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An all-inclusive writeup on calcium supplements and also ferrous ions chelating peptides: Planning, composition along with transport paths.
Purpose Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths in the United States, accounting for 85% of all diagnosed lung cancers and resulting in over 100,000 deaths per year. The main purpose of the current study was to investigate the antiproliferative effects of ethanolic extract of Artemisia maritima in three human lung cancer cell lines along with studying the effects of the herbal extract on cellular apoptosis, G2/M cell cycle arrest and cell migration. Methods The CCK-8 assay was used to determine cell viability. Apoptosis was detected by using acridine orange (AO)/ethidium bromide (EB) staining, annexin V/propidium iodide (PI) assay and western blot. The cell migration was determined by wound healing assay while the effects on cell cycle were evaluated by flow cytometry. Results The results showed that herbal extract of Artemisia maritima decreased the viability of all three cell lines H1299, NCI-H1437, PC-14 dose-dependently with maximum effect on NCI-H1437 cell line. The antiproliferative effects were due to the activation of mitochondrial-dependent apoptotic pathway as seen by fluorescence microscopy which showed chromatin condensation and nuclear fragmentation. This was also associated with increase in Bax and decrease in Bcl-2 levels. Artemisia maritima extract treatment also led to G2/M phase cell cycle arrest along with strong inhibition of cell migration. Conclusions In conclusion, the results of the current study clearly indicate that Artemisia maritima extract exhibits antiproliferative effects in Nonsmall cell lung cancer cells by triggering apoptosis, cell cycle arrest and inhibition of cell migration.Purpose Accounting for significant human morbidity and mortality across the globe, lung cancer is the most prevalent type of cancer as far as incidence and mortality is concerned. MicroRNAs (miRs) have shown an amazing potential to act as therapeutic agents for the management of several human diseases. This study investigated the function of miR-16 in lung cancer. Methods The normal lung cancer cell line MRC3 and lung cancer cell lines SK-MES-1, A549, MS-53 and SK-LU-1 were used in the present study. The qRT-PCR was used for expression profiling of miR-16 and yes associated protein 1 (YAP1). WST-1 assay was used to monitor the proliferation rate. Flow cytometry was used for cell cycle analysis. Apoptosis was examined by DAPI and annexin V/propidium iodide (PI) staining. TargetScan analysis was performed to identify the potential target of miR-16 and western blot analysis was done to estimate the protein expression. Results The gene expression analysis showed miR-16 to be suppressed in lung cancer tissues and cell lines. Overexpression of miR-16 inhibited the growth and metastasis of the DMS-53 lung cancer cells via induction of the apoptotic cell death. Bioinformatic approaches revealed miR-16 exerts its effects by targeting YAP1. YAPI expression was found elevated in lung cancer tissues and its silencing halted the growth of the DMS-53 lung cancer cells. Nonetheless, YAP1 overexpression could reverse the growth inhibitory effects of miR-16. Conclusion Taken together, miR-16 may serve as novel therapeutic target for the treatment of lung cancer.Purpose The main purpose of the current research work was to investigate the anticancer activity of norartocarpetin - a plant derived isoflavone -in human lung carcinoma cells NCI-H460 and normal lung cell line MRC-9 along with studying its effects on cellular apoptosis, DNA damage, cell migration and invasion and Ras/Raf/MAPK signalling pathways. Methods Cell proliferation was examined by CCK-8 assay while effects on apoptosis were evaluated by acridine orange (AO)/ethidium bormide (EB) staining and Comet assay using fluorescence microscopy. In vitro wound healing assay was used for checking the effects on cell migration and transwell assay for invasion while western blot was used to evaluate the effects on the expression of Ras/Raf/MAPK proteins. Results The results showed that Norartocarpetin led to dose-dependent cytotoxic effects in NCI-H460 cells showing an IC50 value of 22 μM while in normal lung cells, the cytotoxic effects were much lower as shown by higher IC50 value of 85 μM. It also led to dose-dependent apoptosis and induced DNA damage as shown by fluorescence microscopy. This molecule also inhibited cell migration and invasion dose-dependently, along with inhibiting MMP-9 expression. Norartocarpetin treatment also led to inhibition of the expression of Ras/Raf/MAPK proteins and also caused S-phase cell cycle arrest in these cells. Conclusion Norartocarpetin has a significant anticancer activity in lung carcinoma cells and these effects are mediated via targeting apoptosis, DNA damage, cell migration and invasion, cell cycle and inhibiting Ras/Raf/MAPK signalling pathways.Purpose The EGFR (Epidermal Growth Factor Receptor) mutations may predict sensitivity and resistance to EGFR-TKIs (Tyrosine Kinases Inhibitors) in metastatic lung adenocarcinoma. The detection of these mutations is usually performed on tumor tissue samples. However, when a biopsy is not feasible or the amount of tissue is limited, circulating tumor DNA (ctDNA) may represent an alternative source for genotyping the tumor. Methods In the first phase of the study, the liquid biopsy was performed in newly diagnosed metastatic lung adenocarcinoma patients with and without EGFR mutations to evaluate the concordance between EGFR mutational analysis on ctDNA by real time PCR and on tissue. In the second phase