Epithelial-to-mesenchymal transition (EMT) is a complex and dynamic cellular process during which epithelial cells lose their polarity and cell adhesion capabilities and subsequently express mesenchymal stem cell-like phenotype, including increased invasiveness, migration, resistance to programmed cell death, and synthesis of extracellular matrix components. Although several studies to date have demonstrated the intricate signalling pathways and important transcriptional regulators that drive EMT, glycolipids are now emerging as a significant modulator of the EMT transition. Alterations in glycolipid composition activate various growth factor signalling networks, which ultimately promote EMT and facilitate tumor development and metastasis. Despite this, there are still big gaps in our understanding of how glycolipid remodelling changes through time and space in the process of EMT and how these changes impact on the tumor microenvironment. Enzyme inhibitors, monoclonal antibodies, glycolipid-based vaccines, synthetic analogues, CRISPR–Cas9, and CAR-T cell therapies are some of the therapeutic strategies under study that have the potential to disrupt the glycolipid-driven EMT-signalling cascade and hinder tumor progression. Collectively, these therapeutic treatments have emerged as intriguing candidates for inhibiting glycolipid-driven EMT signalling and slowing metastatic invasion. The modified expression profiles of glycolipids may serve as valuable biomarkers for the molecular status of EMT and metastatic potential. Capturing these expression patterns may enable patient stratification, early diagnosis, and the identification of novel therapeutic targets. This review aims on recent progress in the use of glycolipid modulation of EMT. Potential therapeutic implications are also discussed here, to bring a new dimension to the cancer therapy.

Monocyte migration is an important process in inflammation and atherogenesis. Identification of the key signalling pathways that regulate monocyte migration can provide prospective targets for prophylactic treatments in inflammatory diseases. Previous research showed that the focal adhesion kinase Pyk2, Src kinase and MAP kinases play an important role in MCP-1-induced monocyte migration. In this study, we demonstrate that MCP-1 induces iPLA2 activity, which is regulated by PKCβ and affects downstream activation of Rac1 and Pyk2. Rac1 interacts directly with iPLA2 and Pyk2, and plays a crucial role in MCP-1-mediated monocyte migration by modulating downstream Pyk2 and p38 MAPK activation. Furthermore, Rac1 is necessary for cell spreading and F-actin polymerization during monocyte adhesion to fibronectin. Finally, we provide evidence that Rac1 controls the secretion of inflammatory mediator vimentin from MCP-1-stimulated monocytes. Altogether, this study demonstrates that the PKCβ/iPLA2/Rac1/Pyk2/p38 MAPK signalling cascade is essential for MCP-1-induced monocyte adhesion and migration.

Aim: AMPK can be considered as an important target molecule for cancer for its unique ability to directly recognize cellular energy status. The main aim of this study is to explore the role of different AMPK activators in managing cancer cell aggressiveness and to understand the mechanistic details behind the process. Main methods: First, we explored the AMPK expression pattern and its significance in different subtypes of lung cancer by accessing the TCGA data sets for LUNG, LUAD and LUSC patients and then established the correlation between AMPK expression pattern and overall survival of lung cancer patients using Kaplan-Meire plot. We further carried out several cell-based assays by employing different wet lab techniques including RT-PCR, Western Blot, proliferation, migration and invasion assays to fulfil the aim of the study. Key findings: center dot Expression of AMPK is correlated with survival and prognosis of lung cancer patients. center dot AMPK activators like Metformin and Phenformin downregulate A549 and HCT-116 cell proliferation and migration via repression of p38MAPK activity, subsequent augmentation of R1 repressor and corresponding downregulation of MAO-A expression/activity resulting reduction in the intracellular ROS. center dot SRT-1720 directly activates AMPK in LKB1 mutant A549 cells either alone or in combination with Metformin resulting regulation of cancer cell aggressiveness. Significance: This study identifies the importance of AMPK activators as a repurposing agent for combating lung and colon cancer cell aggressiveness. It also suggests SRT-1720 as a potent repurposing agent for cancer treatment especially in NSCLC patients where a point mutation is present in LKB1.

