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Alien plants were first recorded in 1937 in the 2 million ha Kruger National Park (KNP, a savanna protected area in South Africa), and attempts to control them began in the mid-1950s. The invasive alien plant control program expanded substantially in the late 1990s, but its overall efficacy has not been determined. We present an assessment of invasive alien plant control operations over several decades in KNP. We based our assessment on available information from a range of control programs funded from various sources, including national public works programs, KNP operational funds, and foreign donor funds. Over ZAR 350 million (~ US$ 27 million) has been spent on control interventions between 1997 and 2016. We found evidence of good progress with the control of several species, notably Opuntia stricta, Sesbania punicea, Lantana camara and several aquatic weeds, often because of effective biological control. On the other hand, we found that over one third (40%) of the funding was spent on species that have subsequently been recognised as being of lower priority, most of which were alien annual weeds. The allocation of funds to non-priority species was sometimes driven by the need to meet additional objectives (such as employment creation), or by perceptions about relative impact in the absence of documented evidence. We also found that management goals were limited to inputs (funds disbursed, employment created, and area treated) rather than to ecological outcomes, and progress was consequently not adequately monitored. At a species level, four out of 36 species were considered to be under complete control, and a further five were under substantial control. Attempts to control five annual species were all considered to be ineffective. On the basis of our findings, we recommend that more studies be done to determine impacts associated with individual invasive alien species; that the criteria used to prioritise invasive alien species be documented based on such assessments, so that management can justify a focus on priority species; and that funding be re-directed to those species that clearly pose greater threats, and for which other solutions (such as biological control) are not an option.
Preeclampsia (PE) remains a leading cause of maternal and perinatal mortality and morbidity worldwide. Its pathogenesis has not been fully elucidated and no causal therapy is currently available. It is of clinical relevance to decipher novel molecular biomarkers. RITA (RBP-J (recombination signal binding protein J)-interacting and tubulin-associated protein) has been identified as a negative modulator of the Notch pathway and as a microtubule-associated protein important for cell migration and invasion. In the present work, we have systematically studied RITA’s expression in primary placental tissues from patients with early- and late-onset PE as well as in various trophoblastic cell lines. RITA is expressed in primary placental tissues throughout gestation, especially in proliferative villous cytotrophoblasts, in the terminally differentiated syncytiotrophoblast, and in migrating extravillous trophoblasts. RITA’s messenger RNA (mRNA) level is decreased in primary tissue samples from early-onset PE patients. The deficiency of RITA impairs the motility and invasion capacity of trophoblastic cell lines, and compromises the fusion ability of trophoblast-derived choriocarcinoma cells. These data suggest that RITA may play important roles in the development of the placenta and possibly in the pathogenesis of PE.
Insulin-like growth factor-1 (IGF-1)-related signaling is associated with prostate cancer progression. Links were explored between IGF-1 and expression of integrin adhesion receptors to evaluate relevance for growth and migration. Androgen-resistant PC3 and DU145 and androgen-sensitive LNCaP and VCaP prostate cancer cells were stimulated with IGF-1 and tumor growth (all cell lines), adhesion and chemotaxis (PC3, DU145) were determined. Evaluation of Akt/mTOR-related proteins, focal adhesion kinase (FAK) and integrin α and β subtype expression followed. Akt knock-down was used to investigate its influence on integrin expression, while FAK blockade served to evaluate its influence on mTOR signaling. Integrin knock-down served to investigate its influence on tumor growth and chemotaxis. Stimulation with IGF-1 activated growth in PC3, DU145, and VCaP cells, and altered adhesion and chemotactic properties of DU145 and PC3 cells. This was associated with time-dependent alterations of the integrins α3, α5, αV, and β1, FAK phosphorylation and Akt/mTOR signaling. Integrin blockade or integrin knock-down in DU145 and PC3 cells altered tumor growth, adhesion, and chemotaxis. Akt knock-down (DU145 cells) cancelled the effect of IGF-1 on α3, α5, and αV integrins, whereas FAK blockade cancelled the effect of IGF-1 on mTOR signaling (DU145 cells). Prostate cancer growth and invasion are thus controlled by a fine-tuned network between IGF-1 driven integrin-FAK signaling and the Akt-mTOR pathway. Concerted targeting of integrin subtypes along with Akt-mTOR signaling could, therefore, open options to prevent progressive dissemination of prostate cancer.