it was performed in EGFR positive patients progressing after first or second generation TKIs in order to detect the T790M mutation. Results In the first phase, a 100% concordance between EGFR on ctDNA and tissue was revealed, leading to validation of the test. In the second phase, 44.8% of patients showed T790M positive result at liquid biopsy. Considering the re-biopsies performed in 31% of the cases, the overall positivity rate of T790M was 58.6%. Sensitivity and specificity were 76% and 75%, respectively. The median time to development of T790M mutation from the start of first line EGFR TKI was 244 days. Conclusions Our experience confirms that liquid biopsy is a valid method to detect sensitizing and resistant EGFR mutations in patients with metastatic lung adenocarcinoma. Nevertheless, in the presence of negative ctDNA analysis, a rebiopsy should be performed whenever possible to confirm this result.Purpose We compared the safety and efficacy of two hypofractionated irradiation schedules for elderly and low performance status patients with inoperable symptomatic non-small cell lung cancer (NSCLC). Methods Patients that entered the study were either unfit or without response concerning chemotherapy. We randomized 14 patients (group A) vs 15 patients (group B) who underwent two different hypofractionated radiotherapy schedules. Group Α patients underwent a scheme of 13x3 Gy, while group B patients received 2x8.5 Gy and one fraction of 6 Gy one week apart. Efficacy was assessed in terms of disease-free survival (DFS), tumor response and overall survival (OS).Toxicity according to RTOG/EORTC criteria and duration of symptoms were also evaluated. Results Median follow up was 3 years. Median age was 64.5 years (group A) and 73 years (group B). Mean values for symptom palliation were higher for group B vs group A (3.20±1.21 vs 2.21±0.97, p=0.037), respectively. EORTC/RTOG toxicity was significantly higher (p=0.046) for group A (1.57±0.51) vs group B (1.13±0.35). this website Duration of toxicity was significantly lower in group B compared to group A (p=0.001). Median OS was similar between groups, while DFS was better in group B than group A (p=0.023). Conclusions Although safe conclusions are difficult to be ascertained, hypofractionated schedule B might be an alternative scheme in elderly and low performance status patients offering adequate palliation, good tumor control and acceptable toxicity.Purpose The current study was set with a purpose to assess the regulatory role of micro RNA (miR)-138 in human lung cancer cells with emphasis on the underlying mechanism of action. Methods RT-PCR based analysis was employed for gene expression studies. MTT assay was used to determine the proliferation rates of lung cancer cells. Colony forming assay was performed for the analysis of colony forming potential. DAPI and Annexin V-FITC/propidium iodide (PI) double staining methods were performed for the analysis of apoptosis. Migration and invasion of cancer cells were assessed using wound healing and transwell assays, respectively. Dual luciferase reporter assay was performed for interactional study. Western blotting was used to determine the protein concentrations. Results Cancer cells had lower levels of miR-138 transcripts. The overexpression of miR-138 reduced the proliferation of cancer cells and cells were seen to form lower number of viable colonies. This was due to the induction of cancer cell apoptosis under miR-138 overexpression. miR-138 also inhibited the metastasis of lung cancer cells. miR-138 was found to interact with SOX4 intracellularly and SOX4 protein levels decreased under miR-138. The anticancer effects of miR-138 were shown to be modulated through SOX4. Conclusion MiRs have a potential to act as molecular markers in cancer prognosis. There is a need to screen for miRs specific to particular types of cancer and to look for their potential to function as anticancer entities at molecular level.Purpose To explore the effect of aquaporin-3 (AQP3) on the functions of lung cancer stem cells (LCSCs), and its molecular mechanism in regulating the differentiation and apoptosis of LCSCs through the Wnt/glycogen synthase kinase-3β (GSK-3β)/β-catenin pathway. Methods The stem cells were selected and the cell lines with low expression of AQP3 were constructed, followed by transcriptome sequencing. LCSCs were transfected with empty lentivirus in control group and transfected with AQP3 shRNA in interference group, and the low expression of AQP3 was inhibited using the Wnt pathway inhibitor XAV939 in interference + inhibitor group. The expressions of AQP3, Wnt/GSK-3β/β-catenin pathway genes, stemness genes, differentiation-related markers and apoptosis proteins in LCSCs were detected. Results In interference group, the pathway genes were highly expressed. The genes in interference group were enriched in the Wnt/GSK-3β/β-catenin pathway. In interference group, the expressions of β-catenin, GSK-3β and signal transducer and activator of transcription 3 (STAT3) were significantly higher, while the expression of adenomatous polyposis coli (APC) was significantly lower (p less then 0.05). The expression of Wnt5α had no difference. In interference group, the expressions of stemness-related genes were obviously higher, while the expression of CDK2 had no difference (p=0.471). Interference group had higher expressions of differentiation markers. Conclusion In conclusion, AQP3 can reduce the differentiation and inhibit the apoptosis of LCSCs through reducing the expressions of Wnt/GSK-3β/β-catenin pathway-related genes such as β-catenin, GSK-3β and STAT3, thereby affecting the tumor progression.
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