scholarly journals The Expression of YKL-40 in Peripheral Blood of Colorectal Cancer and Its Effect on the Proliferation and Angiogenesis of Colorectal Cancer Cells

2021 ◽  
Author(s):  
Shaohui Yang ◽  
Jie Shen ◽  
Yibin Zhao
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Precancerous Lesion ◽  
Colon Cancer Cell ◽  
Lesion Group ◽  
Control Group ◽  
Cancer Group ◽  
Hct 116

Abstract Objective To observe the expression of YKL-40 in the serum of patients with colorectal cancer, and to study the effect of YKL-40 gene on the proliferation and angiogenesis of colon cancer cell lines. Methods The serum of patients with colorectal cancer, precancerous lesions, and healthy controls were collected, and the expression of YKL-40 was detected by enzyme-linked immunosorbent assay (ELISA) technology. Screened cell lines with high expression of YKL-40 from colon cancer cell lines HCT-15, HCT-116, SW480, interfered with YKL-40 gene expression through siRNA technology, and co-cultured with bevacizumab, and detected cells with CCK8 method Proliferation, cell formation test to detect blood vessel formation. Results The mean values of serum YKL-40 in the colorectal cancer group, precancerous lesion group and control group were (178.50±71.91) μg/L, (91.37±35.79) μg/L and (78.23±26.52) μg/L, respectively. The colorectal cancer group (preoperative) was significantly higher than the precancerous lesion group and the control group (P <0.01). The precancerous lesion group was higher than the control group, but the difference between the two was not statistically significant (P = 0.244). The expression of YKL-40 was positively correlated with the stage of colorectal cancer (P <0.05). There was no significant difference in the expression of serum YKL-40 before and after surgery (p=0.07). HCT-116 is a YKL-40 highly expressing cell line. After inhibiting the expression of this gene, the survival rate of the experimental group was 78.75%, which was significantly lower than that of the control group (p<0.05). The angiogenesis test is used to detect the angiogenesis ability. siRNA interference with YKL-40 gene and the addition of bevacizumab can inhibit the angiogenesis ability in vitro. Moreover,the vascular inhibitory effect of bevacizumab in the experimental group was stronger than that in the control group. Conclusion YKL-40 is highly expressed in the peripheral blood of patients with colorectal cancer and is related to the tumor stage. The HCT-116 colon cancer cell line has a high expression of YKL-40. Interfering with the expression of YKL-40 can inhibit cell proliferation and angiogenesis. It suggests that YKL-40 plays an important role in the occurrence and development of colorectal cancer.

scholarly journals Anticancer effects of bifidobacteria on colon cancer cell lines

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zeinab Faghfoori ◽  
Mohammad Hasan Faghfoori ◽  
Amir Saber ◽  
Azimeh Izadi ◽  
Ahmad Yari Khosroushahi
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Rt Pcr ◽  
Anticancer Effects ◽  
Colon Cancer Cell Lines ◽  
Apoptotic Genes

Abstract Background Colorectal cancer (CRC), with a growing incidence trend worldwide, is resistant to apoptosis and has uncontrolled proliferation. It is recently reported that probiotic microorganisms exert anticancer effects. The genus Bifidobacterium, one of the dominant bacterial populations in the gastrointestinal tract, has received increasing attention because of widespread interest in using it as health-promoting microorganisms. Therefore, the present study aimed to assess the apoptotic effects of some bifidobacteria species on colon cancer cell lines. Methods The cytotoxicity evaluations performed using MTT assay and FACS-flow cytometry tests. Also, the effects of five species of bifidobacteria secretion metabolites on the expression level of anti- or pro-apoptotic genes including BAD, Bcl-2, Caspase-3, Caspase-8, Caspase-9, and Fas-R studied by real-time polymerase chain reaction (RT-PCR) method. Results The cell-free supernatant of all studied bifidobacteria significantly decreased the survival rates of colon cancer cells compared with control groups. Flow cytometric and RT-PCR results indicated that apoptosis is induced by bifidobacteria secretion metabolites and the mechanism for the action of bifidobacteria species in CRC prevention could be down-regulation and up-regulation of anti-apoptotic and, pro-apoptotic genes. Conclusions In the present study, different bifidobacteria species showed anticancer activity on colorectal cancer cells through down-regulation and up-regulation of anti-apoptotic and pro-apoptotic genes. However, further studies are required to clarify the exact mechanism of apoptosis induction by bifidobacteria species.

scholarly journals Efficiency of brown seaweed (Sargassum longifolium) polysaccharides encapsulated in nanoemulsion and nanostructured lipid carrier against colon cancer cell lines HCT 116

RSC Advances ◽  
2018 ◽  
Vol 8 (29) ◽  
pp. 15973-15984 ◽  
Author(s):  
Saghya Infant Shofia ◽  
Kannan Jayakumar ◽  
Amitava Mukherjee ◽  
Natarajan Chandrasekaran
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Brown Seaweed ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Nanostructured Lipid Carrier ◽  
Brown Seaweeds ◽  
Colon Cancer Cell Lines ◽  
Hct 116

Bioactive polysaccharides extracted from brown seaweeds have potent antioxidant, antitumor, antibacterial, antiviral, anti-inflammatory activities and nanomedicine applications.