In the quest of recognizing hazardous nitro-aromatic compounds in water, two pyridinefunctionalized Schiff-base chemosensors, DMP ((E)-N-(3,4-dimethoxybenzylidene)(pyridin-2-yl) methanamine)) and MP (4-((E)-((pyridin-2-yl)methylimino)methyl)-2-ethoxyphenol) have been synthesized to detect mutagenic 2,4,6-Trinitrophenol (TNP) in soil, water as well as cellular matrices by producing turn-off emission responses as a combined consequence of PET and RET processes. Several experimental analyses including ESI-MS, FT-IR, photoluminescence, 1H NMR titration, and the theoretical calculations ascertained the formation and sensing efficacies of the chemosensors. The analytical substantiations revealed that structural variation of the chemosensors played a significant role in improving the sensing efficiency, which would certainly be worthwhile in developing small molecular TNP sensors. The present work depicted that the electron density within the MP framework was more than that of DMP due to the intentional incorporation of -OEt and -OH groups. As a result, MP represented a strong interaction mode towards the electron-deficient TNP with a detection limit of 39 mu M.

The objective of the study was to assess the optimum frying condition of fish considering the multiple perspectives (retention of nutritional quality indices [NQI], reduction of preparation time, and improvement of health benefit) to satisfy consumer-preferred sensory attributes by controlling the most impactful process variables (temperature, time, and oil amount). The multi-criteria decision-making (MCDM) approach is appropriate to handle the numerous conflicting criteria and numerous multiple objectives. First, an artificial neural network (ANN) model was developed to build a non-linear correlation between the cooking process parameters and NQI by an automatic exhaustive search of all available algorithms and activation functions. All the NQI are conflicting in nature. Therefore, the ANN-based multi-objective genetic algorithm was implemented to obtain the Pareto optimal solutions to improve all NQI simultaneously. Five optimised conditions were selected amongst the Pareto optimal solutions, satisfying the above-mentioned multiple criteria. Finally, a well-known MCDM approach, the analytical hierarchy process (AHP), was applied for sensory analysis to evaluate the overall acceptance of the optimised conditions based on the relative importance of consumers' general sensory modalities (flavour, colour & appearance, and taste). Furthermore, the following condition (140.01 & DEG;C, 7.62 min, 47.87 ml oil/kg of fish) was selected as the most accepted in terms of all quality attributes that may be implemented as the standard condition in domestic and industrial purposes.

The complex [Pt(AEP)Cl2]; C-1 (where, AEP = 1-(2-Aminoethyl) pyrrolidine) and its hydrolyzed diaqua form cis-[Pt(AEP)(H2O)2]2+; C-2 were synthesized for their bioactivity and in vitro kinetic study with bioactive thiol group (-S-H) containing ligands (like; L-cysteine and N-ac -L-cysteine) for their biological importance for 'drug reservoir' activity. The Thermal Gravimetric Analysis (TGA) was executed to confirm about the weight loss due to coordinated water molecules at high temperature range. At pH 4.0, the substitution behavior of C-2 with the thiols was studied in pseudo-first order reaction condition. The interaction mechanism of thiols with complex C-2 to their corresponding thiol substituted C-3 [Pt(AEP)(L-cys)] and C-4 [Pt(AEP)(N-ac-L-cys)] (where L-cys = L-cysteine and N-ac-L-cys =N-ac -L-cysteine) were proposed from their thermodynamical activation parameters (Delta H/=and Delta S/=), which were obtained from Eyring equation. DNA and BSA binding activity of the complexes C-1 to C-4 were investigated by gel electrophoresis technique, spectroscopic titration and viscosity methods. The binding activity of the complexes with DNA and BSA was evaluated using a theoretical approach molecular docking study. The drug-like nature of the complexes is supported by the prediction of activity spectra for substance (PASS) from 2D structure of the Pt(II) complexes. Structural optimization, HOMO-LUMO energy calculation, Molecular electrostatic potential surface, NBO and TD-DFT calculation were executed by using density functional theory (DFT) with Gaussian 09 software package to pre-assessment of biological activity of the complexes. DFT-based descriptors were determined from the HOMO-LUMA energy to be related with the ability of binding affinity of Pt(II) complexes towards DNA and BSA to the formation of their corresponding adducts. The anticancer property of the design complexes were examined on HCT116 (colorectal carcinoma) cancer cell lines and as well as human normal cell NKE (Normal Kidney Epithelial) and compared with the recognised anticancer drug cisplatin. The Reactive Oxygen Species (ROS) production was assessed by DCFDA assay in presence of the Pt(II) complexes.

