Analysing the HERV-K env, np9, rec and gag expression in cervical tissues.

Cervical cancer is considered to be the fourth common cancer. It is assumed that numerous risk factors, especially infectious ones, can have a detrimental effect on cervical cancer. In this study, we evaluated the expression of Herv-K env, np9, rec and gag in cervical tissues. After RNA extraction and cDNA sensitizing of 12 cervical cancer tissues and CIN3, 51 CIN1,2 and 18 normal ones, Herv-K env, np9, rec and gag were assessed using quantitative real-time PCR analysis. There was a decrease in the level of HERV-K env expression in cervical cancer and CIN 1-3 in compression with normal tissues. Cervical cancer and CIN3 indicated the most increase in expression. Meanwhile, we observed an increase in gag and rec expression in CIN 1,2; although cervical cancer and CIN 3 had a decrease in rec and gag expression, we did not report any changes in np expression. In conclusion, given the relationship between HERV-associated genes and cervical cancer, our study suggests that these genes can be useful for cancer diagnosis. However, further investigations are needed to provide a better perspective about the effectiveness of these genes in the diagnostic strategies of gastrointestinal cancer. These results are just an observation that could open a wider investigation to test the correlation between the expression of these genes and cervical cancer.

The interplay between EBV and KSHV viral products and NF-κB pathway in oncogenesis.

Among the DNA tumor viruses Epstein-Barr virus (EBV) and Kaposi sarcoma herpesvirus (KSHV), account for a considerable percentage of virus-associated cancers. Deregulation of transcription factors signaling pathways is one of the most significant oncogenic characteristics of EBV and KSHV. NF-κB is a transcription factor that play a remarkable role in oncogenesis because of its function as a master regulator of a spectrum of genes involved in physiological and pathophysiological process. Constitutive activation of NF-κB is a frequent and well-described event in many human malignancies. Compelling evidence represent EBV and KSHV are capable of targeting different components of NF-κB cascade. Here, we summarized recent findings to clarify the precise relationship between dysregulation of NF-κB and EBV and KSHV-related malignancies. This essay also emphasizes on contribution of various viral products in developing cancer through alteration of NF-κB signaling pathway.

Epidemiology of herpes simplex and varicella zoster virus in cerebrospinal fluid of patients suffering from meningitis in Iran.

From the early 18th century that "meningitis" outbreak was firstly recorded in Geneva, it is one of the alarming health problems worldwide. Different infectious risk factors may contribute to the progression of meningitis. Herpes simplex virus (HSV) and Varicella-zoster virus (VZV) are just some noticeable risk factors among many involved in the progression of this disease. In this study, 415 meningitis suspected patients were recruited with some symptoms, such as fever, headache, nausea or vomiting, seizure, rash, dizziness from four different hospitals of Iran and molecular examinations of samples were performed by using specific primers of HSV½ and VZV via real-time PCR. Out of 415 included patient 41 (9.8 %) were VZV and six (1.4 %) cases were HSV ½ positive. Fever was the most frequent symptom by 315 (76 %) of patients with median temperature of 38 °C in all included patients. The median WBS counts of CSF in VZV positive, HSV½ positive, and all included cases were 1567 × 106 /L, 1257 × 106 /L, and 766 × 106 /L (range 0-21200), respectively. In conclusion, as the rate of VZV infection was high among children patients and it was associated with the absence of vaccination program for chickenpox in Iran, we suggested that VZV is one of the plausible hallmarks in meningitis.

Cdc6 expression is induced by HPV16 E6 and E7 oncogenes and represses E-cadherin expression.

Cervical cancer is one of the most common cancers in women worldwide, and its development is related to two viral oncoproteins E6 and E7 from high-risk human papillomaviruses. Aberrant expression of E-cadherin is associated with epithelial-to-mesenchymal transition (EMT), and it is frequently seen in cervical cancer. However, the underlying mechanisms involved in E-cadherin suppression in cervical cancer are not clear. We studied the effects of human papillomavirus 16 (HPV16) E6 and E7 on E-cadherin and Cdc6 (cell division cycle 6) expression in the HCT-116 cell line. We also assessed the relationship between Cdc6 and E-cadherin expression in cells expressing HPV16 E6 and E7 proteins. The results showed that HPV16 E6 and E7 proteins reduce E-cadherin expression, and HPV16 E6-expressing cells undergo a more profound suppression of E-cadherin compared with cells expressing HPV16 E7. Our results also revealed that HPV16 E6 and E7 oncoproteins induce Cdc6 expression, whereas suppression of Cdc6 protein by short hairpin RNA restores E-cadherin expression. Induction of Cdc6 expression in HCT-116 cells was greater with E6 than with E7, a finding that was consistent with the corresponding changes in E-cadherin expression. These observations suggest that Cdc6 overexpression is an important factor for E-cadherin reduction in cells expressing HPV16 E6 and E7 proteins and may have an important role in the metastasis of HPV-associated cancers.Cancer Gene Therapy advance online publication, 11 November 2016; doi:10.1038/cgt.2016.51.

The effect of oxamflatin on the E-cadherin expression in gastric cancer cell line.

Gastric cancer is among the leading causes of cancer-related death, and the symptoms are commonly characterized in advanced stages. Histone acetylation is among the most important epigenetic alterations occurring during cancer development. In addition, reduced E-cadherin expression is a major contributor in the process of tumor cell invasion and metastasis. Oxamflatin is a histone deacetylase inhibitor that has been suggested as a promising anti-tumor agent; yet its effect on the viability and invasion of gastric tumor cells is unclear. We aimed to assess the impact of oxamflatin on the viability of gastric tumor cells and expression of E-cadherin as a marker of tumor invasion susceptibility. In this study, MKN-45 cells were treated with 1, 2.5 and 5 mM oxamflatin and followed by MTT assay after 24-48 h of incubation. To determine E-cadherin expression in treated cells, total RNA was extracted and reverse transcribed to complementary DNA, followed by quantitative real-time PCR. MTT results showed that the viability of MKN-45 cells declines with increasing concentrations of oxamflatin. The results of quantitative real-time PCR showed increased expression of E-cadherin following treatment with oxamflatin at the concentration of 2.5 mM compared with 1 mM. The present results showed that oxamflatin can induce E-cadherin expression and also reduce cell viability in the MKN-45 cell line. On the basis of these findings, oxamflatin can be further considered for the prevention of tumor metastasis.