Daniela Catanzaro's scientific contributionswhile working at University of Padova (Padova, Italy) and other institutions

Publications (10)

Publications citing this author (65)

    • Similarly, Quer elicited a spectacular extent of G2/M phase cell cycle arrest in HepG2 tumor cell line [70]. The reduction of cyclin D1 level that could be linked to the G1/S phase alteration has been found in Quer-treated human ovarian carcinoma and osteosarcoma cell lines [53]. Furthermore, results also demonstrated that Quer suppressed the viability of HeLa cells by inducing G2/M phase cell cycle arrest and mitochondrial apoptosis through a p53- dependent mechanism [71].
    [Show abstract] [Hide abstract] ABSTRACT: Despite extensive efforts done in the recent decades, cancer has still remained an incurable disorder. On the other hand, there is no doubt that different natural compounds possess a huge potential to suppress the promotion and progression of tumorigenesis, and numerous studies have described the possible molecular mechanisms of such substances. Probably one of the most efficient ways to hinder the multiplication of cancer cells is to arrest their cell cycle progression. Therefore, in the current article, a detailed review is presented about the arrest of cell cycle in different phases followed by exposure of cancer cells to two natural dietary agents, quercetin, and ursolic acid. Both these compounds have previously been shown to exert anticancer properties, whereas pleiotropic action mechanisms were proposed. The current work describes a variety of molecules occupied in regulation of cell cycle progression and transition between different phases initiated by treatment of cancer cells with the respective flavonoid and triterpenoid. It is clear that better knowledge about the processes and molecules involved in cell cycle, as well as possibilities to modulate such mechanisms by natural compounds, may lead to the development of more efficient and targeted chemopreventive and chemotherapeutic strategies in the future.
    Full-text · Article · Oct 2016 · Oxidative medicine and cellular longevity
    • Discussion Galluzzi et al. previously reported that cisplatin increases intracellular ROS levels [6]. Tumor drug resistance is closely related to their antioxidant capacity [12, 31], and the antioxidant capacity of tumor cells is also closely related to their metabolism. Early studies reported that CC cells from the liver had primary cisplatin resistance [2, 3] .
    [Show abstract] [Hide abstract] ABSTRACT: The tumor cells have some metabolic characteristics of the original tissues, and the metabolism of the tumor cells is closely related to autophagy. However, the mechanism of autophagy and metabolism in chemotherapeutic drug resistance is still poorly understood. In this study, we investigated the role and mechanism of autophagy and glucose metabolism in chemotherapeutic drug resistance by using cholangiocarcinoma QBC939 cells with primary cisplatin resistance and hepatocellular carcinoma HepG2 cells. We found that QBC939 cells with cisplatin resistance had a higher capacity for glucose uptake, consumption, and lactic acid generation, and higher activity of the pentose phosphate pathway compared with HepG2 cells, and the activity of PPP was further increased after cisplatin treatment in QBC939 cells. It is suggested that there are some differences in the metabolism of glucose in hepatocellular carcinoma and cholangiocarcinoma cells, and the activation of PPP pathway may be related to the drug resistance. Through the detection of autophagy substrates p62 and LC3, found that QBC939 cells have a higher flow of autophagy, autophagy inhibitor chloroquine can significantly increase the sensitivity of cisplatin in cholangiocarcinoma cells compared with hepatocellular carcinoma HepG2 cells. The mechanism may be related to the inhibition of QBC939 cells with higher activity of the PPP, the key enzyme G6PDH, which reduces the antioxidant capacity of cells and increases intracellular ROS, especially mitochondrial ROS. Therefore, we hypothesized that autophagy and the oxidative stress resistance mediated by glucose metabolism may be one of the causes of cisplatin resistance in cholangiocarcinoma cells. It is suggested that according to the metabolism characteristics of tumor cells, inhibition of autophagy lysosome pathway with chloroquine may be a new route for therapeutic agents against cholangiocarcinoma.
    Full-text · Article · Mar 2017
    • In all the individuals described in this report it is striking that despite the mitochondrial defect being homoplasmic and present in all tissues clinical disease was restricted to the kidney , although we acknowledge that other organs may be affected at a subclinical level. This situation is similar to the organ specific effect of mutations in mt tRNA Ile , which primarily cause hypertrophic cardiomyopathy [20][21] and of mutations in NADH dehydrogenase causing Leber's hereditary optic neuropathy [22] . Taken together, the contrasting effects of these mutations should offer a powerful route to understanding how mitochondrial defects cause disease in different tissues.
