scholarly journals Anticancer effects of fucoxanthin and fucoxanthinol on colorectal cancer cell lines and colorectal cancer tissues

2015 ◽  
Vol 10 (3) ◽  
pp. 1463-1467 ◽  
Author(s):  
KAZUTO TAKAHASHI ◽  
MASASHI HOSOKAWA ◽  
HIROYUKI KASAJIMA ◽  
KAZUTERU HATANAKA ◽  
KAZUHIRO KUDO ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Anticancer Effects ◽  
Colorectal Cancer Cell Lines ◽  
Cancer Tissues

scholarly journals ADAMTS9 is Silenced by Epigenetic Disruption in Colorectal Cancer and Inhibits Cell Growth and Metastasis by Regulating Akt/p53 Signaling

2017 ◽  
Vol 44 (4) ◽  
pp. 1370-1380 ◽  
Author(s):  
Ling Chen ◽  
Jun Tang ◽  
Yixiao Feng ◽  
Shuman Li ◽  
Qin Xiang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Promoter Methylation ◽  
Methylation Status ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Matrix Assembly ◽  
Colorectal Cancer Cell Lines ◽  
Cancer Tissues

Background/Aims: ADAMTS (disintegrin-like and metalloproteinase with thrombospondin motifs) proteins are extracellular zinc metalloproteinases that play an important role in extracellular matrix assembly and degradation, connective tissue structuring, angiogenesis, and cell migration. Multiple studies suggest that ADAMTS proteins (e.g. ADAMTS9) can act as tumor suppressors. In gastric, esophageal, and nasopharyngeal carcinomas ADAMTS9 is frequently down-regulated by promoter methylation. Whether ADAMTS9 can function as a tumor suppressor gene (TSG) in colorectal cancer is still unclear. Methods: We performed immunohistochemistry, RT-PCR, and qRT-PCR, to examine the expression of ADAMTS9 in colorectal cancer cell lines and primary colorectal cancer tissues. Methylation-specific PCR was also carried out to investigate the promoter methylation status of ADAMTS9. We also explored the functions of ADAMTS9 in colorectal cancer cell lines through in vitro experiments. Results: ADAMTS9 expression was down-requlated or silenced in 83.3% (5/6) of colorectal cancer cell lines, and frequently repressed in 65.6% (21/32) of colorectal cancer tissues. Down-regulation of ADAMTS9 was partially due to promoter methylation. Exogenous expression of ADAMTS9 in colorectal cancer cell lines inhibited cell proliferation and migration through the regulation of cell cycle and apoptosis. In addition, ADAMTS9 prevented the activation of Akt, and its downstream targets in colorectal cancer cell lines. Conclusion: Our findings suggest ADAMTS9 is a TSG in colorectal cancer.

Long non-coding RNA Linc00525 as a prognostic factor to regulate proliferation and apoptosis in colorectal cancer.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e15085-e15085 ◽  
Author(s):  
Peng Peng ◽  
Qin Zheng
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Qrt Pcr ◽  
Proliferation And Apoptosis ◽  
Colorectal Cancer Cell Lines ◽  
Cancer Tissues

e15085 Background: Colorectal cancer (CRC) is one of the most common digestive system tumors and poses a serious threat to human health. More and more studies have shown that long noncoding RNAs (lncRNAs) play an important role in the occurrence and development of various tumors. They regulate a variety of cancer biology, such as proliferation, apoptosis, invasion and metastasis. Abnormally expressed lncRNAs are closely related to colorectal cancer. The purpose of this study was to find lncRNAs associated with the development of colorectal cancer and to explore its function and mechanism. Methods: (1) By analyzing the expression profile of lncRNAs in colorectal cancer-normal tissues in GEO databases, the abnormal expression of lncRNA LINC00525 was screened. Colorectal cancer tissues, adjacent normal colon tissues and colorectal cancer cell lines (HCT116, DLD1, HT-29, SW480) were detected by qRT-PCR. We analyzed the relationship between expression of LINC00525 and clinical features. (2) The biological functions of LINC00525 in HCT116, DLD1 and SW480 were peformed in vitro by MTT, clone formation assay, EDU and flow cytometry. (3) The effect of LINC00525 on tumorigenesis in vivo was evaluated by nude mice model. (4) The expression of lncRNA LINC00525 was knocked down in colorectal cancer cell lines (HCT116, SW480), and the mRNA expression levels of P15, P21, P27 and KLF2 were detected by qRT-PCR. Results: (1) Microarray data and qRT-PCR verification showed that the expression of lncRNA LINC00525 in colorectal cancer tissues and colorectal cancer cell lines was significantly upregulated. The overexpression of LINC00525 was positively correlated with clinical stage and tumor size. (2) Knockdown of LINC00525 in colorectal cancer cell lines could inhibit cancer cell proliferation and induce apoptosis. In SW480 and HCT116 cell lines, cells were arrested in G0/G1 phase after knocking down LINC00525. (3) Subcutaneous xenograft experiments in nude mice further confirmed that knockdown of LINC00525 could inhibit the tumor growth. (4) After knocking down the expression of LINC00525 in HCT116 and SW480 cell lines, the expression of mRNAs of tumor suppressor genes P15, P21, P27 and KLF2 increased. Conclusions: Our studies suggested that LINC00525 was significantly upregulated in colorectal cancer tissues. Mechanism studies had shown that LINC00525 could regulate the expression of KLF2, P15, P21 and P27 in CRC cell lines, and then affect cell proliferation and apoptosis.

