The Inhibitory Effects of Lactobacillus Reuteri’s Cell Wall on Cell Proliferation in the HCT-116 Colorectal Cancer Cell Line

Background: Colorectal cancer (CRC) is the third and a second common cancer in men and women respectively in the world and about 1.4 million new cases diagnosed in 2012. The normal gut microflora consists of bacterial species. One group of them is probiotics, which confer a health benefit to the host. Lactobacillus reuteri (L.reuteri) is known as a probiotic, which lead to the prevention of colorectal cancer. The aim of this study was to assess the inhibitory effects of Lactobacillus reuteri’s cell wall on cell proliferation in the colorectal cancer HCT-116 cell line.Materials and Methods: The cells of HCT-116 cell line were grown at 37ᵒC, 5% CO2. L.reuteri was obtained from the Iranian Biological Resource Center and cultured in the MRS Broth at 37ᵒC for 48h anaerobically. The cell wall was prepared by the freezing-thawing procedure. So the inhibitory effect of L.reuteri on the growth and proliferation of HCT-116 cells was assessed by MTT assay.Results: The cell wall from L.reuteri inhibited cell proliferation on colorectal cancer HCT-116 cell line. It showed dose- and –time dependent inhibition.Conclusion: These results demonstrated that cell wall of L.reuteri inhibits cell proliferation of HCT-116 cell line

Modulation of transforming growth factor-beta signaling transducers in colon adenocarcinoma cells induced by staphylococcal enterotoxin B

Colorectal cancer (CRC) is a notable cause of cancer-associated mortality worldwide, making it a pertinent topic for the study of cancer and its treatment. Staphylococcal enterotoxin B (SEB), an enterotoxin produced by Staphylococcus aureus, has been demonstrated to exert anticancer and antimetastatic effects due to its ability to modify cell immunity and cellular signaling pathways. In the current study, SEB was investigated, including whether it exerts its growth inhibitory effects on colon adenocarcinoma cells. This may occur through the manipulation of a key tumor growth factor, termed transforming growth factor-beta (TGF-beta), and its signaling pathway transducer, Smad2/3. The human colon adenocarcinoma HCT116 cell line was treated with different concentrations of SEB, and cell number was measured using MTT assay at different treatment times. Smad2/3 RNA expression level was analyzed in untreated or SEB-treated cells using quantitative polymerase chain reaction, which indicated significant differences between cell viability and Smad2/3 expression levels. SEB effectively downregulated Smad2/3 expression in the HCT116 cells at concentrations of 1 and 2 mu g/ml (P=0.0021 and P=0.0017, respectively). SEB concentrations that were effective at inhibiting Smad2/3 expression were correlated with those able to inhibit the proliferation of the cancer cells. SEB inhibited Smad2/3 expression at the mRNA level in a concentration- and time-dependent manner. The present study thus proposed SEB as an agent able to significantly reduce Smad2/3 expression in colon cancer cells, provoking moderate TGF-beta growth signaling and the reduction of tumor cell proliferation

Viral Infections in Intensive Care Unit Patients

Background and Aim: Viral infections in the intensive care units (ICUs) often involve the central nervous system or respiratory tract. These infections can cause significant morbidity and mortality. Science the fact that there is effective treatment against some viruses, knowing the viruses that cause infections in ICU can be a great help in managing these patients. Hence, the study reviewed the major viruses in the ICU. Materials and Methods: We searched published articles on trends of viral infections in the intensive care units (ICUs). The articles were retrieved from databases of PubMed, Scopus, Google Scholar, and MEDLINE. Conclusion: Due to the significant outbreak of viruses in the ICU and the presence of effective treatments against some viruses, knowing the important viruses in this area and rapid diagnosing and treatment can be importan

Modulation of transforming growth factor-β signalling transducers in colon adenocarcinoma cells induced by staphylococcal enterotoxin B

Colorectal cancer (CRC) is a notable cause of cancer-associated mortality worldwide, making it a pertinent topic for the study of cancer and its treatment. Staphylococcal enterotoxin B (SEB), an enterotoxin produced by Staphylococcus aureus, has been demonstrated to exert anticancer and antimetastatic effects due to its ability to modify cell immunity and cellular signaling pathways. In the current study, SEB was investigated, including whether it exerts its growth inhibitory effects on colon adenocarcinoma cells. This may occur through the manipulation of a key tumor growth factor, termed transforming growth factor-β (TGF-β), and its signaling pathway transducer, Smad2/3. The human colon adenocarcinoma HCT116 cell line was treated with different concentrations of SEB, and cell number was measured using MTT assay at different treatment times. Smad2/3 RNA expression level was analyzed in untreated or SEB-treated cells using quantitative polymerase chain reaction, which indicated significant differences between cell viability and Smad2/3 expression levels. SEB effectively downregulated Smad2/3 expression in the HCT116 cells at concentrations of 1 and 2 μg/ml (P=0.0021 and P=0.0017, respectively). SEB concentrations that were effective at inhibiting Smad2/3 expression were correlated with those able to inhibit the proliferation of the cancer cells. SEB inhibited Smad2/3 expression at the mRNA level in a concentration- and time-dependent manner. The present study thus proposed SEB as an agent able to significantly reduce Smad2/3 expression in colon cancer cells, provoking moderate TGF-β growth signaling and the reduction of tumor cell proliferation

