scholarly journals Fatty change of the liver microenvironment influences the metastatic potential of colorectal cancer

2020 ◽  
Vol 101 (5) ◽  
pp. 162-170
Author(s):  
Satoshi Masaki ◽  
Yoshimi Hashimoto ◽  
Shoma Kunisho ◽  
Akiko Kimoto ◽  
Yasuhiko Kitadai
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Potential ◽  
Fatty Change

scholarly journals PLAC1 Enhances Metastatic Potential and is Associated with PI3K/AKT/NF-κB Signaling Pathway in Colon Cancer

2019 ◽  
Author(s):  
JIachi Ma ◽  
Shoukai Zhang ◽  
Danru Liang ◽  
Lei Li ◽  
Jun Du ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Endothelial Cells ◽  
Cancer Cells ◽  
Umbilical Vein ◽  
Metastatic Potential ◽  
Dependent Manner ◽  
Human Colorectal Cancer ◽  
Colorectal Cancer Cells ◽  
Metastatic Process ◽  
Ht 29

Abstract Background: To better explore the underlying mechanism of liver metastatic formation by placenta-specific protein 1 (PLAC1) in human colorectal cancer, we investigated the proliferation, invasion and angiogenic capabilities of human colorectal cancer cell lines with different liver metastatic potentials as well as the mechanism of action of PLAC1 in the metastatic process. Methods: The expression of PLAC1 was detected by reverse transcriptase PCR, western blot and real-time PCR. The effect of PLAC1 on metastatic potential was determined by proliferation, invasion, and angiogenesis assays, including an in vitro coculture system consisting of cancer cells and vascular endothelial cells that were used to detect the relationship between cancer cells and angiogenesis. In addition, we also determined PLAC1 downstream targets that preferentially contribute to the metastatic process. Results: PLAC1 was expressed in HT-29, WiDr and CaCo-2 colorectal cancer cells but not in Colo320 colorectal cancer cells. PLAC1 could not only significantly enhance the proliferation of CoLo320 and human umbilical vein endothelial cells (HUVECs) but could also promote the invasion of CoLo320 cells. The angiogenesis of HUVECs was enhanced by PLAC1 in a dose-dependent manner. In cocultured systems, angiogenesis was significantly increased by coculture with HT-29 cells. In addition, PLAC1 could promote angiogenesis in coculture with HT-29 cells. Furthermore, PLAC1-enhanced metastatic potential of colorectal cancer cells was dependent on activation of the PI3K/Akt/NF-κB pathway. Conclusions: The activation of PI3K/Akt/NF-κB signaling by PLAC1 may be critical for the metastasis of colorectal cancer cells. According to our results, we suggest that modification of PLAC1 function might be a promising new therapeutic approach to inhibit the aggressive spread of colorectal cancer.

scholarly journals The Cuban Propolis Component Nemorosone Inhibits Proliferation and Metastatic Properties of Human Colorectal Cancer Cells

2020 ◽  
Vol 21 (5) ◽  
pp. 1827 ◽  
Author(s):  
Yahima Frión-Herrera ◽  
Daniela Gabbia ◽  
Michela Scaffidi ◽  
Letizia Zagni ◽  
Osmany Cuesta-Rubio ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Metastatic Potential ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Colorectal Cancer Cells ◽  
Folk Remedies ◽  
Main Component