Single Investigation of the Role of APC2 in Colorectal Cancer

2020 ◽  
Author(s):  
Yingwei Jiao ◽  
Qiang Liu ◽  
Hongbo Zhao ◽  
Xianzhen Hu ◽  
Jinlong Sun ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tumor Invasion ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Mrna Levels ◽  
Colorectal Cancer Cell Lines ◽  
Cancer Tissues

Abstract BackgroundAPC2 is as a homolog of adenomatous polyposis coli (APC) that has comparable functions in cancer, and is located on chromosome 19p13.3. It is an important signaling pathway protein in many cancers and diseases. For example, in ovarian cancer, APC2 serves as an important tumor suppressor through the induction of the WNT signaling pathway, inhibiting tumor invasion and growth. In colorectal cancer, APC2 was shown to be an important protein for inhibiting tumor invasion and metastasis. In the present study, APC2 was shown to be an important regulatory pathway protein that cooperates with microRNA bidirectional regulation to induce phenotypic changes in colorectal cancer.MethodsThrough measurements in colorectal cancer tissue samples (RT-PCR and immunohistochemistry), we found that the APC2 gene may play a role in the occurrence and development of colorectal cancer patients. We selected colorectal cancer cell lines as the research carrier of the APC2 gene. We changed the expression of APC2 gene in colorectal cancer cell lines by silencing the APC2 gene and up-regulating the APC2 gene, and then used cell cycle, MTT and western blot methods to measure its possible effects on colorectal cancer mechanisms.ResultWe found that the expression of APC2 in normal mucosal tissues in colorectal cancer tissues is was than that of matched colorectal cancer tissues, both at the protein and mRNA levels. We then tested colorectal cancer cell lines for gene silencing and up-regulation. We found that silencing the expression of the APC2 gene effectively advanced the cycle in colorectal cancer cells. In subsequent protein testing, we found that the proteins of the relevant cycle checkpoints changed accordingly. We found the opposite in cell lines after up-regulating the expression of the APC2 gene. By contrast, the SW480 cell line with k-ras mutation in the key pathway did not produce relevant changes by up-regulating the expression of the APC2 gene.ConclusionLow expression levels of the APC2 gene in colorectal cancer inhibit the progression of colorectal cancer cell lines through the RAS signaling pathway and hinders the occurrence and development of colorectal cancer.

scholarly journals Promoter hypermethylation of theADAM23gene in colorectal cancer cell lines and cancer tissues

2009 ◽  
Vol 124 (6) ◽  
pp. 1258-1262 ◽  
Author(s):  
Jin-Sung Choi ◽  
Kyung-Hee Kim ◽  
You-Kyung Jeon ◽  
Sung-Hee Kim ◽  
Sang-Geun Jang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Promoter Hypermethylation ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Colorectal Cancer Cell Lines ◽  
Cancer Tissues

IGF2 knockdown in two colorectal cancer cell lines decreases survival, adhesion and modulates survival-associated genes

Tumor Biology ◽  
2016 ◽  
Vol 37 (9) ◽  
pp. 12485-12495 ◽  
Author(s):  
Michael A. Rogers ◽  
Verena Kalter ◽  
Moritz Strowitzki ◽  
Martin Schneider ◽  
Peter Lichter
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Colorectal Cancer Cell Lines

EXTL3/EXTR1 alterations in colorectal cancer cell lines.

1999 ◽  
Author(s):  
T Arai ◽  
Y Akiyama ◽  
H Nagasaki ◽  
N Murase ◽  
S Okabe ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Colorectal Cancer Cell Lines

scholarly journals DNA methylator and mismatch repair phenotypes are not mutually exclusive in colorectal cancer cell lines

Oncogene ◽  
2000 ◽  
Vol 19 (7) ◽  
pp. 943-952 ◽  
Author(s):  
Martha M Pao ◽  
Gangning Liang ◽  
Yvonne C Tsai ◽  
Zhenggang Xiong ◽  
Peter W Laird ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Mismatch Repair ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colorectal Cancer Cell ◽  
Colorectal Cancer Cell Lines
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