Folic acid inhibition of EGFR-mediated proliferation in human colon cancer cell lines

1999 ◽  
Vol 277 (6) ◽  
pp. C1142-C1148 ◽  
Author(s):  
Richard Jaszewski ◽  
Ahmed Khan ◽  
Fazlul H. Sarkar ◽  
Omer Kucuk ◽  
Martin Tobi ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Folic Acid ◽  
Tyrosine Kinase ◽  
Cell Lines ◽  
Cancer Cell ◽  
Kinase Activity ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Hct 116

Although accumulating evidence suggests a chemopreventive role for folic acid in colon cancer, the regulation of this process in unknown. We hypothesize that supplemental folic acid exerts its chemopreventive role by inhibiting mucosal hyperproliferation, an event considered to be central to the initiation of carcinogenesis in the gastrointestinal tract. The present investigation examines the effect of supplemental folic acid on proliferation of Caco-2 and HCT-116 colon cancer cell lines. Furthermore, because certain tyrosine kinases, particularly epidermal growth factor receptor (EGFR), play a role in regulating cell proliferation, we also examined the folic acid-induced changes in tyrosine kinase activity and expression of EGFR. In Caco-2 and HCT-116 cells, maintained in RPMI 1640 medium containing 1 μg/ml folic acid, we observed that the supplemental folic acid inhibited proliferation in a dose-dependent manner. Pretreatment of HCT-116 and Caco-2 cell lines with supplemental folic acid (1.25 μg/ml) completely abrogated transforming growth factor-α (TGF-α)-induced proliferation in both cell lines. Tyrosine kinase activity and the relative concentration of EGFR were markedly diminished in both cell lines following a 24-h exposure to supplemental folic acid. The folic acid-induced inhibition of EGFR tyrosine kinase activity in colon cancer cell lines was also associated with a concomitant reduction in the relative concentration of the 14-kDa membrane-bound precursor form of TGF-α. In conclusion, our data suggest that supplemental folic acid is effective in reducing proliferation in two unrelated colon cancer cell lines and that EGFR tyrosine kinase appears to be involved in regulating this process.

Dual Targeting of the Epidermal Growth Factor Receptor Using the Combination of Cetuximab and Erlotinib: Preclinical Evaluation and Results of the Phase II DUX Study in Chemotherapy-Refractory, Advanced Colorectal Cancer

2012 ◽  
Vol 30 (13) ◽  
pp. 1505-1512 ◽  
Author(s):  
Andrew J. Weickhardt ◽  
Tim J. Price ◽  
Geoff Chong ◽  
Val Gebski ◽  
Nick Pavlakis ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Growth Factor Receptor ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Epidermal Growth

Purpose This preclinical and phase II study evaluated the efficacy and safety of the combination of cetuximab and erlotinib in metastatic colorectal cancer (mCRC). Patients and Methods The activity and mechanism of action of the combination of cetuximab plus erlotinib were investigated in vitro in colorectal cancer cell lines. In the clinical study, patients with chemotherapy-refractory mCRC were treated with cetuximab 400 mg/m2 as a loading dose and then weekly cetuximab 250 mg/m2 with erlotinib 100 mg orally daily. The primary end point was response rate (RR), which was evaluated separately in KRAS wild-type (WT) versus KRAS mutant tumors. Secondary end points included toxicity, progression-free survival (PFS), and overall survival. Target accrual was 50 patients, with a one-stage design. Results Preclinical studies demonstrated synergistic activity of cetuximab and erlotinib cotreatment on growth inhibition of colon cancer cell lines both as a result of enhanced inhibition of the epidermal growth factor receptor pathway and differential effects on STAT3. In the clinical study, 50 patients were enrolled, with 48 patients evaluable for response. The overall RR was 31% (95% CI, 26% to 57%), with a median PFS of 4.6 months (95% CI, 2.8 to 5.6 months). RR was 41% (95% CI, 26% to 57%) in KRAS WT tumors, with a median PFS of 5.6 months (95% CI, 2.9 to 5.6 months). There was no response in 11 patients with KRAS mutations. Frequent grade 3 and 4 toxicities were rash (48%), hypomagnesaemia (18%), and fatigue (10%). Conclusion The combination of cetuximab and erlotinib synergistically inhibits growth of colon cancer cell lines, achieves promising efficacy in patients with KRAS WT mCRC, and merits evaluation in further randomized studies.

