Evaluation of anti-epithelial-mesenchymal transition property of Garcinia mangostana rind extract

Background Epithelial-mesenchymal transition (EMT) helps solid tumors to lose their intercellular adhesive property and drives metastasis. As mangosteen fruit is known for many beneficial effects including antimicrobial, antioxidant, and anti-tumorigenic properties and has been used widely in traditional medicine, we interrogated its possible anti-metastatic effect on MCF-7 breast cancer cells. Results We found that aqueous mangosteen rind extract (MRE) inhibited growth of MCF-7 and altered the transcript levels of ERα, ERβ, and EGFR genes. Additionally, the MRE changed the expression of important markers of EMT, E-Cadherin, N-Cadherin, Snail, and MMP-9. Moreover, MRE inhibited migration of MCF-7 cells. Conclusion The results suggest that MRE suppresses growth and inhibits epithelial-mesenchymal transition in MCF-7 cells.

Role of CRISPR/Cas9 in Genetic Manipulation of ROS1 and EGFR Genes using Synthego Platform

Mutations and fusions in kinase enzymes are often observed in cancer prognosis. The growth and survival of tumor cells depend on the activation of kinase enzymes which when activated unrestrained can lead to the uncontrolled division of malignant lung cells. Thus, their inhibition is viewed as a promising and effective anti-cancer therapy. ROS1 and EGFR are two tyrosine kinases that have been explored as the genes responsible for Non-Small Cell Lung Cancer (NSCLC). By interrupting the unchecked division of these genes, the development of malignant lung cancer cells can be blocked. The results show 4 of the top-line RNAs for altering the gene quality as well as the target sequences relevant to cleavage by that gRNA, 4 for each gene. We propose a genetic approach of controlling the ROS1 and EGFR genes guided by CRISPR/Cas-9 to guarantee fewer symptoms and an increasingly powerful treatment, by the use of computational tools.

Surveying the Expression of CDH1 and EGFR Genes in Patients with Anthracosis and Its Relationship with Lung Carcinoma

Introduction: Anthracosis is known as the black lung disease and studies have shown relationships between the disease and lung carcinoma. In addition, the expression of CDH1 and EGFR genes can be used as the prognostic of anthracosis. The present study surveys the expression of CDH1 and EGFR genes in anthracosis patients and its relationship with non-small cells lung carcinoma. Methodology: Thirty anthracosis patients diagnosed by a specialist participated in the study. The subjects were asked to sign an informed letter of consent and then, to examine the expression of CDH1 and EGFR genes through real-time PCR, tissue samples were collected. Afterward, the relationship of expression of the biomarkers with tumor staging and cancer progress was examined. Results: Mean age of the patients was 48±10.5 years. As the reference gene, 18sRNA was adopted and comparison of mean CTs at the center and edges of lesions showed no significant difference. As to CDH1 gene at the center of lesions, 12 cases out of 30 were positive, which indicates 40% sensitivity; while at the edges, 20 cases out 30 were positive. Comparison of the positive rates of CDH1 gene at the center and edges of the lesions indicated a significant difference (P-value<0.001). Moreover and with regard to EGFR gene at the center of lesions, 19 cases out 30 were positive (sensitivity = 63.3%) and five cases out of 30 were positive at the edges of lesions (control). There was also a significant difference between the positive cases of EGFR gene at the center and edges of the lesions (P-value<0.001). Clearly, the positive cases of CDH1 at the edges were higher than that at the center, while in the case of EGFR gene, positive cases at the center were higher than that at the edges. It is notable that to obtan results with higher accuracy entails increasing the sensitivity level. Following similar studies and to have higher accuracy, the experiments were carried out with three iterations. Conclusion: In general, the results indicated a sort of relationship between anthracosis and lung carcinoma. To prove such relationship on a more solid ground, more studies with larger number of subjects are needed.

329 Primary and Secondary Glioblastomas are Driven by Distinct Forms of Fusion Oncoproteins

INTRODUCTION The role of chromosomal rearrangement in neoplastic transformation has been well-studied in number of cancers. However, the area remains under-studied in high-grade gliomas. METHODS We performed RNA-seq of 272 gliomas, identifying 214 fusion transcripts. Additional review of the literature identified an additional 772 fusion transcripts in the published literature. Analysis was performed pertaining to rearrangement hot-spots and recurrent fusion transcripts. RESULTS >The most common form of fusion transcript arose from joining of sequences from the same chromosome (76%) rather than sequences from difference chromosomes. Frequency of fusion transcript increased with advanced tumor grade. More fusion transcripts are found in the classical subtype of glioblastoma (P = 0.012), particularly in tumors with amplification of EGFR. Fusion transcripts were most commonly mapped to chromosomes 7 and 12, suggesting these chromosomes contain hots-spots for chromosomal rearrangement. For primary glioblastomas, the most prevalent fusion transcripts involved 1) segments of the EGFR sequence fused to other segments of EGFR or to sequences derived from non-EGFR genes (5.6%) or 2) fusion between FGFR and TACC (FGFR3-TACC3 (3.8%) and FGFR1-TACC1 (0.5%)). PTPRZ1-MET fusions are unique in that they are predominantly found in secondary glioblastomas. All three classes of the encoded fusion proteins have been shown to modulate aspects of glioblastoma biology, including tumorigenesis and invasion. CONCLUSION While ∼50% of glioblastoma harbor fusion transcripts, the occurrence of “driver” fusion transcripts is a relative rarity (<5%). Primary and secondary glioblastomas harbor distinct forms of “driver” fusion transcripts.