scholarly journals Abundance, fatty acid composition and saturation index of neutral lipids are significantly different between isogenic primary and metastatic colon cancer cell lines

2019 ◽  
Author(s):  
Rimsha Munir ◽  
Jan Lisec ◽  
Carsten Jaeger ◽  
Nousheen Zaidi
Keyword(s):  
Colon Cancer ◽  
Neutral Lipids ◽  
Saturation Index ◽  
Carcinoma Cells ◽  
Metastatic Colon Cancer ◽  
Colon Carcinoma Cells ◽  
Metabolic Genes ◽  
Colon Cancer Cell Lines ◽  
Sw620 Cells ◽  
Ce Content

AbstractLipid droplets, the dynamic organelles that store triglycerides (TG) and cholesterol esters (CE), are highly accumulated in colon cancer cells. This work studies the TG and CE subspecies profile in colon carcinoma cells lines, SW480 derived from primary tumor, and SW620 derived from a metastasis of the same tumor. It was previously reported that the total TG and CE content is dramatically higher in SW620 cells; however, TG and CE subspecies profile has not been investigated in detail. The presented work confirms that total TG and CE content is significantly higher in SW620 cells. Moreover, the FA-composition of TGs is significantly altered in SW620 cells, with significant decrease in the abundance of saturated triglycerides. This resulted in significantly decreased TG saturation index in SW620 cells. The saturation index of CEs was also significantly decreased in SW620 cells. The saturation indices of some other major lipid classes were either similar or only moderately different between SW480 and SW620 cells. We also compared the expression of metabolic genes that may regulate these changes in the lipidomic profiles.

scholarly journals Abundance, fatty acid composition and saturation index of neutral lipids in colorectal cancer cell lines

2021 ◽  
Author(s):  
Rimsha Munir ◽  
Jan Lisec ◽  
Carsten Jaeger ◽  
Nousheen Zaidi
Keyword(s):  
Fatty Acid ◽  
Cell Lines ◽  
Lipid Droplets ◽  
Neutral Lipids ◽  
Saturation Index ◽  
Carcinoma Cell Lines ◽  
Fa Composition ◽  
Colorectal Cancer Cell Lines ◽  
Sw620 Cells ◽  
Ce Content

Lipid droplets, the dynamic organelles that store triglycerides (TG) and cholesterol esters (CE), are highly accumulated in colon cancer cells. This work studies the TG and CE subspecies profile in colon carcinoma cell lines, SW480 derived from primary tumor, and SW620 derived from a metastasis of the same tumor. It was previously reported that the total TG and CE content is dramatically higher in SW620 cells; however, TG and CE subspecies profile has not been investigated in detail. The work presented here confirms that the total TG and CE content is significantly higher in the SW620 cells. Moreover, the fatty acid (FA) composition of TG is significantly altered in the SW620 cells, with significant decrease in the abundance of saturated triglycerides. This resulted in a significantly decreased TG saturation index in the SW620 cells. The saturation index of CE was also significantly decreased in the SW620 cells.

scholarly journals Kallikrein 6 is a mediator of K-RAS-dependent migration of colon carcinoma cells

2008 ◽  
Vol 389 (6) ◽  
Author(s):  
Rebecca S. Henkhaus ◽  
Eugene W. Gerner ◽  
Natalia A. Ignatenko
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Small Interference Rna ◽  
Colon Carcinoma Cells ◽  
Kallikrein 6

Abstract Kallikrein 6 (KLK6) is a trypsin-like serine peptidase whose relevance in various types of cancers is currently being explored. Previous studies have shown that KLK6 mRNA is upregulated in colon and gastric cancers; however, the regulatory mechanisms and phenotypic consequences of this upregulation are largely unknown. Activating K-RAS mutations are common in colon cancer, occurring in approximately 50% of cases. We have recently reported the upregulation of KLK6 mRNA in Caco2 human colon cancer cells stably transfected with a mutant K-RAS allele (K-RASG12V). In this study we examined the pattern of K-RAS-dependent KLK6 expression and secretion in colon cancer cells. Using pharmacological inhibitors of pathways downstream of K-RAS, we could show that the PI3K and p42/44 MAPK pathways play an important role in the induction of KLK6 in mutant K-RAS-expressing colon cancer cells. Increased KLK6 expression enhanced colon cancer cell migration through laminin and Matrigel. Inhibition of KLK6 using small interference RNA treatment or a specific KLK6 antibody in Caco2 cells stably expressing the mutant K-RAS and in SW480 cells carrying a mutation in the K-RAS oncogene resulted in a reduction in invasiveness through cell culture inserts. These data support the oncogenic role of KLK6 in colorectal cancer.

scholarly journals pH-operated hybrid silica nanoparticles with multiple H-bond stoppers for colon cancer therapy

RSC Advances ◽  
2015 ◽  
Vol 5 (80) ◽  
pp. 64932-64936 ◽  
Author(s):  
C. Théron ◽  
A. Gallud ◽  
S. Giret ◽  
M. Maynadier ◽  
D. Grégoire ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Therapy ◽  
Silica Nanoparticles ◽  
Cancer Cells ◽  
Cyanuric Acid ◽  
Carcinoma Cells ◽  
Controlled Delivery ◽  
Chemotherapeutic Drug ◽  
Colon Carcinoma Cells ◽  
Hybrid Silica

Controlled delivery of a chemotherapeutic drug from pH-sensitive hybrid silica nanocarriers efficiently targets colon carcinoma cells. The drug, blocked by cyanuric acid as stopper, is autonomously released inside the cancer cells.

