hsp90β isoforms and NVP-BEP800, a specific inhibitor of Hsp90β, in tumor angiogenesis is rarely mentioned.MethodsImmunohistochemistry and statistical analysis was used to evaluate the correlation between Hsp90β expression, CD31 endothelial cell-dependent vessel density, and VEGFRs expression in tissue samples of 96 HCCs. Kaplan-Meier survival analysis and COX proportional hazards analysis the relation of Hsp90β and prognosis. HUVEC cells were transfected with Hsp90β or treated with NVP-BEP800, and then cell proliferation, migration, invasion and tube formation were investigated. The VEGFR1 and VEGFR2 expression was determined by Western blot and immunofluorescence. The VEGFR1 and VEGFR2 promoter activities were detected by dual luciferase report system. In vivo, the angiogenesis promotion of Hsp90β and anti-angiogenesis efficacy of NVP-BEP800 was tested in HCC xenograft models. Histological analysis was performed on tumor samples to evaluate Hsp90β, VEGFRs expression and MVD.ResultsThis study investigated the correlation between Hsp90β expression and CD31+ endothelial cell-dependent vessel density. Hsp90β promoted VEGFRs expression by increasing their promoter activities. The proliferation, migration, invasion, and tube formation activities of human endothelial cells significantly increased when Hsp90β was overexpressed. NVP-BEP800 down-regulated VEGFRs expression to significantly reduce tubular differentiation, as well as endothelial cell proliferation, migration, and invasion. Furthermore, NVP-BEP800 decreased VEGFR1 and VEGFR2 promoter activities. In vivo, Hsp90β promoted VEGFRs and CD31 expression in human hepatocellular carcinoma tumor xenografts and was associated with increased tumor microvessel density. After 18 days of treatment with 30 mg/kg/day NVP-BEP800, VEGFRs and CD31 expression significantly decreased.ConclusionHsp90β induced endothelial cell-dependent tumor angiogenesis by activating VEGFRs transcription. NVP-BEP800 has potential as a therapeutic strategy for inhibiting tumor angiogenesis by decreasing endothelial cell progression and metastasis. It can help develop a therapeutic strategy for tumor treatment through the inhibition of endothelial cell progression and metastasis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-017-0640-9) contains supplementary material, which is available to authorized users.

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“…Tumor fragments were subcutaneously implanted into pockets made in each side of the lower back of SCID mice. When the tumor size reached 100 to 200 mm 3 , the samples (called F1) were divided into pieces for in vivo passaging to construct F2 tumors and then F3 constructed as described above (28). When the F3 tumor size reached 100 to 200 mm 3 , 1 Â 10 7 TU lentiviral particles carrying circ-10720 in HBSS was intratumorally injected into Twist1-Low groups (Twist1-Lowþcirc-10720 groups) and HBSS group as control (Twist1-Lowþcontrol group); 10 OD circ-10720 siRNA was intratumorally injected into Twist1-High groups (Twist1-Highþcirc-10720 siRNA groups) and control siRNA injection as control (Twist1-Highþcontrol siRNA group).…”

Section: Patient-derived Xenograft Modelmentioning

confidence: 99%

Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma

et al. 2018

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Twist is a critical epithelial-mesenchymal transition (EMT)-inducing transcription factor that increases expression of vimentin. How Twist1 regulates this expression remains unclear. Here, we report that Twist1 regulates Cullin2 (Cul2) circular RNA to increase expression of vimentin in EMT. Twist1 bound the Cul2 promoter to activate its transcription and to selectively promote expression of Cul2 circular RNA (circ-10720), but not mRNA. circ-10720 positively correlated with Twist1, tumor malignance, and poor prognosis in hepatocellular carcinoma (HCC). Twist1 promoted vimentin expression by increasing levels of circ-10720, which can absorb miRNAs that target vimentin. circ-10720 knockdown counteracted the tumor-promoting activity of Twist1 and in patient-derived xenograft and diethylnitrosamine-induced TetOn-Twist1 transgenic mouse HCC models. These data unveil a mechanism by which Twist1 regulates vimentin during EMT. They also provide potential therapeutic targets for HCC treatment and provide new insight for circular RNA (circRNA)-based diagnostic and therapeutic strategies. A circRNA-based mechanism drives Twist1-mediated regulation of vimentin during EMT and provides potential therapeutic targets for treatment of HCC. http://cancerres.aacrjournals.org/content/canres/78/15/4150/F1.large.jpg .

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Evaluation of anti-tumorigenic activity of BP3B against colon cancer with patient-derived tumor xenograft model

Cited by 11 publications

References 36 publications

Systematic Review of Patient-Derived Xenograft Models for Preclinical Studies of Anti-Cancer Drugs in Solid Tumors

Systematic Review of Patient-Derived Xenograft Models for Preclinical Studies of Anti-Cancer Drugs in Solid Tumors

Hsp90β promoted endothelial cell-dependent tumor angiogenesis in hepatocellular carcinoma

Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma

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