    [Show abstract] [Hide abstract] ABSTRACT: Author summary Mitochondria provide the cell’s energy through respiration, using glucose and oxygen to produce ATP. Critical components for this process are encoded by maternally inherited mitochondrial DNA. Mutations in mitochondrial DNA usually affect organs that use energy intensively, notably the brain, eyes and muscles. Here we have discovered a variant in the promoter region of mitochondrial DNA in a large family with kidney disease and normal function in other organs. We show that patient-derived mitochondria do not generate energy normally and have reduced promoter activity, leading to loss of mitochondrial gene expression. We also identify similar mutations that might provide a mechanism for other cases of unexplained inherited kidney disease: two families with reduced cellular respiration carry mutations affecting mitochondrial phenylalanine tRNA, normally required for mitochondrial protein translation. Together, this study provides the first example of a disease-causing mutation in the mitochondrial promoter, and also establishes that the kidney is particularly sensitive to different mutations in mitochondrial DNA. As these can arise from a mutation in the promoter region of mitochondrial DNA or in the tRNA itself, and both reduce the amount of mitochondrial phenylalanine tRNA, this may provide a potential unifying mechanism for mitochondrially inherited kidney disease.
    Full-text · Article · Mar 2017
    • Growing evidence from epidemiological studies suggests a positive association between reduction in the incidence diabetes and the consumption of a diet rich in phenols [128]. Several biological beneficial properties have been documented for dietary phenols including antioxidant [129], anti-allergic [130], anti-viral [131], anti-microbial [132], anti-proliferative [133], anti-carcinogenic [134], free radical scavenging [135] and regulation of cell cycle arrest [136]. Phenol-rich foods increase plasma antioxidant capacity, and this incidence may be explained by acceptance of electron from reactive oxygen species (ROS), thus forming relatively stable phenoxyl radicals (Clifford).
    [Show abstract] [Hide abstract] ABSTRACT: Diabetes is a metabolic, endocrine disorder which is characterized by hyperglycemia and glucose intolerance due to insulin resistance. Extensive research has confirmed that inflammation is closely involved in the pathogenesis of diabetes and its complications. Patients with diabetes display typical features of an inflammatory process characterized by the presence of cytokines, immune cell infiltration, impaired function and tissue destruction. Numerous anti-diabetic drugs are often prescribed to diabetic patients, to reduce the risk of diabetes through modulation of inflammation. However, those anti-diabetic drugs are often not successful as a result of side effects; therefore, researchers are searching for efficient natural therapeutic targets with less or no side effects. Natural products’ derived bioactive molecules have been proven to improve insulin resistance and associated complications through suppression of inflammatory signaling pathways. In this review article, we described the extraction, isolation and identification of bioactive compounds and its molecular mechanisms in the prevention of diabetes associated complications.
    Full-text · Article · Aug 2016
    • The results of our lymphocyte proliferation assay showed that the BS extracts exerted a significant stimulatory effect on B+ cell proliferation, possibly mediated by an enhanced number of Th17 + cells. Many authors have demonstrated that B. serrata extracts turn out to be effective in the treatment of diseases such as inflammatory bowel disease and osteoarthritis in which inflammation and/or oxidative stress exert an important pathogenic role [2, 13, 30, 46]. However, BS extracts also exerted beneficial effects in some autoimmune diseases, such as rheumatoid arthritis [1], where chronic inflammation and an aberrant autoimmune response are hallmarks of the disease [47].
    [Show abstract] [Hide abstract] ABSTRACT: Boswellia serrata (BS) is an important traditional medicinal plant that currently represents an interesting topic for pharmaceutical research since it possesses several pharmacological properties (e.g., anti-inflammatory, antimicrobial, and antitumour). The safety and versatility of this dietary supplement should allow for its use in numerous pathological conditions; however the quality of the extracts needs to be standardized to increase the clinical success rate resulting from its use. In the present study, different commercially available B. serrata extracts were employed to compare their AKBA content and in vitro antioxidant power. Furthermore, their ability to modulate the immune system regulatory properties was investigated. Our results showed that the AKBA content varied from 3.83±0.10 to 0.03±0.004 %, with one sample in which it was not detectable. The highest antioxidant power and phenolic content were shown by the same extract, which also exhibited the highest AKBA concentration. Finally, the BS extracts showed the ability to influence the regulatory and effector T-cell compartments. Our results suggest that frankincense should be further investigated for its promising potentiality to modulate not only inflammation/oxidative stress but also immune dysregulation, but attention should be paid to the composition of the commercial extracts.
    Full-text · Article · Jan 2017