A series of pyrrolidine-based Pd(II) complexes, [Pd(AEP)Cl-2] (C-1), [Pd(AEP)(OH2)(2)](2+)(C-2), [Pd(AEP)(L-cys)](+) (C-3), [Pd(AEP)(N-ac-L-cys)](C-4), [Pd(AEP)(GSH)] (C-5), and [Pd(AEP)(DL-meth)](2+) (C-6)(where, AEP = 1-(2-aminoethyl)pyrrolidine, L-cys = l-cysteine,N-ac-L-cys = N-acetyl-l-cysteine, GSH =glutathione, and DL-meth = dl-methionine), as anticancerdrug candidates have been synthesized and characterized. The DNA bindingproperty of the complexes was executed by gel electrophoresis andspectrophotometric and viscometric methods, and their interactionwith BSA was also investigated by various spectroscopic methodologies.The binding activity of the Pd(II) complexes with DNA and BSA wereassessed to evaluate their binding mode and binding constants. Moleculardocking was performed to correlate with the experimental results onthe interaction of the complexes with DNA and BSA. The changes inthe microenvironmental and structural properties of BSA are monitoredby a synchronous and 3D fluorescence study. The structural propertieswere evaluated by DFT and TD-DFT studies. The anticarcinogenic activityof the Pd(II) complexes was assessed by PASS prediction software tocorroborate with the experimental results of the anticancer activityof the complexes. The ROS generation in cancer cell lines has beeninvestigated, and the cell death mechanism through apoptosis was confirmedby measuring the protein expression. All these complexes have excellentanticancer activity compared to ancillary ligands. The cancer cellline (HCT116) shows almost similar or better cell inhibition activitywhen treated with the Pd(II) complexes compared to cisplatin, whereasthe adverse effect is minimum on a normal cell (NKE). Both the Pd(II)and Pt(II) complexes carrying the same ligands reveal almost similarantiproliferative activity.

Colorectal cancer (CRC) is the third most diagnosed and second leading cause of cancer-related death worldwide. Limitations with existing treatment regimens have demanded the search for better treatment options. Different phytochemicals with promising anti-CRC activities have been reported, with the molecular mechanism of actions still emerging. This review aims to summarize recent progress on the study of natural phenolic compounds in ameliorating CRC using in vivo models. This review followed the guidelines of the Preferred Reporting Items for Systematic Reporting and Meta-Analysis. Information on the relevant topic was gathered by searching the PubMed, Scopus, ScienceDirect, and Web of Science databases using keywords, such as “colorectal cancer” AND “phenolic compounds”, “colorectal cancer” AND “polyphenol”, “colorectal cancer” AND “phenolic acids”, “colorectal cancer” AND “flavonoids”, “colorectal cancer” AND “stilbene”, and “colorectal cancer” AND “lignan” from the reputed peer-reviewed journals published over the last 20 years. Publications that incorporated in vivo experimental designs and produced statistically significant results were considered for this review. Many of these polyphenols demonstrate anti-CRC activities by inhibiting key cellular factors. This inhibition has been demonstrated by antiapoptotic effects, antiproliferative effects, or by upregulating factors responsible for cell cycle arrest or cell death in various in vivo CRC models. Numerous studies from independent laboratories have highlighted different plant phenolic compounds for their anti-CRC activities. While promising anti-CRC activity in many of these agents has created interest in this area, in-depth mechanistic and well-designed clinical studies are needed to support the therapeutic use of these compounds for the prevention and treatment of CRC.

Parkinson's disease (PD) is linked to & alpha;-synuclein (aS) aggregation and deposition of amyloid in the substantia nigra region of the brain tissues. In the current investigation we produced two distinct classes of aS oligomer of differed protein conformation, stability and compared their toxic nature to cultured neuronal cells. Lyophilized oligomer (LO) was produced in storage of aS at-20 degrees C for 7 days and it was enriched with loosely hold molten globule like structure with residues having preferences for & alpha;-helical conformational space. The size of the oligomer was 4-5.5 nm under AFM. This kind of oligomer exhibited potential toxicity towards neuronal cell lines and did not transform into compact 8-sheet rich amyloid fiber even after incubation at 37 degrees C for several days. Formation of another type of oligomer was often observed in the lag phase of aS fibrillation that often occurred at an elevated temperature (37 degrees C). This kind of heat induced oligomer (IO) was more hydrophobic and relatively less toxic to neuronal cells compared to lyophilized oligomer (LO). Importantly, initiation of hydrophobic zipping of aS caused the transformation of IO into thermodynamically stable 8-sheet rich amyloid fibril. On the other hand, the presence of molten globule like conformation in LO, rendered greater toxicity to cultured neuronal cells.

