Prevalence of herpes simplex, varicella zoster and Cytomegalovirus in tumorous and adjacent tissues of patients, suffering from colorectal cancer in Iran

Abstract Background Colorectal cancer (CRC) can be considered as a result of multiple risks factors, and the significant role of infectious ones, especially viral diseases could not be underestimated. Despite endorsed attempts to identify the accelerating effects of different herpes viridea, such as HSV-1, HSV2, VZV and CMV on the deterioration of different kinds of malignancy, the relationship between these viruses and CRC have not successfully been understood. Taking advantages of these facts, we assessed the role of these viruses on CRC progression. Methods In this case-control study, 88 cancerous specimens and 70 their adjacent paraffin-embedded tissues from Modares Hospital between 2011 and 2019 were collected. We extracted the DNA of each tissue and investigated the presence of HSV-1, HSV2, VZV and CMV. Results Our data indicated the presence of HSV-1 DNA in the three control samples; however, we could not find an obvious relationship between HSV2, VZV, CMV infection and this type of cancer. The presence of HSV-1 DNA in control tissues introduced HSV-1 as a probable factor for the killing of colorectal cancer cells. Conclusions we supposed that HSV-1 can function as an inhibitor of colon cancer progresion, but it is required to studied more in order to find the role of this virus on CRC.

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LPS Upregulated VEGFR-3 Expression Promote Migration and Invasion in Colorectal Cancer via a Mechanism of Increased NF-κB Binding to the Promoter of VEGFR-3

Cellular Physiology and Biochemistry ◽

10.1159/000447868 ◽

2016 ◽

Vol 39 (5) ◽

pp. 1665-1678 ◽

Cited By ~ 13

Author(s):

Guangwei Zhu ◽

Qiang Huang ◽

Wei Zheng ◽

Yongjian Huang ◽

Jin Hua ◽

...

Keyword(s):

Colorectal Cancer ◽

Cancer Cells ◽

Neutralizing Antibody ◽

High Expression ◽

Migration And Invasion ◽

Colorectal Cancer Cells ◽

Cancer Tissues ◽

The Relationship

Background and Aim: Lipopolysaccharide(LPS) could promote the progression of colorectal cancer, but the specific regulatory mechanisms are largely unknown. So, this study aim to clarify the mechanisms that LPS upregulated VEGFR-3, which promotes colorectal cancer cells migration and invasion with a mechanism of increased NF-κB bind to the promoter of VEGFR-3. Methods: The present study examined the VEGFR-3 expression in colorectal cancer tissues and analyzed the relationship between the VEGFR-3 expression with clinical parameters. PCR, Western blot, CCK-8, colone formation assay, and Transwell assay detected that LPS promoted the migration and invasion and the role of VEGFR-3 in the process of colorectal carcinoma in vitro. Used the methods of promoter analysis, EMSA assay and ChIP assay to explore the mechanisms LPS increased the expression of VEGFR-3. Results: VEGFR-3 was significantly high expression in the colorectal cancer tissues. And the high expression was associated with the TNM stage and lymph node metastasis of colorectal cancer. LPS could promote the migration and invasion, which could be blocked by the neutralizing antibody IgG of VEGFR-3. And found that -159 nt to +65 nt was the crucial region of VEGFR-3 promoter. And detected that the NF-κB was important transcription factor for the VEGFR-3 promoter. And LPS could increase NF-κB binding to VEGFR-3 promoter and upregulated the expression of VEGFR-3 to exert biological functions. Conclusion: We have elucidated the relationship between LPS and the VEGFR-3 expression and revealed that VEGFR-3 play very important role in the process of LPS promoting the migration and invasion of colorectal cancer cells. Further illuminated the mechanism that LPS upregulated VEGFR-3 expression via increased NF-κB bind to the promoter of VEGFR-3.

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Gly972Arg Variant of Insulin Receptor Substrate 1 Gene and Colorectal Cancer Risk in Overweight/Obese Subjects

The International Journal of Biological Markers ◽

10.5301/jbm.5000159 ◽

2016 ◽

Vol 31 (1) ◽

pp. 68-72 ◽

Cited By ~ 3

Author(s):

Touraj Mahmoudi ◽

Keivan Majidzadeh-A ◽

Khatoon Karimi ◽

Hamid Farahani ◽

Reza Dabiri ◽

...