Lentivirus-Mediated Knockdown of NOB1 Suppresses the Proliferation of Colon Cancer Cells

2014 ◽  
Vol 52 (05) ◽  
pp. 429-435 ◽  
Author(s):  
Y. Liu ◽  
H. Huang ◽  
B. Yuan ◽  
L. Zhuang ◽  
T. Luo ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Colony Formation ◽  
Ribosome Biogenesis ◽  
Carcinoma Cells ◽  
G1 Phase ◽  
Flow Cytometry Analysis ◽  
Colon Cancer Cells ◽  
Endogenous Gene ◽  
Colon Cancer Cell Lines

AbstractNOB1 is important for ribosome biogenesis and protein degradation. Previous studies showed that it could regulate the growth and colony-formation ability of ovarian, breast and hepatocellular carcinoma cells. However, its function in colon cancer cells is largely unknown. In this study, we found that NOB1 could express in 6 different colon cancer cell lines. Lentivirus-mediated shRNA targeted NOB1 could suppress the endogenous gene expression. NOB1 depletion significantly inhibited cell proliferation and colony formation ability, as determined by MTT and colony formation assays. Flow cytometry analysis showed NOB1 silencing arrested cell cycle in G0 / G1 phase. Moreover, the percentage of cells at sub-G1 phase dramatically increased after NOB1 knockdown. These results indicate that NOB1 may play an important role in the growth and tumorigensis of colon cancer and knockdown of NOB1 may be a potential therapeutic method for colon cancer in the future.

scholarly journals MicroRNA-4284 inhibits colon cancer epithelial-mesenchymal transition by down-regulating Perilipin 5

STEMedicine ◽  
2021 ◽  
Vol 2 (6) ◽  
pp. e85
Author(s):  
Xiaofei Miao ◽  
Zengyao Li ◽  
Ye Zhang ◽  
Tong Wang
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Metastatic Colon Cancer ◽  
Mesenchymal Transition ◽  
Colon Cancer Cell Lines ◽  
Perilipin 5

Background: MicroRNA (miR) has been suggested in the development of several types of cancer; yet, the exact function of miR-4284 in colon cancer remains elusive. Methods: MiR-4284 expression was assessed in normal colon cell line CCD-18Co, and HT-29 and SW480 cell lines representing human colon cancer. Potential target gene of miR-4284 was predicted using TargetScanHuman, and experimentally verified using luciferase report assay. Wound-healing, cell invasion and attachment were evaluated to determine the effect of miR-4284 on the migration, invasion, and metastatic properties of colon cancer cell lines. Expression of epithelial-mesenchymal transition (EMT) phenotypic protein hallmarks, including N-cadherin, E-cadherin, as well as Vimentin, was also evaluated. Results: MiR-4284 was significantly decreased in colon cancer cell lines, and Perilipin 5 (PLIN5) was found to be directly targeted by miR-4284. Ectopic expression of miR-4284 significantly reduced endogenous expression level of PLIN5 in colon cancer cell lines, suppressing migration, invasion, and metastatic phenotypes. In addition, re-introducing miR-4284 reversed the expression profile of EMT markers. Conclusion: Our findings for the first time identify miR-4284 as an anti-tumor miRNA in colon cancer, which acts to reduce PLIN5 and inhibit EMT, leading to inhibited colon cancer tumorigenesis. These results highlight the potential of miR-4284 as a therapeutic target in metastatic colon cancer.

CJK-7, a Novel Flavonoid from Paulownia tomentosa Triggers Cell Death Cascades in HCT-116 Human Colon Carcinoma Cells via Redox Signaling

2018 ◽  
Vol 18 (3) ◽  
pp. 428-437 ◽  
Author(s):  
Mahendra Pal Singh ◽  
Ki Hun Park ◽  
Tejinder Pal Khaket ◽  
Sun Chul Kang
Keyword(s):  
Colon Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Paulownia Tomentosa ◽  
Colon Carcinoma Cells ◽  
Human Colon Carcinoma ◽  
Hct 116

Background: Colon cancer is the second most common cancer to cause death worldwide. About half of colon cancers patients require adjuvant therapy to control relapse following surgical resection. Therefore, abolition of tumor cell progression using an effective chemotherapeutic agent holds a feasible approach to treat patients suffering from colon cancer. In the present study, we evaluated the effects of geranylated flavonoid CJK-7, isolated from Paulownia tomentosa on HCT-116 human colon carcinoma cells. Materials and Methods: The effects of CJK-7 as an active component on HCT-116 cells programmed cell death and its underlying molecular mechanism were examined by using MTT assay, morphological assessment, H2DCFDA staining, Fura-2AM staining, Hoechst-33342 staining, comet assay, Acridine orange staining, mitochondrial membrane potential (ΔΨm) assay and Western blot analyses. Results and Conclusion: The results revealed that, CJK-7 was capable of inducing caspase-dependent cell death events in cancer cells. Moreover, it was involved in up-regulation of autophagy signaling as evidenced by enhanced expression of LC3I/II. We also noticed stimulated expression of endoplasmic reticulum stress markers and phosphorylation of c-Jun NH2-terminal kinase (JNK), which was associated with up-regulated expression of p53, PUMA, Atg5 and Beclin-1, and down-regulation of Bcl-2, stressing the interaction of ROS on the aforementioned signaling. Furthermore, exposure to ROS scavengers (N-acetyl-l-cysteine (NAC), and JNK-specific inhibitor SP600125) significantly reversed the effects of CJK-7 by down-regulating apoptosis and autophagy signatures in HCT-116 cancer cells. Collectively our findings clarify the ROS-dependent regulatory effect of CJK-7 on programmed cell death signaling events in HCT-116 cancer cells while depicting its virile pro-oxidant capacity.

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