scholarly journals Malignant transformation of host stromal fibroblasts derived from the bone marrow traced in a dual-color fluorescence xenograft tumor model

2015 ◽  
Vol 34 (6) ◽  
pp. 2997-3006 ◽  
Author(s):  
XINGLIANG DAI ◽  
HUA CHEN ◽  
YANMING CHEN ◽  
JINDING WU ◽  
HAIYANG WANG ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Malignant Transformation ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Stromal Fibroblasts ◽  
Dual Color ◽  
Xenograft Tumor Model

scholarly journals Hepatitis C virus-induced tumor-initiating cancer stem-like cells activate stromal fibroblasts in a xenograft tumor model

Hepatology ◽  
2017 ◽  
Vol 66 (6) ◽  
pp. 1766-1778 ◽  
Author(s):  
Reina Sasaki ◽  
Pradip Devhare ◽  
Ratna B. Ray ◽  
Ranjit Ray
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Stromal Fibroblasts ◽  
Xenograft Tumor Model

scholarly journals Wnt5b-induced PCP/JNK Activation Promotes PD-L1 Expression and the Malignant Phenotype of Non-small Cell Lung Cancer 

2020 ◽  
Author(s):  
Guangping Wu ◽  
Yuan Luo ◽  
Yusai Xie ◽  
Yang Han ◽  
Di Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Model ◽  
Small Cell ◽  
Xenograft Tumor ◽  
Small Cell Lung ◽  
Malignant Phenotype ◽  
Membrane Recruitment ◽  
Xenograft Tumor Model

Abstract Background: Wnt5b is noncanonical Wnt ligand, and programmed-death ligand 1 (PD-L1) is a targeted agent for immunotherapy, but the mechanism by which Wnt5b regulates PD-L1 expression in non-small cell lung cancer (NSCLC) is unclear. Methods: Wnt5b and PD-L1 expressions were detected in NSCLC specimens by immunohistochemistry. The interrelationship connecting Wnt5b with PD-L1 was verified using dual-luciferase assay, immunofluorescence, coimmunoprecipitation, western blot，real-time PCR and xenograft tumor model. Results: Wnt5b and PD-L1 expressions were positively correlated in NSCLC specimens. Five-year survival time in the group with their coexpression was significantly lower than that without coexpression. Under the effect of Wnt5b, Frizzled-3 (Fzd3) initiated Dishevellde-3 (Dvl-3) membrane recruitment via DEP domain by Dvl-3 phosphorylation, contributing to activate PCP/JNK signaling through the small GTPase Rac1, and then upregulate PD-L1 expression and promote the malignant phenotype of NSCLC in vivo and in vitro. After PD-L1 antibody treatment, Wnt5b induced tumor growth was inhibited significantly in xenograft tumor model. Conclusion: We demonstrate a new signal transduction pathway: Wnt5b initiates Dvl-3 membrane recruitment via DEP domain by Fzd3 so as to promote Rac1–PCP/JNK–PD-L1 pathway, which provides a potential target for clinical intervention and immunotherapy in lung cancer.

miR-9-5p Promotes β-Catenin-Activated Epithelial-To-Mesenchymal Transition of Triple-Negative Breast Cancer Via Targeting LZTS2

2020 ◽  
Author(s):  
Jie Zhang ◽  
Lina Zhang ◽  
Jianlong Wang ◽  
Jing Zhao ◽  
Xuelian Zhao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Triple Negative Breast Cancer ◽  
Nuclear Export ◽  
Triple Negative ◽  
Tumor Model ◽  
Migration And Invasion ◽  
Xenograft Tumor ◽  
Xenograft Tumor Model ◽  
Low Expression