scholarly journals MicroRNA silencing of CNN1 and CNN2 protein family members regulates biology processes in colorectal cancer by targeting the p53 signal pathway

2020 ◽  
Author(s):  
Fuda Huang ◽  
Mingwei Wei ◽  
Anmin Wang ◽  
Ya Zhang ◽  
Zebang Qin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Expression Levels ◽  
Colon Cancer Cell Lines ◽  
Cancer Tissues

Abstract BackgroundCalponin was first defined as a striated muscle troponin T-like protein that binds actin thin filaments to regulate smooth muscle contraction. There are few studies of CNN1 and CNN2 in colorectal cancer, and the roles these two genes play in colorectal cancer cell lines and the mechanisms by which they act are unknown.MethodsWe used immunohistochemistry to identify expression of the two genes in the cancer tissues. RT-PCR was used to measure expression levels of microRNA. W performed western blots to measure changes in signaling pathways in the context of expression interference.Meanwhile, the same method was used to measure binding relationship between the two genes and key pathway proteins. To determine the relationship between microRNA and gene mRNA, we used the reporter gene method. We used the chi-square and t-test methods to analyze the significance and correlations of the data.Results and conclusionsExpression levels of CNN1 were lower in colon cancer tissues than in normal mucosal tissues. After downregulating CNN1, the cell cycle in colon cancer cell lines progressed quickly, and the expression of related pathway proteins also increased. Expression levels of CNN2 were higher in colon cancer tissues, and its downregulation significantly inhibited cell cycle progression in colon cancer cell lines. We confirmed correlations between the expression of microRNA and CNN2 using data analysis.Bars indicate ± standard errors.*p < 0.05; **p < 0.01 compared with the control. The inhibition of the expression of CNN2 mRNA using microRNA was confirmed using western blot. The combination of the two at the mechanism level was also demonstrated using the reporter gene method.

scholarly journals Anticancer effects of Bifidobacteria on colon cancer cell lines

2021 ◽  
Author(s):  
Zeinab Faghfoori ◽  
Mohammad Hasan Faghfoori ◽  
Amir Saber ◽  
Azimeh Izadi ◽  
Ahmad Yari Khosroushahi
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Rt Pcr ◽  
Anticancer Effects ◽  
Colon Cancer Cell Lines ◽  
Apoptotic Genes

Abstract Background: Colorectal cancer (CRC), with a growing incidence trend worldwide, is resistant to apoptosis and have the uncontrolled proliferation. It is recently reported that probiotic microorganisms exert anticancer effects. The genus Bifidobacterium, one of the dominant bacterial populations in the gastrointestinal tract, has received increasing attention because of widespread interest in using as health-promoting microorganisms. Therefore, the present study aimed to assess the apoptotic effects of some bifidobacteria species on colon cancer cell lines.Methods: The cytotoxicity evaluations performed using MTT assay and FACS-flow cytometry tests. Also, the effects of five species of bifidobacteria secretion metabolites on the expression level of anti- or pro-apoptotic genes including BAD, Bcl-2, Caspase-3, Caspase-8, Caspase-9, and Fas-R studied by real-time polymerase chain reaction (RT-PCR) method. Results: The cell-free supernatant of all studied bifidobacteria significantly decreased the survival rates of colon cancer cells compared with control groups. Flow cytometric and RT-PCR results indicated that apoptosis is induced by bifidobacteria secretion metabolites and the mechanism for the action of bifidobacteria species in CRC prevention could be down-regulation and up-regulation of anti-apoptotic and, pro-apoptotic genes.Conclusions: In the present study, different bifidobacteria species showed anticancer activity on colorectal cancer cells through down-regulation and up-regulation of anti-apoptotic and pro-apoptotic genes. However, further studies are required to clarify the exact mechanism of apoptosis induction by bifidobacteria species.

scholarly journals Comprehensive polar metabolomics and lipidomics profiling discriminates the transformed from the non-transformed state in colon tissue and cell lines

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Caroline Rombouts ◽  
Margot De Spiegeleer ◽  
Lieven Van Meulebroek ◽  
Lynn Vanhaecke ◽  
Winnok H. De Vos
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
High Resolution Mass Spectrometry ◽  
Cancer Cell Line ◽  
Colon Cancer Cell ◽  
Colon Tissue ◽  
Tissue Samples ◽  
Cellular Models