Cytotoxic Activity of Rosa Damascene Mill, Allium sativum, Allium Hirtifolium Boiss, and Prosopis Farcta Extracts on Human Cervical Carcinoma Cell Line

Background: Cervical cancer is one of the major reasons of cancer-related mortality. Human papillomavirus is the most common sexually transmitted viral infection, which can lead to cervical cancer. There is no powerful chemotherapeutic agent for HPV infection and cervical cancer. Some plants have the proper potential to be used for treatment of cervical cancer caused by HPV type 18.Materials and Methods: In this study, cytotoxic effect of extract of four indigenous Iranian plants including Rosa damascene mill, Allium sativum, Allium hirtifolium boiss and Prosopis farcta were investigated on the HeLa cell line. HeLa cells were incubated with different concentrations of extracts and then the cell viability was measured by MTT assay.Results: The viable cell numbers were decreased by increase of the extracts concentration. The Allium sativum showed the higher cytotoxicity in all concentrations than the other ones. Afterwards, Allium hirtifolium Boiss, Rosa damascene mill, and Prosopis farcta showed maximum efficiency to decrease cell viability, respectively.Conclusion: The above four mentioned plants might be used for death of HeLa cell harboring HPV type 18. Therefore, they could be employed as a chemotherapeutic agent in the cervical cancer treatment in future

Homeodomain protein transforming growth factor beta-induced factor 2 like, X-linked function in colon adenocarcinoma cells

A member of homeodomain protein namely TGIF2LX has been implicated as a tumor suppressor gene in human malignancy as well as in spermatogenesis. However, to our knowledge, dynamic functional evidence of the TGIF2LX has not yet been provided. The aim of the present study was to investigate the human TGIF2LX target gene(s) using a cDNA-AFLP as a differential display method. A pEGFP-TGIF2LX construct containing the wild-type TGIF2LX cDNA was stably transfected into SW48 cells. UV microscopic analysis and Real-time RT-PCR were used to confirm TGIF2LX expression. The mRNA expressions of TGIF2LX in transfected SW48 cells, the cells containing empty vector (pEGFP-N), and untransfected cells were compared. Also, a Real-time PCR technique was applied to validate cDNA-AFLP results. The results revealed a significant down-regulation and up-regulationby TGIF2LX of Nir1 and Nir2 genes, respectively. The genes are engaged in the cell morphogenesis process. Our findings may provide new insight into the complex molecular pathways underlying colorectal cancer development

Transcriptional regulation of E-cadherin and oncoprotein E7 by valproic acid in HPV positive cell lines

Objective(s): Valproic acid (VPA) has proven to be as one of the most promising useful drug with anticancer properties. In this study, we investigate the VPA effects on E-cadherin expression in HeLa, TC1, MKN45, and HCT116 cell lines. This study assesses the effects of VPA on human papillomavirus E7 expression in HPV positive cell lines. Materials and Methods: Cell lines were treated by 2 mmol/l VPA and expression of E-cadherin and E7 was analyzed by quantitative real-time PCR. Student�s t test and ANOVA were used to determine changes in expression levels. Results: The results revealed that mean of E-cadherin expression is increased by VPA 1.8 times in HCT116 and MKN45 cell lines, also the mean of E-cadherin mRNA levels is up-regulated 2.9 times in HeLa and TC1 cell lines. So, E-cadherin augmentation induced by VPA in HeLa and TC-1, HPV positive cell lines, is higher than HPV negative cell lines MKN45 and HCT116. The mean of HPV E7 expression is decreased by VPA, 4.6 times in in HeLa and TC-1 cell lines. Conclusion: This study demonstrates that re-expression of E-cadherin by VPA in HPV positive cell lines is more than HPV negative cell lines. Whereas, HPV E7 reduces the expression of E-cadherin, reduction of HPV E7 expression by VPA is related to more augmentation of E-cadherin in HPV positive cell lines. So, this study demonstrates that VPA has more anticancer properties in HPV positive cell lines, and could potentially be a promising candidate for cervical cancer treatment. © 2016, Mashhad University of Medical Sciences. All rights reserved

Prevalence of Epstein–Barr virus, Human Papillomavirus and Porphyromonas Gingivalis in Oral Cancer