The majority of deaths related to colorectal cancer (CRC) are associated with the metastatic process. Alternative therapeutic strategies, such as traditional folk remedies, deserve attention for their potential ability to attenuate the invasiveness of CRC cells. The aim of this study is to investigate the biological activity of brown Cuban propolis (CP) and its main component nemorosone (NEM) and to describe the molecular mechanism(s) by which they inhibit proliferation and metastatic potential of 2 CRC cell lines, i.e., HT-29 and LoVo. Our results show that CP and NEM significantly decreased cell viability and inhibited clonogenic capacity of CRC cells in a dose and time-dependent manner, by arresting the cell cycle in the G0/G1 phase and inducing apoptosis. Furthermore, CP and NEM downregulated BCL2 gene expression and upregulated the expression of the proapoptotic genes TP53 and BAX, with a consequent activation of caspase 3/7. They also attenuated cell migration and invasion by inhibiting MMP9 activity, increasing E-cadherin and decreasing β-catenin and vimentin expression, proteins involved in the epithelial–mesenchymal transition (EMT). In conclusion NEM, besides displaying antiproliferative activity on CRC cells, is able to decrease their metastatic potential by modulating EMT-related molecules. These finding provide new insight about the mechanism(s) of the antitumoral properties of CP, due to NEM content.

scholarly journals De Novo Fatty Acid Synthesis-Driven Sphingolipid Metabolism Promotes Metastatic Potential of Colorectal Cancer

2018 ◽  
Vol 17 (1) ◽  
pp. 140-152 ◽  
Author(s):  
Naser Jafari ◽  
James Drury ◽  
Andrew J. Morris ◽  
Fredrick O. Onono ◽  
Payton D. Stevens ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Metastatic Potential ◽  
Acid Synthesis ◽  
Sphingolipid Metabolism

Abstract 5279: LPS-TLR4 binding increases metastatic potential of colorectal cancer cells

2010 ◽  
Author(s):  
Rich YC Hsu ◽  
Carlos HF Chan ◽  
Jonathan D. Spicer ◽  
Mathieu C. Rousseau ◽  
Rushika Perera ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Metastatic Potential ◽  
Colorectal Cancer Cells

scholarly journals Expression of HTRA Genes and Its Association with Microsatellite Instability and Survival of Patients with Colorectal Cancer

2020 ◽  
Vol 21 (11) ◽  
pp. 3947
Author(s):  
Dorota Zurawa-Janicka ◽  
Jarek Kobiela ◽  
Tomasz Slebioda ◽  
Rafal Peksa ◽  
Marcin Stanislawowski ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Microsatellite Instability ◽  
Survival Data ◽  
Patient Survival ◽  
Mrna Level ◽  
Metastatic Potential ◽  
Colorectal Carcinogenesis ◽  
Cancer Tissue ◽  
Protein Levels ◽  
High Level

HtrA proteases regulate cellular homeostasis and cell death. Their dysfunctions have been correlated with oncogenesis and response to therapeutic treatment. We investigated the relation between HtrA1-3 expression and clinicopathological, and survival data, as well as the microsatellite status of tumors. Sixty-five colorectal cancer patients were included in the study. The expression of HTRA1-3 was estimated at the mRNA and protein levels by quantitative PCR and immunoblotting. Microsatellite status was determined by high-resolution-melting PCR. We found that the HTRA1 mRNA level was higher in colorectal cancer tissue as compared to the unchanged mucosa, specifically in primary lesions of metastasizing cancer. The levels of HtrA1 and HtrA2 proteins were reduced in tumor tissue when compared to unchanged mucosa, specifically in primary lesions of metastasizing disease. Moreover, a decrease in HTRA1 and HTRA2 transcripts’ levels in cancers with a high level of microsatellite instability compared to microsatellite stable ones has been observed. A low level of HtrA1 or/and HtrA2 in cancer tissue correlated with poorer patient survival. The expression of HTRA1 and HTRA2 changes during colorectal carcinogenesis and microsatellite instability may be, at least partially, associated with these changes. The alterations in the HTRA1/2 genes’ expression are connected with metastatic potential of colorectal cancer and may affect patient survival.

scholarly journals Relationship Between Increased Fucosylation and Metastatic Potential in Colorectal Cancer

2016 ◽  
Vol 108 (9) ◽  
pp. djw210 ◽  
Author(s):  
Takahiro Osuga ◽  
Rishu Takimoto ◽  
Michihiro Ono ◽  
Masahiro Hirakawa ◽  
Makoto Yoshida ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Potential
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