scholarly journals A comprehensive look at the role of hyperlipidemia in promoting colorectal cancer liver metastasis

2018 ◽  
Vol 9 (16) ◽  
pp. 2981-2986 ◽  
Author(s):  
Yimin Shen ◽  
Caihua Wang ◽  
Yuezhong Ren ◽  
Jun Ye
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Colorectal Cancer Liver Metastasis

A meta-analysis exploring the role of PET and PET-CT in the management of potentially resectable colorectal cancer liver metastasis.

2018 ◽  
Vol 36 (15_suppl) ◽  
pp. 3547-3547
Author(s):  
Julian Daza Vargas ◽  
Natalie Solis ◽  
Sameer Parpia ◽  
Steven Gallinger ◽  
Carol-Anne Moulton ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Meta Analysis ◽  
Colorectal Cancer Liver Metastasis ◽  
Pet Ct

scholarly journals Bimodal role of Kupffer cells during colorectal cancer liver metastasis

2013 ◽  
Vol 14 (7) ◽  
pp. 606-613 ◽  
Author(s):  
Shu Wen Wen ◽  
Eleanor I Ager ◽  
Christopher Christophi
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Kupffer Cells ◽  
Colorectal Cancer Liver Metastasis

scholarly journals LncRNA MIR17HG promotes colorectal cancer liver metastasis by mediating a glycolysis-associated positive feedback circuit

Oncogene ◽  
2021 ◽  
Author(s):  
Senlin Zhao ◽  
Bingjie Guan ◽  
Yushuai Mi ◽  
Debing Shi ◽  
Ping Wei ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Metastatic Tumor ◽  
Feedback Circuit ◽  
Colorectal Cancer Liver Metastasis ◽  
Positive Feedback Circuit

AbstractGlycolysis plays a crucial role in reprogramming the metastatic tumor microenvironment. A series of lncRNAs have been identified to function as oncogenic molecules by regulating glycolysis. However, the roles of glycolysis-related lncRNAs in regulating colorectal cancer liver metastasis (CRLM) remain poorly understood. In the present study, the expression of the glycolysis-related lncRNA MIR17HG gradually increased from adjacent normal to CRC to the paired liver metastatic tissues, and high MIR17HG expression predicted poor survival, especially in patients with liver metastasis. Functionally, MIR17HG promoted glycolysis in CRC cells and enhanced their invasion and liver metastasis in vitro and in vivo. Mechanistically, MIR17HG functioned as a ceRNA to regulate HK1 expression by sponging miR-138-5p, resulting in glycolysis in CRC cells and leading to their invasion and liver metastasis. More interestingly, lactate accumulated via glycolysis activated the p38/Elk-1 signaling pathway to promote the transcriptional expression of MIR17HG in CRC cells, forming a positive feedback loop, which eventually resulted in persistent glycolysis and the invasion and liver metastasis of CRC cells. In conclusion, the present study indicates that the lactate-responsive lncRNA MIR17HG, acting as a ceRNA, promotes CRLM through a glycolysis-mediated positive feedback circuit and might be a novel biomarker and therapeutic target for CRLM.

scholarly journals Exosomal ANGPTL1 attenuates colorectal cancer liver metastasis by regulating Kupffer cell secretion pattern and impeding MMP9 induced vascular leakiness

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Kai Jiang ◽  
Haiyan Chen ◽  
Yimin Fang ◽  
Liubo Chen ◽  
Chenhan Zhong ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Kupffer Cell ◽  
Cell Secretion ◽  
Gene Expressions ◽  
Protein Levels ◽  
Normal Tissues ◽  
Mmp9 Expression ◽  
Stat3 Signaling Pathway

Abstract Background Angiopoietin-like protein 1 (ANGPTL1) has been proved to suppress tumor metastasis in several cancers. However, its extracellular effects on the pre-metastatic niches (PMNs) are still unclear. ANGPTL1 has been identified in exosomes, while its function remains unknown. This study was designed to explore the role of exosomal ANGPTL1 on liver metastasis in colorectal cancer (CRC). Methods Exosomes were isolated by ultracentrifugation. The ANGPTL1 level was detected in exosomes derived from human CRC tissues. The effects of exosomal ANGPTL1 on CRC liver metastasis were explored by the intrasplenic injection mouse model. The liver PMN was examined by vascular permeability assays. Exosomal ANGPTL1 localization was validated by exosome labeling. The regulatory mechanisms of exosomal ANGPTL1 on Kupffer cells were determined by RNA sequencing. qRT-PCR, Western Blot, and ELISA analysis were conducted to examine gene expressions at mRNA and protein levels. Results ANGPTL1 protein level was significantly downregulated in the exosomes derived from CRC tumors compared with paired normal tissues. Besides, exosomal ANGPTL1 attenuated liver metastasis and impeded vascular leakiness in the liver PMN. Moreover, exosomal ANGPTL1 was mainly taken up by KCs and regulated the KCs secretion pattern, enormously decreasing the MMP9 expression, which finally prevented the liver vascular leakiness. In mechanism, exosomal ANGPTL1 downregulated MMP9 level in KCs by inhibiting the JAK2-STAT3 signaling pathway. Conclusions Taken together, exosomal ANGPTL1 attenuated CRC liver metastasis and impeded vascular leakiness in the liver PMN by reprogramming the Kupffer cell and decreasing the MMP9 expression. This study suggests a suppression role of exosomal ANGPTL1 on CRC liver metastasis and expands the approach of ANGPTL1 functioning.

Matrix metalloproteinase 2 and 9 activity in patients with colorectal cancer liver metastasis

2003 ◽  
Vol 90 (12) ◽  
pp. 1556-1564 ◽  
Author(s):  
E. T. Waas ◽  
T. Wobbes ◽  
R. M. L. M. Lomme ◽  
J. DeGroot ◽  
T. Ruers ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Colorectal Cancer Liver Metastasis

Higher Tumor Burden Neutralizes Negative Margin Status in Hepatectomy for Colorectal Cancer Liver Metastasis

2018 ◽  
Vol 26 (2) ◽  
pp. 593-603 ◽  
Author(s):  
Masanori Oshi ◽  
Georgios Antonios Margonis ◽  
Yu Sawada ◽  
Nikolaos Andreatos ◽  
Jin He ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Tumor Burden ◽  
Margin Status ◽  
Negative Margin ◽  
Colorectal Cancer Liver Metastasis
Sign in / Sign up

Export Citation Format

Share Document