scholarly journals Pien Tze Huang inhibits tumor cell proliferation and promotes apoptosis via suppressing the STAT3 pathway in a colorectal cancer mouse model

2012 ◽  
Author(s):  
Jun Peng
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Mouse Model ◽  
Tumor Cell ◽  
Tumor Cell Proliferation ◽  
Stat3 Pathway ◽  
Pien Tze Huang

scholarly journals RIP3 promotes colitis-associated colorectal cancer by controlling tumor cell proliferation and CXCL1-induced immune suppression

Theranostics ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 3659-3673 ◽  
Author(s):  
Zhen-Yu Liu ◽  
Ming Zheng ◽  
Yi-Ming Li ◽  
Xin-Yu Fan ◽  
Jian-Chao Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Immune Suppression ◽  
Tumor Cell Proliferation

scholarly journals Mathematical Modeling of Tumor Cell Proliferation Kinetics and Label Retention in a Mouse Model of Lung Cancer

2013 ◽  
Vol 73 (12) ◽  
pp. 3525-3533 ◽  
Author(s):  
Yanyan Zheng ◽  
Helen Moore ◽  
Alexandra Piryatinska ◽  
Trinidad Solis ◽  
E. Alejandro Sweet-Cordero
Keyword(s):  
Mathematical Modeling ◽  
Lung Cancer ◽  
Cell Proliferation ◽  
Mouse Model ◽  
Tumor Cell ◽  
Tumor Cell Proliferation ◽  
Proliferation Kinetics

scholarly journals Cancer-Preventive Role of Bone Marrow-Derived Mesenchymal Stem Cells on Colitis-Associated Colorectal Cancer: Roles of Gut Microbiota Involved

2021 ◽  
Vol 9 ◽  
Author(s):  
Ruohang He ◽  
Chaoqun Han ◽  
Ying Li ◽  
Wei Qian ◽  
Xiaohua Hou
Keyword(s):  
Colorectal Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Tumor Cell ◽  
Rna Sequencing ◽  
Ribosomal Rna ◽  
Tumor Cell Proliferation

BackgroundMesenchymal stem cells (MSCs) treatment showed promising results in inflammatory bowel disease in both rodent models and patients. Nevertheless, previous studies conducted conflicting results on preclinical tumor models treated with MSCs concerning their influence on tumor initiation and progression. This study is designed to demonstrate the role of bone marrow-derived MSCs and the potential mechanism in the colitis-associated colon cancer (CAC) model.MethodsBone marrow-derived MSCs were isolated from green fluorescent protein-transgenic mice, cultured, and identified by flow cytometry. Azoxymethane and dextran sulfate sodium were administrated to establish the CAC mouse model, and MSCs were infused intraperitoneally once per week. The mice were weighed weekly, and colon length, tumor number, and average tumor size were assessed after the mice were killed. MSC localization was detected by immunofluorescence staining; tumor cell proliferation and apoptosis were measured by immunohistochemistry staining of Ki-67 and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling assay, respectively. The colonic tumor tissues were isolated for RNA-seq, and fecal samples were collected for 16S ribosomal RNA sequencing of the microbiome.ResultsAfter injection intraperitoneally, MSCs migrated to the intestine and inhibited the initiation of colitis-associated colorectal cancer. This inhibition effect was marked by less weight loss, longer colon length, and reduced tumor numbers. Moreover, MSCs reduced tumor cell proliferation and induced tumor cell apoptosis. Furthermore, MSCs could inhibit chronic inflammation assessed by RNA-sequencing and promote gut microbiome normalization detected by 16S ribosomal RNA sequencing.ConclusionThe results proved that MSCs could migrate to the colon, inhibit chronic inflammation, and regulate gut microbiome dysbiosis to suppress the development of CAC.

scholarly journals Cyclodextrin-based host-guest complexes loaded with regorafenib for colorectal cancer treatment

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Hongzhen Bai ◽  
Jianwei Wang ◽  
Chi Uyen Phan ◽  
Qi Chen ◽  
Xiurong Hu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Tumor Microenvironment ◽  
Tumor Cell ◽  
Tumor Cell Proliferation ◽  
Therapeutic Targeting ◽  
Potential Strategy ◽  
Colorectal Cancer Treatment ◽  
Channel Type

AbstractThe malignancy of colorectal cancer (CRC) is connected with inflammation and tumor-associated macrophages (TAMs), but effective therapeutics for CRC are limited. To integrate therapeutic targeting with tumor microenvironment (TME) reprogramming, here we develop biocompatible, non-covalent channel-type nanoparticles (CNPs) that are fabricated through host-guest complexation and self-assemble of mannose-modified γ-cyclodextrin (M-γ-CD) with Regorafenib (RG), RG@M-γ-CD CNPs. In addition to its carrier role, M-γ-CD serves as a targeting device and participates in TME regulation. RG@M-γ-CD CNPs attenuate inflammation and inhibit TAM activation by targeting macrophages. They also improve RG’s anti-tumor effect by potentiating kinase suppression. In vivo application shows that the channel-type formulation optimizes the pharmacokinetics and bio-distribution of RG. In colitis-associated cancer and CT26 mouse models, RG@M-γ-CD is proven to be a targeted, safe and effective anti-tumor nanomedicine that suppresses tumor cell proliferation, lesions neovascularization, and remodels TME. These findings indicate RG@M-γ-CD CNPs as a potential strategy for CRC treatment.

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