AbstractColorectal cancer (CRC) is the fourth most lethal disease worldwide. Despite an urgent need for therapeutic advance, selective target identification in a preclinical phase is hampered by molecular and metabolic variations between cellular models. To foster optimal model selection from a translational perspective, we performed untargeted ultra-high performance liquid chromatography coupled to high-resolution mass spectrometry-based polar metabolomics and lipidomics to non-transformed (CCD841-CON and FHC) and transformed (HCT116, HT29, Caco2, SW480 and SW948) colon cell lines as well as tissue samples from ten colorectal cancer patients. This unveiled metabolic signatures discriminating the transformed from the non-transformed state. Metabolites involved in glutaminolysis, tryptophan catabolism, pyrimidine, lipid and carnitine synthesis were elevated in transformed cells and cancerous tissue, whereas those involved in the glycerol-3-phosphate shuttle, urea cycle and redox reactions were lowered. The degree of glutaminolysis and lipid synthesis was specific to the colon cancer cell line at hand. Thus, our study exposed pathways that are specifically associated with the transformation state and revealed differences between colon cancer cell lines that should be considered when targeting cancer-associated pathways.

scholarly journals Expression of AEG-1 mRNA and protein in colorectal cancer patients and colon cancer cell lines

2012 ◽  
Vol 10 (1) ◽  
pp. 109 ◽  
Author(s):  
Sebastian Gnosa ◽  
Yang-Mei Shen ◽  
Chao-Jie Wang ◽  
Hong Zhang ◽  
Johannes Stratmann ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Patients ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Colorectal Cancer Patients

scholarly journals P08.02 Berberine-loaded liposome formulation enhance the phagocytic activity of liposomal imiquimod towards colon cancer cell lines

2020 ◽  
Vol 8 (Suppl 2) ◽  
pp. A50.1-A50
Author(s):  
M Mianowska ◽  
M Zaremba-Czogalla ◽  
A Zygmunt ◽  
J Gubernator
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cell Surface ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Liposomal Formulations ◽  
Colon Cancer Cell Lines

BackgroundColorectal cancer is the third most commonly diagnosed malignant tumor, taking fourth place in terms of cause of cancer deaths worldwide.1 Unfortunately, the ability of the immune system to distinguish its own from foreign cells is often limited. One of the overexpressed receptors is receptor CD47 - widely distributed glycoprotein on the cell surface of various kind of tumors. It plays a role as ‘don’t eat me’ signal by binding with receptor SIRPα, presents on the cell surface of macrophages.2 Calreticulin, protein occurring on the surface of tumor cells and phagocytes, acts as protein with pro-phagocytic properties. Several natural bioactive substances are predicted to induce immunogenic cell death by translocation calreticulin on the surface of cancer cells which significantly increases the efficiency of their phagocytosis. Moreover, one of the well-known TLR-7 receptor agonists - imiquimod, is involved in phosphorylation of Bruton’s tyrosine kinase leading to the appearance of calreticulin on the surface of macrophages, which increases the efficiency of phagocytosis of tumor cells.3 Combination therapy composed of berberine and imiquimod can be highlighted as effective immunotherapy for colon cancer. However, such an approach remains very limited. Liposomes can serve as promising carriers for targeting delivery and controlled release of anti-cancer agents.Material and MethodsLiposomes were prepared by the thin-film hydration method followed by extrusion. Human colon cancer cell line (LS180 I SW620) and human monocytic cell line (THP-1) were used for experiments. Calreticulin was detected by using confocal microscopy.ResultsThe work presented aimed to develop novel liposomal formulations of berberine and imiquimod which were examined for their efficacy in combination against colorectal cancer cell lines. Liposomal formulations of both compounds were successfully prepared using active loading method with different pH generating agents. All loading methods showed desired characteristics in terms of mean liposome size and polydispersity. The encapsulation efficiency was higher than 95% for almost all used formulations. The in vitro study proved cytotoxicity of berberine loaded liposomal formulations on tested colon cancer cell lines. The results of the immunofluorescence staining indicated that the both compounds triggered calreticulin on the cell surface (colon cancer or macrophages).ConclusionsThe combination of both substances in the liposomal form may generate a synergistic effect on phagocytosis of colon cancer cells.ReferencesArnold M, Sierra MS, Laversanne M, et al. Global patterns and trends in colorectal cancer incidence and mortality. Gut 2017;66:683–691.Sick E, Jeanne A, Schneider C, Dedieu S, Takeda K, Martiny L. CD47 update: a multifaceted actor in the tumor microenvironment of potential therapeutic interest, Br J Pharmacol 2012, 167(7):1415–30.M. Feng, et al., Macrophages eat cancer cells using their own calreticulin as a guide: Roles of TLR and Btk. PNAS 2015;112( 7):2145–2150.Disclosure InformationM. Mianowska: B. Research Grant (principal investigator, collaborator or consultant and pending grants as well as grants already received); Significant; National Science Center, Poland. M. Zaremba-Czogalla: None. A. Zygmunt: None. J. Gubernator: None.

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