Background: Hepatocellular carcinoma (HCC) is a common malignant tumor worldwide with a poor prognosis. Amounting studies revealed that long non-coding RNAs (lncRNAs) show important roles in various biological processes. The purpose of this study was to explore the biological
function and potential molecular mechanism of CASC7 in HCC. Methods: CASC7 expression in HCC cell lines was detected by qRT-PCR. The expressions of CASC7 and miR-340-5p were changed by transfection of miR-340-5p mimic, the CASC7 overexpression and knockdown plasmids. The interaction
between CASC7 and miR-340-5p was assessed by a Dual-Luciferase reporter assay. The biological functions of CASC7 were evaluated by CCK-8, colony formation assay, ROS assay kit, immunofluorescence and flow cytometry (FCM). Results: CASC7 was upregulated in HCC cell lines. CASC7 overexpression
significantly promoted cell proliferation, as well as inhibited apoptosis and oxidative stress. In contrast, CASC7 knockdown could reverse these above changes. The result of the Dual-luciferase reporter assay revealed that CASC7 directly targeted miR-340-5p and negatively regulated its expression.
In addition, CASC7 promoted proliferation and inhibited apoptosis of HCC cells through activating Nrf2 pathway by downregulating miR-340-5p. Conclusions: In summary, CASC7 promotes HCC tumorigenesis and progression through the Nrf2 pathway by targeting miR-340-5p, which may provide
a new target for therapy of HCC.
Objective: Our research was to discuss effects and mechanism of lncRNA TUG1 in NSCLC by vitro study. Methods: A549 and H1299 cells were divided into NC, pcDNA 3.1 and lncRNA TUG1 groups. Measuring cell proliferation using CCK-8 assay, cell apoptosis by flow cytometry,
invasion cell number by transwell and wound healing rate by wound healing assay. Relative gene and protein expressions by RT-qPCR and WB assay. Results: Compared with NC group, the cell proliferation rate, invasion cell number and wound healing rate were significantly depressed in A549
and H1299 cell lines (P < 0.001, respectively). By RT-qPCR and WB assay, lncRNA TUG1 gene expression were significantly increased (P < 0.001, respectively); E-cadherin gene and protein expression were significantly up-regulation, and N-cadherin and Vimentin gene and protein
expressions were significantly depressed compared with those of NC group in A549 and H1299 cell lines (P < 0.001, respectively). Conclusion: lncRNA TUG1 had effects to suppress NSCLC cell biological activities by regulation EMT relative gene and proteins expression in vivo
Abstract Persea lingue Ness is a tree species that lives mainly in temperate forests of south-central Chile. Its leaves are used in ethnomedicine, the fruit is a drupe similar to that of the avocado and has not been studied. The aim of this study was to determine the cytotoxicity in leukemia cell and antibacterial activity, along with some chemical content characteristics of P. lingue fruit and leaf extracts. The antibacterial activity was determined by the inhibition of bacterial growth in liquid medium assay against Gram-positive and Gram-negative bacteria. The leukemia cell lines Kasumi-1 and Jurkat were used to evaluate the cytotoxic activity by using propidium iodide and AlamarBlue assays. Total phenolic, flavonoid, condensed tannin, alkaloid and lipid contents were evaluated in the fruit and in the leaf extracts. The antioxidant activity of both extracts were also elavaluated. Leaf extract presented the highest content of total phenols, condensed tannins and flavonoids, and also the highest antioxidant activity. While the fruit extract has a higher amount of lipids and alkaloids and the high antibacterial activity against Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus, Bacillus megaterium and Micrococcus luteus. The leaf extract only showed activity against M. luteus. Concerning the cytotoxic activity, only the fruit extract showed cytotoxicity against the cell lines Jurkat and Kasumi-1. P. lingue fruit extract is a potential source of biologically active molecules for the development of new drugs to be used in some types of leukemia, as well as antibacterial agent.
Abstract Colorectal cancer (CRC) is a disease with high incidence worldwide. As of 2018, it is the second leading cause of cancer deaths in the world. In Saudi Arabia, the incidence of this disease has been increasing in the younger population. Both genetic and lifestyle factors may have contributed to its increased incidence and pathogenesis. Monosodium glutamate (MSG) is a food flavor enhancer that can be found in many commercial foods, and it can sometimes be used as a substitute to table salt. MSG has been investigated for its possible genotoxicity, yielding controversial results. In the present study, the effect of MSG on cell viability and its effect on expression of APC, BECN1, and TP53 genes in SW620 and SW480 colon cancer cell lines were studied. TP53 is a tumor suppressor gene that functions in modifying DNA errors and/or inducing apoptosis of damaged cells, and both APC and BECN1 genes are involved in CRC and are of importance in cellular growth and metastasis. Cancer cell viability was analyzed using MTT assay, and the results showed a significant increase in the number of viable cells after 24 h of treatment with MSG with different concentrations (0.5, 1.0, 10, 50, and 100mM). Moreover, gene expression results showed a significant increase in the expression levels of APC and BECN1 under specified conditions in both cell lines; conversely, TP53 showed a significant decrease in expression in SW620 cells. Thus, it can be concluded that MSG possibly confers a pro-proliferative effect on CRC cells.
High expression of E74-like factor 3 (ELF3) has been reported in type 1 endometrial cancer (EC). Bioinformatics analysis predicted a positive correlation with ELF3 and mucin 1 (MUC1)/hypoxiainducible factor 1α (HIF-1α), a previously identified cancer-promoting
pathway. This study focused on the MUC1/HIF-1α-involved action mechanism of ELF3 in EC. ELF3 expression in EC cell lines was measured by RT-qPCR and western blot analysis. Following the expression of ELF3 was silent, cell proliferation was examined using CCK-8 and colony formation
assay, cell migration and invasion were observed using wound healing and transwell assays. The effect of ELF1 silencing on MUC1/HIF-1α expression was detected by western blot. Rescue experiments incorporating pcDNA3.1(+)/MUC1 explored the interaction between ELF3 and MUC1/HIF-1α
in EC cell proliferation, migration and invasion. ELF3 was found to be expressed at a high level in EC cell lines, and the silencing of it effectively inhibited EC cell proliferation. Moreover, ELF silencing also inhibited the migration and invasion of EC cells. Consistent with the database
prediction, a positive correlation between ELF3 and MUC1/HIF-1α was observed. More importantly, MUC1 overexpression abated the promotive effect of ELF3 silencing on EC cell proliferation, migration and invasion. ELF3 promotes EC cell proliferation, migration and invasion by regulating
MUC1/HIF-1α pathway. Thus, ELF3 as well as MUC1/HIF-1α pathway may be particle targets in the treatment of EC.
The work presented here demonstrates the utility of a two-step algorithm for environmental poliovirus surveillance based on: preselection of sewage samples tested for the presence of enteroviral genetic material-RT-PCR assay and detection of infectious viruses by cell culture technique (L20B for polioviruses and RD for polio and other non-polio enteroviruses). RD and L20B cell lines were tested to determine their sensitivity for isolation of viruses from environmental samples (sewage). Finally, we wanted to determine if sewage concentration affects the results obtained for RT-PCR and cell cultures.