This study depicted the effect of IL-13 and 13(S)HpODE (the endogenous product during IL-13 activation) in the process of cancer cell apoptosis. We examined the role of both IL-13 and 13(S)HpODE in mediating apoptotic pathway in three different in vitro cellular models namely A549 lung cancer, HCT116 colorectal cancer and CCF52 GBM cells. Our data showed that IL-13 promotes apoptosis of A549 lung carcinoma cells through the involvement of 15-LO, PPARγ and MAO-A. Our observations demonstrated that IL-13/13(S)HpODE stimulate MAO-A-mediated intracellular ROS production and p53 as well as p21 induction which play a crucial role in IL-13-stimulated A549 cell apoptosis. We further showed that 13(S)HpODE promotes apoptosis of HCT116 and CCF52 cells through the up-regulation of p53 and p21 expression. Our data delineated that IL-13 stimulates p53 and p21 induction which is mediated through 15-LO and MAO-A in A549 cells. In addition, we observed that PPARγ plays a vital role in apoptosis as well as in p53 and p21 expression in A549 cells in the presence of IL-13. We validated our observations in case of an in vivo colon cancer tumorigenic study using syngeneic mice model and demonstrated that 13(S)HpODE significantly reduces solid tumor growth through the activation of apoptosis. These data thus confirmed that IL-13 > 15-LO>13(S)HpODE > PPARγ>MAO-A > ROS > p53>p21 axis has a major contribution in regulating cancer cell apoptosis and further identified 13(S)HpODE as a potential chemo-preventive agent which can improve the efficacy of cancer treatment as a combination compound.

Uniform and healthy seeds of green gram cv. Pratap (SG-1) were treated with two mutagens, gamma rays (physical mutagen) and EMS (chemical mutagen) alone and in combination. The two hundred forty M1 progenies were laid in randomized block design with three replications during Kharif, 2017 to raise M2 generation. Analysis of variance discloses significant differences among the treatments for all the eight characters studied. It was observed that in general, the combination dose, i.e., 200 Gy+0.2% EMS gave superior results in almost all the yield attributing characteristics. High heritability coupled with high genetic advance was recorded for seed yield per plant, which indicates the predominance of additive gene action. Number of pods per plant followed by pod length showed high significant positive correlation with seed yield per plant. The character number of pods per cluster had shown positive correlation with seed yield per plant, but path analysis revealed its negative direct effect on seed yield.

The oxygenation of polyunsaturated fatty acids such as arachidonic and linoleic acid through enzymes like lipoxygenases (LOXs) are common and often leads to the production of various bioactive lipids that are important both in acute inflammation and its resolution and thus in disease progression. Amongst the several isoforms of LOX that are expressed in mammals, 15-lipoxygenase (15-LOX) has shown to be crucial in the context of inflammation. Moreover, being expressed in cells of the immune system, as well as in epithelial cells; the enzyme has been shown to crosstalk with a number of important signalling pathways. Mounting evidences from recent reports suggest that 15-LOX has anti-cancer activities which are dependent or independent of its metabolites, and is executed through several downstream pathways like cGMP, PPAR, p53, p21 and NAG-1. However, it is still unclear whether the up-regulation of 15-LOX is associated with cancer cell apoptosis. Monoamine oxidase A (MAO-A), on the other hand, is a mitochondrial flavoenzyme which is believed to be involved in the pathogenesis of atherosclerosis and inflammation and in many other neurological disorders. MAO-A has also been reported as a potential therapeutic target in different types of cancers like prostate cancer, lung cancer etc. In this review, we discussed about the role of fatty acids and their lipid mediators in cancer cell apoptosis. Here we particularly focused on the contribution of oxidative enzymes like 15-LOX and MAO-A in mediating apoptosis in lung cancer cell after fatty acid induction.