Keyword(s):

Colorectal Cancer ◽

Insulin Receptor ◽

Case Control Study ◽

Insulin Receptor Substrate ◽

Protective Effects ◽

Insulin Receptor Substrate 1 ◽

Pcr Rflp ◽

Obese Subjects ◽

Control Study

Background Given the major role of obesity and insulin resistance (IR) in colorectal cancer (CRC), we investigated whether genetic variants in ghrelin ( GHRL), resistin ( RETN) and insulin receptor substrate 1 ( IRS1) were associated with CRC risk. Methods This study was conducted as a case-control study, and 750 subjects, including 438 controls and 312 patients with CRC, were enrolled and genotyped using the PCR-RFLP method. Results No significant differences were observed for GHRL (rs696217), RETN (rs3745367) and IRS1 (rs1801278, Gly972Arg or G972R) gene variants between the cases and controls. However, the IRS1 G972R R allele compared with the G allele and the G972R RR+GR genotype compared with the GG genotype appeared to be markers of decreased CRC susceptibility in the overweight/obese subjects (p = 0.024; odds ratio [OR] = 0.42, 95% confidence interval [95% CI], 0.20-0.91; and p = 0.048; OR = 0.42, 95% CI, 0.17-0.99, respectively). Furthermore, the R allele and RR+GR genotype were also associated with decreased risks for obesity in the patients with CRC (p = 0.007; OR = 0.35, 95% CI, 0.15-0.77; and p = 0.015; OR = 0.35, 95% CI, 0.15-0.72, respectively). Conclusions In accordance with previous studies, our findings suggest that the IRS1 G972R R allele and RR+GR genotype have protective effects for CRC in overweight/obese patients and for obesity in patients with CRC. Nevertheless, further studies are required to confirm these findings.

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The essential role of TAp73 in bortezomib-induced apoptosis in p53-deficient colorectal cancer cells

Scientific Reports ◽

10.1038/s41598-017-05813-z ◽

2017 ◽

Vol 7 (1) ◽

Cited By ~ 19

Author(s):

Yasamin Dabiri ◽

Sara Kalman ◽

Clara-Marie Gürth ◽

Jee Young Kim ◽

Viola Mayer ◽

...

Keyword(s):

Colorectal Cancer ◽

Cancer Cells ◽

Essential Role ◽

Colorectal Cancer Cells ◽

Induced Apoptosis

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Assessment of TRPV4 Channel and Its Role in Colorectal Cancer Cells

Biomedical & Pharmacology Journal ◽

10.13005/bpj/1683 ◽

2019 ◽

Vol 12 (2) ◽

pp. 629-638

Author(s):

N. N. Bahari ◽

S. Y. N. Jamaludin ◽

A. H. Jahidin ◽

M. N. Zahary ◽

A. B. Mohd Hilmi

Keyword(s):

Colorectal Cancer ◽

Cell Cycle ◽

Cell Death ◽

Cancer Cells ◽

Human Colorectal Cancer ◽

Expression Levels ◽

Pharmacological Modulation ◽

Colorectal Cancer Cells ◽

Ht 29

The transient receptor potential vanilloid member 4 (TRPV4) is a non-selective calcium (Ca2+)-permeable channel which is widely expressed in different types of tissues including the lungs, liver, kidneys and salivary gland. TRPV4 has been shown to serve as a cellular sensor where it is involved in processes such as osmoregulation, cell volume regulation and thermoregulation. Emerging evidence suggests that TRPV4 also plays important roles in several aspects of cancer progression. Despite the reported roles of TRPV4 in several forms of cancers, the role of TRPV4 in human colorectal cancer remains largely unexplored. In the present study, we sought to establish the potential role of TRPV4 in colorectal cancer by assessing TRPV4 expression levels and investigating whether TRPV4 pharmacological modulation may alter cell proliferation, cell cycle and cell death in colorectal cancer cells. Quantitative real-time PCR analysis revealed that TRPV4 mRNA levels were significantly lower in HT-29 cells than normal colon CCD-18Co cells. However, TRPV4 mRNA was absent in HCT-116 cells. Pharmacological activation of TRPV4 with GSK1016790A significantly enhanced the proliferation of HT-29 cells while TRPV4 inhibition using RN 1734 decreased their proliferation. Increased proliferation in GSK1016790A-treated HT-29 cells was attenuated by co-treatment with RN 1734. Pharmacological modulation of TRPV4 had no effect on the cell cycle progression but promoted cell death in HT-29 cells. Taken together, these findings suggest differential TRPV4 expression levels in human colorectal cancer cells and that pharmacological modulation of TRPV4 produces distinct effects on the proliferation and induces cell death in HT-29 cells.

