Chitosan-encapsulated naringenin promotes ROS mediated through the activation of executioner caspase-3.

We previously reported that chitosan nanoparticle-encapsulated Naringenin (CS-NPs/NAR) could scavenge free radicals at lower doses and be cytotoxic to cancer cells. The current study continues to focus on the mechanism behind CS-NPs/NAR-induced breast cancer cell (MDA-MB-231) death. MDA-MB-231 cells were treated with higher concentrations (100, 200, and 200 µg) of Chitosan nanoparticles (CS-NPs), naringenin (NAR), and chitosan-encapsulated naringenin (CS-NPs/NAR). The cell viability, proliferation, and oxidative stress parameters, such as nitric oxide [NO], xanthine oxidase (XOD), and xanthine dehydrogenase (XDH) levels, were analyzed. ROS levels were determined through DCFDA analysis. MTT-based cell cytotoxicity and BrdU cell proliferation analysis depicted the cytotoxicity effects (37% and 29% for 24 and 48 h) and exhibited a reduction in the proliferation of MDA-MB-231 by CS-NPs/NAR. A significant increase in NO content, XOD, a decrease in XDH, and an increase in ROS levels were observed upon treatment with CS-NPs/NAR. Fluorescent images suggested the increase in the ROS level upon treatment with CS-NPs/NAR in cancer cells, and the results suggested that it could induce apoptosis. Further, to confirm this, the activity of caspase-3 was analyzed through western blotting, and the result suggested that the higher concentration of CS-NPs/NAR has increased the activation of procaspase3 when compared to free NAR. Hence, the current investigation concludes that high doses of CS-NPs/NAR induce and increase oxidative stress and so increased activation of procaspase3 may lead to cancer cell apoptosis and reduction in cell proliferation.

Long non-coding RNAs: an overview on miRNA sponging and its co-regulation in lung cancer.

Lung cancer is the most devastating cause of death among all cancers worldwide, and non-small cell lung cancer (NSCLC) accounts for 80% of all the lung cancer cases. Beyond common genetic research and epigenomic studies, the extraordinary investigations of non-coding RNAs have provided insights into the molecular basis of cancer. Existing evidence from various cancer models highlights that the regulation of non-coding RNAs is crucial and that their deregulation may be a common reason for the development and progression of cancer, and competition of cancer therapeutics. Non-coding RNAs, such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are increasingly recognized as potential cancer biomarkers for early detection and application of therapeutic strategies. The miRNAs have gained importance as master regulators of target mRNAs by negatively regulating their expression. The lncRNAs function as both tumor suppressors and oncogenes, and also compete with miRNAs that influence the translational inhibition processes. This review addresses the role of lncRNAs in lung cancer development, highlights their mechanisms of action, and provides an overview of the impact of lncRNAs on lung cancer survival and progression via miRNA sponging. The improved understanding of lung cancer mechanisms has opened opportunities to analyze molecular markers and their potential therapeutics.

Long noncoding RNAs: role and contribution in pancreatic cancer.

Noncoding RNAs are proclaimed to be expressed in various cancer types and one such type is found to be pancreatic ductal adenocarcinoma (PDAC). The long noncoding RNAs (LncRNAs) affect the migration, invasion, and growth of tumor cells by playing important roles in the process of epigenesis, post-transcription, and transcriptional regulation along with the maintenance of apoptosis and cell cycle. It is quite subtle whether the alterations in lncRNAs would impact PDAC progression and development. This review throws a spotlight on the lncRNAs associated with tumor functions: MALAT-1, HOTAIR, HOXA13, H19, LINC01559, LINC00460, SNHG14, SNHG16, DLX6-AS1, MSC-AS1, ABHD11-AS1, DUXAP8, DANCR, XIST, DLEU2, etc. are upregulated lncRNAs whereas GAS5, HMlincRNA717, MIAT, LINC01111, lncRNA KCNK15-AS1, etc. are downregulated lncRNAs inhibiting the invasion and progression of PDAC. These data provided helps in the assessment of lncRNAs in the development, metastasis, and occurrence of PDAC and also play a vital role in the evolution of biomarkers and therapeutic agents for the treatment of PDAC.