Nutritional quality indices of fish deteriorate drastically during frying. In this study, using Catla catla fish and mustard oil (culinary media), extensive experiments are carried out varying the temperature, time, and oil amount to attain the best nutritional quality indices of fried fish with a tuned combination of cooking parameters. An artificial neural network (ANN) is developed to select the best model to find a nonlinear correlation between the frying conditions and nutritional quality indices. ANN-based metaheuristic optimization methodologies, namely genetic algorithm (GA), differential evolution, firefly optimization, and gray wolf optimization (GWO), are applied to optimize the best cooking conditions. Among these, GWO is most promising for optimizing favorable inputs, practical optimal solutions, and reasonable execution time. As outputs are conflicting, multi-objective genetic algorithm (MOGA) is implemented for their simultaneous optimization with optimum values of process variables for health benefit, reducing frying time, and minimizing the wastage of culinary media. The MOGA successfully improves the omega-3/omega-6 fatty acids, polyunsaturated fatty acids/saturated fatty acids, cis/trans fatty acids ratio, and index of atherogenicity values up to 40.43%, 65.35%, 137%, and 83.84%, respectively, satisfying the multi-objective criteria. Practical applications The conventional frying process of fish is successfully optimized by the developed hybrid "model-optimization" topology that improves the nutrient value of fried fish significantly. The developed neural model automatically searches all available algorithms and activation functions exhaustively to select the best model. All single-objective and multi-objective genetic algorithms integrated with an artificial neural network can attain the optimum successfully for all outputs by a unique tuned cooking condition. Operators can choose the preferred solution among many Pareto optimal combinations as per their needs. Furthermore, this developed, generic topology provides a tool for process modification and optimization of other food process engineering methods.

Asian Sea bass (Lates calcarifer), a popular fish, is cultured and consumed in several countries for its commercial benefits and delectable taste. In this study, the biochemical parameters and fatty acids (FA) composition of Lates calcarifer in raw and fried (with mustard oil) conditions were compared for samples treated under three different ways: fresh, frozen, and sun-dried. From the final outcome, it was observed that after frying the protein content deteriorated significantly for all experimental conditions. Scrutiny of fried sample pointed to an increment in neutral lipid content (4.91%) along with trans FA that may pose a threat to health of the consumers. Contrastingly, after frying the loss of saturated FA to a great extent was countered by the increment of beneficial monounsaturated and polyunsaturated FA (MUFA and PUFA). From the nutritional view point, it was revealed that frying improved the nutritional quality indices (NQI) not only for sun-dried or frozen samples but also for fresh samples nullifying the adverse effect of trans FA because of the presence of low concentration of saturated FA along with high percentage of MUFA and PUFA. However, NQI deteriorated typically after sun-drying and freezing. Principal component analysis (PCA) bi-plot further suggested high positive correlation of fried condition to lipid profile but none of the NQI were significantly affected either on sun-drying or on freezing. From the present study, finally it can be recommended that frying is a suitable method to preserve the nutritional values of L. calcarifer.

Inflammation is a condition through which the body responds to infection or tissue injury. It is typically characterized by the expression of a plethora of genes involved in inflammation, that are regulated by transcription factors, transcriptional co‑regulators, and chromatin remodeling events. Differential mitotically heritable patterns of gene expression without changes in the DNA sequence are essentially controlled by epigenetic regulation. Epigenetic mechanisms, such as histone modifications and DNA methylation have a profound effect on inflammatory gene transcription. Histone protein modifications, which include acetylation and the ubiquitination of lysine residues, the methylation of lysine and arginine, and the phosphorylation of serine have been found to modulate chromatin dynamics, thus altering the levels of gene expression. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) regulate the addition and removal of acetyl groups from lysine residues on histones respectively. Nuclear factor (NF)‑κB, tumor necrosis factor (TNF)‑α and interleukin (IL)‑6 are the pro‑inflammatory genes known to promote inflammatory responses in cells. By contrast, 15‑lipoxygenase‑1 (15‑LOX‑1) and monoamine oxidase‑A (MAO‑A) are the genes that can act against inflammation in certain specific conditions. 15‑LOX‑1, a lipid peroxidative enzyme, is associated with the development of inflammatory disorders, such as atherosclerosis, rheumatoid arthritis, asthma and renal injury. MAO‑A catalyzes degradation of biogenic amines and has been reported to cause oxidative stress, atherosclerosis and neuroinflammation. 15‑LOX‑1 has been shown to be co‑expressed along with MAO‑A, in both primary human monocytes and A549 lung carcinoma cells upon treatment with Th2 cytokines, such as IL‑4 and IL‑13. The present review aimed to discuss the HAT‑ and HDAC‑mediated epigenetic machinery which governs the expression of pro‑inflammatory genes, such as IL‑6, TNF‑α, etc., as well as the expression of anti‑inflammatory genes, such as 15‑LOX‑1 and MAO‑A, responsible for modulating the process of inflammation. On the whole, the present review aims to provide deeper insight into the underlying molecular mechanisms involved in the epigenetic regulation of inflammation, which may have novel implications in designing small molecule inhibitors that target the epigenetic machinery for the effective treatment of a variety of inflammation‑related diseases.