Abstract Background: Leucine zipper tumor suppressor 2 (LZTS2), an emerging tumor-suppressor, is attenuated in multiple cancers including prostate, lung and colon cancer. However, its expression and upstream regulatory mechanisms in triple negative breast cancer (TNBC) still remain unknown.Materials and methods: The expression of LZTS2 in TNBC and matched para-carcinoma tissues was detected with immunohistochemistry. The correlations between LZTS2 expression and clinicopathological parameters were analyzed. Kaplan-Meier analysis was performed to determine the prognostic role of LZTS2 for TNBC patients. CCK-8, wound healing and transwell assay were used to detect the effect of LZTS2 overexpression on the proliferation, migration and invasion ability, respectively. The bioinformation algorithms were used to reveal the potential upstream regulatory miRNA. Then, dual-luciferase reporter assay was performed to confirm the regulatory effect of the chosen miRNA on the expression of LZTS2. miR-9-5p inhibitor was used to determine the effect of miR-9-5p on the subcellular localization of β-catenin. Then, western blotting was performed to reveal the effect of miR-9-5p on EMT-related proteins in TNBC cells. Xenograft tumor model was established to reveal the effect of miR-9-5p on TNBC progression in vivo.Results: Low expression of LZTS2 was observed in 62 of 95 cases of TNBC tissue. Low expression of LZTS2 was correlated with poor postoperative DFS and OS of TNBC patients. LZTS2 could inhibit the proliferation, migration and invasion ability of TNBC cells. LZTS2 could be downregulated by miR-9-5p in TNBC, and the nuclear export of β-catenin was suppressed. Consequently, miR-9-5p inhibitor downregulated E-cadherin and upregulated N-cadherin, Twist and Vimentin in TNBC cells. Xenograft tumor model showed that miR-9-5p inhibitor could upregulate the expression of LZTS2 and induce nuclear export of β-catenin in TNBC.Conclusions: miR-9-5p contributes to β-catenin-activated EMT via downregulating LZTS2, and thus promotes TNBC progression.

scholarly journals TUFT1 promotes metastasis and chemoresistance in triple negative breast cancer through the TUFT1/Rab5/Rac1 pathway

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Weiguang Liu ◽  
Jianjun Han ◽  
Sufang Shi ◽  
Yuna Dai ◽  
Jianchao He
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Multivariate Analyses ◽  
Tumor Model ◽  
Rab Gtpase ◽  
Xenograft Tumor ◽  
Mechanistic Studies ◽  
Xenograft Tumor Model

Abstract Background Triple negative breast cancer (TNBC) is a breast cancer (BC) subtype that is characterized by its strong invasion and a high risk of metastasis. However, the specific mechanisms underlying these phenotypes are unclear. TUFT1 plays an important role in BC and impacts the proliferation and survival of BC cells. Recent studies have shown that TUFT1 mediates intracellular lysosome localization and vesicle transport by regulating Rab GTPase, but the relevance of this activity in TNBC is unknown. Therefore, our aim was to systematically study the role of TUFT1 in the metastasis and chemoresistance of TNBC. Methods We measured TUFT1, Rab5-GTP, and Rac1-GTP expression levels in samples of human TNBC by immunohistochemistry (IHC) and conducted univariate and multivariate analyses. shRNA-mediated knockdown and overexpression, combined with transwell assays, co-immunoprecipitation, a nude mouse xenograft tumor model, and GTP activity assays were used for further mechanistic studies. Results TUFT1 expression was positively correlated with Rab5-GTP and Rac1-GTP in the TNBC samples, and co-expression of TUFT1 and Rab5-GTP predicted poor prognosis in TNBC patients who were treated with chemotherapy. Mechanism studies showed that TUFT1 could activate Rab5 by binding to p85α, leading to activation of Rac1 through recruitment of Tiam1, and concurrent down-regulation of the NF-κB pathway and proapoptotic factors, ultimately promoting metastasis and chemoresistance in TNBC cells. Conclusions Our findings suggest that the TUFT1/Rab5/Rac1 pathway may be a potential target for the effective treatment of TNBC.

scholarly journals Early detection of antiangiogenic treatment responses in a mouse xenograft tumor model using quantitative perfusion MRI

2014 ◽  
Vol 3 (1) ◽  
pp. 47-60 ◽  
Author(s):  
Reshmi Rajendran ◽  
Wei Huang ◽  
Annie Mei Yee Tang ◽  
Jie Ming Liang ◽  
Stephanie Choo ◽  
...  
Keyword(s):  
Early Detection ◽  
Tumor Model ◽  
Perfusion Mri ◽  
Xenograft Tumor ◽  
Antiangiogenic Treatment ◽  
Mouse Xenograft ◽  
Quantitative Perfusion ◽  
Xenograft Tumor Model ◽  
Treatment Responses

Tumor Accumulation of NIR Fluorescent PEG–PLA Nanoparticles: Impact of Particle Size and Human Xenograft Tumor Model

ACS Nano ◽  
2011 ◽  
Vol 5 (11) ◽  
pp. 8710-8720 ◽  
Author(s):  
Andreas Schädlich ◽  
Henrike Caysa ◽  
Thomas Mueller ◽  
Frederike Tenambergen ◽  
Cornelia Rose ◽  
...  
Keyword(s):  
Particle Size ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Xenograft Tumor Model ◽  
Tumor Accumulation
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