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Nei Endonuclease VIII-Like1 (NEIL1) Inhibits Apoptosis of Human Colorectal Cancer Cells

BioMed Research International ◽

10.1155/2020/5053975 ◽

2020 ◽

Vol 2020 ◽

pp. 1-11

Author(s):

Wanjuan Xue ◽

Yongcheng Liu ◽

Ningning Xin ◽

Jiyu Miao ◽

Juan Du ◽

...

Keyword(s):

Colorectal Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Human Colon ◽

Caspase 9 ◽

Human Colon Cancer ◽

Expression Levels ◽

Colorectal Cancer Cells ◽

Human Colorectal Cancer Cells

The study is aimed at investigating the role of Nei endonuclease VIII-like1 (NEIL1) in the pathogenesis of colorectal cancer (CRC). The human CRC (HCT116 and SW480) cells were subjected to the siRNA silencing and recombinant plasmid overexpression of NEIL1. Transfection of siNEIL1 significantly inhibited the cell growth. It also increased the Bax expression levels, while it decreased the Bcl-2 expression levels in human CRC cells, leading the Bax/Bcl-2 balance toward apoptosis. Moreover, the apoptosis was promoted through the caspase-9 signaling pathway. One the other hand, high expression of NEIL1 promoted the cell viability and reduced the apoptosis, inducing the balance of Bax/Bcl-2 in the human colon cancer cells to be antiapoptotic. In addition, the caspase-9 signaling pathway inhibited apoptosis, contrary to the results obtained by downregulating NEIL1 expression. Furthermore, NEIL1 was negatively regulated by miR-7-5p, indicating that miR-7-5p inhibited the NEIL1 expression after transcription. Overexpression of miR-7-5p reversed the effects of NEIL1 on these CRC cells. In conclusion, NEIL1 promotes the proliferation of CRC cells, which is regulated negatively by miR-7-5p. These findings suggest that NEIL1 is a potential therapeutic target for CRC.

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The role of spermidine/spermine N1-acetyltransferase in determining response to chemotherapeutic agents in colorectal cancer cells

Molecular Cancer Therapeutics ◽

10.1158/1535-7163.mct-06-0303 ◽

2007 ◽

Vol 6 (1) ◽

pp. 128-137 ◽

Cited By ~ 35

Author(s):

Wendy L. Allen ◽

Estelle G. McLean ◽

John Boyer ◽

Andrea McCulla ◽

Peter M. Wilson ◽

...

Keyword(s):

Colorectal Cancer ◽

Cancer Cells ◽

Chemotherapeutic Agents ◽

Colorectal Cancer Cells

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The Association between Serum Bilirubin Levels and Colorectal Cancer Risk: Results from the Prospective Cooperative Health Research in the Region of Augsburg (KORA) Study in Germany

Antioxidants ◽

10.3390/antiox9100908 ◽

2020 ◽

Vol 9 (10) ◽

pp. 908

Author(s):

Nazlisadat Seyed Khoei ◽

Gabriele Anton ◽

Annette Peters ◽

Heinz Freisling ◽

Karl-Heinz Wagner

Keyword(s):

Colorectal Cancer ◽

Health Research ◽

High Performance ◽

A Priori ◽

Antioxidant Properties ◽

Positive Association ◽

Population Based ◽

Inverse Association ◽

Control Study

Emerging studies have suggested that bilirubin, particularly unconjugated bilirubin (UCB), has substantial anti-inflammatory and antioxidant properties that protect against oxidative stress-associated diseases such as cancer. Few observational studies have investigated the etiological role of bilirubin in colorectal cancer (CRC) development. In this case-control study, nested in the population-based prospective cohort of the Cooperative Health Research in the Region of Augsburg (KORA) study in south Germany, pre-diagnostic circulating UCB concentrations were measured by high-performance liquid chromatography in 77 CRC cases and their individually matched controls. Multivariable unconditional logistic regression was used to estimate the odds ratios (OR) and 95% confidence intervals (CI) for associations between log-transformed UCB levels (log-UCB), standardized per one-standard-deviation (one-SD) increment, and CRC risk. The models were a priori stratified by sex based on previous evidence. In the fully adjusted models, each one-SD increment in log-UCB was indicative of a positive association with CRC risk (OR, 1.20; 95% CI, 0.52–2.79) among men, and of an inverse association (OR, 0.76; 95% CI, 0.34–1.84) among women (Pheterogeneity = 0.4 for differences between men and women). We found little evidence for sex-specific associations of circulating bilirubin with CRC risk, and further studies are needed to confirm or refute the potential associations.

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