Background: Multiple risk factors are supposed to progress oral cavity carcinoma and among them, the role ofneither bacterial nor viral infections should be underestimated. Despite relentless efforts, the accelerating effectsof human papillomavirus (HPV), Epstein–Barr virus (EBV), and Porphyromonas gingivalis (P. gingivalis) onoral cancer has not yet been recognized successfully. Taking advantage of these facts, in this study we evaluatedthe prevalence of HPV, EBV, and P. gingivalis in oral cavity carcinoma.Materials and Methods: A total of 43 oral cavity cancerous tissues and 29 healthy oral ones were collected fromLoghman Hospital, Tehran, Iran, between 2016 and 2018. After DNA extraction, the prevalence of HPV, EBV,and P. gingivalis was evaluated by PCR.Results: There were 53.5 well-differentiated (15 male, 9 female), 41.8% moderate (10 male, 5 female), and4.7% poor (1 male, 3 female) adenocarcinoma paraffin-embedded tissue samples. PCR analysis has shownthat there were 1 HPV (age: 46; moderate adenocarcinoma) and 1 EBV (age: 62; moderate adenocarcinoma)positive in different samples. No P. gingivalis was found and there was not any infected tissue with both EBVand HPV. In 31% of control tissues, blisters were observed and in 51.7% there was no mucus. We did not findany association between age, sex, and HPV, EBV positive samples.Conclusion: As sample size can affect the results of epidemiological and clinical study, and due to the lownumber of positive samples in this study, we concluded that HPV, EBV, and P. gingivalis may not have adetrimental effect on the progression of oral cancer, but further studies are needed

Low presence of papillomavirus and its lack of correlation with clinicopathological factors in breast cancer: a case control study

Background and Objectives: Breast cancer is currently the most commonly diagnosed neoplasm in women worldwide. There is evidence that human papillomavirus (HPV) infection may play a key role in breast cancer aggressiveness, but results are conflicting across studies. The aim of this study was to investigate the presence of the HPV viral genome in benign and malignant breast tissue samples and its clinicopathological characteristics of cancer. Materials and Methods: In this case-control study, 100 formalin-fixed paraffin-embedded (FFPE) of breast cancer and 100 blocks of non-cancerous breast tissue were selected as a control group from the pathology department of Imam Khomeini Hospital in Ahvaz from 2020-2022. The presence of HPV was detected using nested PCR including MY09/11 primers and sequencing were performed for virus genotyping. Results: The present study enrolled 100 subjects each in two cancer and control groups with a mean age of 52.81±13.23 and 35.77±11.65, respectively. The risk of cancer in HPV-infected patients is almost 5 times higher than in HPV-negative individuals, it is not statistically significant (OR =4.99, 95% CI 0.35 to 72.15, p=0.238). The prevalence of HPV in the cancer and control groups was 7% and 1%, respectively and HPVs detected in two groups were of the HPV 16 genotype. Although the chance of ER and PR expression, lymphvascular involvement, perineural invasion, and higher tumor grade was higher in HPV-positive subjects than in HPV-negative subjects, this was not statistically significant (OR>1, p>0.05). Conclusion: Based on studies reporting the existence of sequences of different high-risk HPV types (oncogenes) in breast cancer tissues, this study confirmed the hypothesis of a possible infectious cause in the development of breast cancer. So far, however, the results have been controversial and inconclusive. Further studies with large sample sizes are needed to demonstrate the link between HPV and breast cancer

Evaluation of antitumor activity of a TGF-beta receptor I inhibitor (SD-208) on human colon adenocarcinoma.

BACKGROUND: Transforming growth factor-β (TGF-β) pathway is involved in primary tumor progression and in promoting metastasis in a considerable proportion of human cancers such as colorectal cancer (CRC). Therefore, blockage of TGF-β pathway signaling via an inhibitor could be a valuable tool in CRC treatment. METHODS: To evaluate the efficacy of systemic targeting of the TGF-β pathway for therapeutic effects on CRC, we investigated the effects of a TGβRI (TGF-β receptor 1) or TβRI kinase inhibitor, SD-208, on SW-48, colon adenocarcinoma cells. In this work, in vitro cell proliferation was studied by methyl thiazolyl tetrazolium (MTT) and bromo-2'-deoxyuridine (BrdU) assays. Also, the histopathological and immunohistochemical evaluations were conducted by hematoxylin and eosin, and Ki-67 and CD34 markers were stained, respectively. RESULTS: Our results showed no significant reduction in cell proliferation and vessel formation (170 ± 70 and 165 ± 70, P > 0.05) in treated SW-48 cells with SD-208 compared to controls. CONCLUSION: Our data suggested that SD-208 could not significantly reduce tumor growth and angiogenesis in human colorectal cancer model at least using SW-48 cells