Prostate cancer (PCa) is a major cause of mortality and morbidity in men. Available therapies yield limited outcome. We explored anti-PCa activity in a polyphenol-rich fraction of Bergenia ligulata (PFBL), a plant used in Indian traditional and folk medicine for its anti-inflammatory and antineoplastic properties. PFBL constituted of about fifteen different compounds as per LCMS analysis induced apoptotic death in both androgen-dependent LNCaP and androgen-refractory PC3 and DU145 cells with little effect on NKE and WI38 cells. Further investigation revealed that PFBL mediates its function through upregulating ROS production by enhanced catalytic activity of Monoamine oxidase A (MAO-A). Notably, the differential inactivation of NRF2-antioxidant response pathway by PFBL resulted in death in PC3 versus NKE cells involving GSK-3β activity facilitated by AKT inhibition. PFBL efficiently reduced the PC3-tumor xenograft in NOD-SCID mice alone and in synergy with Paclitaxel. Tumor tissues in PFBL-treated mice showed upregulation of similar mechanism of cell death as observed in isolated PC3 cells i.e., elevation of MAO-A catalytic activity, ROS production accompanied by activation of β-TrCP-GSK-3β axis of NRF2 degradation. Blood counts, liver, and splenocyte sensitivity analyses justified the PFBL safety in the healthy mice. To our knowledge this is the first report of an activity that crippled NRF2 activation both in vitro and in vivo in response to MAO-A activation. Results of this study suggest the development of a novel treatment protocol utilizing PFBL to improve therapeutic outcome for patients with aggressive PCa which claims hundreds of thousands of lives each year.

MCP-1-induced monocyte chemotaxis is a crucial event in inflammation and atherogenesis. Identifying the important signal transduction pathways that control monocyte chemotaxis can unravel potential targets for preventive therapies in inflammatory disease conditions. Previous studies have shown that the focal adhesion kinase Pyk2 plays a critical role in monocyte motility. In this study, we investigated the MCP-1-mediated activation of Pyk2 (particularly by the phosphorylation of Tyr402) in primary human peripheral blood monocytes. We showed that MCP-1 induces Src phosphorylation in a similar time frame and that the MCP-1-induced Pyk2 tyrosine phosphorylation is controlled by the Src family kinase. We also report, in this study, that PKCβ, an isoform of PKC, is required for both Src and Pyk2 activation/phosphorylation in response to MCP-1 stimulation. We identified Lyn as the specific Src kinase isoform that is activated by MCP-1 and acts upstream of Pyk2 in primary monocytes. Furthermore, Lyn is found to be indispensable for monocyte migration in response to MCP-1 stimulation. Moreover, our coimmunoprecipitation studies in monocytes revealed that PKCβ, Pyk2, and Lyn exist constitutively in a molecular complex. To our knowledge, our study has uncovered a novel PKCβ-Lyn-Pyk2 signaling cascade in primary monocytes that regulates MCP-1-induced monocyte adhesion and migration.

Monoamine oxidase-A (MAO-A), a pro-oxidative enzyme catalyzes the oxidative deamination of endogenous and exogenous monoamines/neurotransmitters like dopamine, serotonin, norepinephrine or tyramine and converting them into their corresponding aldehydes and reactive oxygen species (ROS). Hyperactivity of MAO-A has been shown to be involved in depression, neuro-degeneration including Parkinson’s and Alzheimer’s diseases, neuropsychiatric disorders and cardiovascular diseases. Our recent results however demonstrated the involvement of MAO-A in promoting aggressiveness of lung carcinoma. We found both constitutive and inducible expression of MAO-A in non-small cell lung cancer cells H1299 and in A549 lung epithelial carcinoma cells. By using knockout (by CRISPR-Cas9 gene editing technology) or knockdown (using MAO-A specific esiRNA) MAO-A cells we demonstrated the role of MAO-A in promoting lung cancer aggressiveness and epithelial to mesenchymal transition (EMT). From our observations, we can conclude that MAO-A may be considered as a potential therapeutic target for the intervention and treatment of lung carcinoma.