The management of invasive alien species (IAS) in protected areas has become increasingly important in recent years. In this study, we analyse IAS management in the bilateral National Park Thayatal-Podyjí at the Austrian-Czech border. Based on two surveys from the years 2001 and 2010 and on annual management data from 2001-2010 we analyse changes in distribution and the efficiency of IAS management of three invasive alien plants (Fallopia × bohemica, Impatiens glandulifera, Robinia pseudoacacia). In 2010, the three study species had invaded 161 ha (2%) of the study area. Despite a decade of management, F. × bohemica has become widespread, whereas I. glandulifera distribution has decreased strongly. The most widespread species, R. pseudoacacia, has declined substantially in cover, but the area invaded has increased. From 2001 to 2010, annual management effort declined by about half. Management effort per hectare and decade was highest for F. × bohemica (2,657 hours), followed by R. pseudoacacia (1,473 hours) and I. glandulifera (270 hours). Management effort for achieving the same amount of reduction in population size and cover was highest for R. pseudoacacia, followed by F. × bohemica and I. glandulifera. We conclude that substantial effort and resources are necessary to successfully manage the study species and have to be provided over prolonged time periods, and thus continued management of these species is recommended. We highly recommend a systematic approach for monitoring the efficiency of IAS management projects in protected areas.
The microtubule (MT) cytoskeleton is crucial for cell motility and migration by regulating multiple cellular activities such as transport and endocytosis of key components of focal adhesions (FA). The kinesin-13 family is important in the regulation of MT dynamics and the best characterized member of this family is the mitotic centromere-associated kinesin (MCAK/KIF2C). Interestingly, its overexpression has been reported to be related to increased metastasis in various tumor entities. Moreover, MCAK is involved in the migration and invasion behavior of various cell types. However, the precise molecular mechanisms were not completely clarified. To address these issues, we generated CRISPR/dCas9 HeLa and retinal pigment epithelium (RPE) cell lines overexpressing or downregulating MCAK. Both up- or downregulation of MCAK led to reduced cell motility and poor migration in malignant as well as benign cells. Specifically, it’s up- or downregulation impaired FA protein composition and phosphorylation status, interfered with a proper spindle and chromosome segregation, disturbed the assembly and disassembly rate of FA, delayed cell adhesion, and compromised the plus-tip dynamics of MTs. In conclusion, our data suggest MCAK act as an important regulator for cell motility and migration by affecting the actin-MT cytoskeleton dynamics and the FA turnover, providing molecular mechanisms by which deregulated MCAK could promote malignant progression and metastasis of tumor cells.
This study was designed to investigate whether epigenetic modulation by histone deacetylase (HDAC) inhibition might circumvent resistance towards the mechanistic target of rapamycin (mTOR) inhibitor temsirolimus in a prostate cancer cell model. Parental (par) and temsirolimus-resistant (res) PC3 prostate cancer cells were exposed to the HDAC inhibitor valproic acid (VPA), and tumor cell adhesion, chemotaxis, migration, and invasion were evaluated. Temsirolimus resistance was characterized by reduced binding of PC3res cells to endothelium, immobilized collagen, and fibronectin, but increased adhesion to laminin, as compared to the parental cells. Chemotaxis, migration, and invasion of PC3res cells were enhanced following temsirolimus re-treatment. Integrin α and β receptors were significantly altered in PC3res compared to PC3par cells. VPA significantly counteracted temsirolimus resistance by down-regulating tumor cell–matrix interaction, chemotaxis, and migration. Evaluation of integrin expression in the presence of VPA revealed a significant down-regulation of integrin α5 in PC3res cells. Blocking studies demonstrated a close association between α5 expression on PC3res and chemotaxis. In this in vitro model, temsirolimus resistance drove prostate cancer cells to become highly motile, while HDAC inhibition reversed the metastatic activity. The VPA-induced inhibition of metastatic activity was accompanied by a lowered integrin α5 surface level on the tumor cells.
Tumor progression and pregnancy share many common features, such as immune tolerance and invasion. The invasion of trophoblasts in the placenta into the uterine wall is essential for fetal development, and is thus precisely regulated. Its deregulation has been implicated in preeclampsia, a leading cause for maternal and perinatal mortality and morbidity. Pathogenesis of preeclampsia remains to be defined. Microarray-based gene profiling has been widely used for identifying genes responsible for preeclampsia. In this review, we have summarized the recent data from the microarray studies with preeclamptic placentas. Despite the complex of gene signatures, suggestive of the heterogeneity of preeclampsia, these studies identified a number of differentially expressed genes associated with preeclampsia. Interestingly, most of them have been reported to be tightly involved in tumor progression. We have discussed these interesting genes and analyzed their potential molecular functions in preeclampsia, compared with their roles in malignancy development. Further investigations are warranted to explore the involvement in molecular network of each identified gene, which may provide not only novel strategies for prevention and therapy for preeclampsia but also a better understanding of cancer cells. The trophoblastic cells, with their capacity for proliferation and differentiation, apoptosis and survival, migration, angiogenesis and immune modulation by exploiting similar molecular pathways, make them a compelling model for cancer research.
Die gegenseitige Beeinflussung von Bracheäckern und Trocken- und Halbtrockenrasen wurde entlang eines Transektes (48 m lang, gegliedert in 24 Flächen à 2 x 2 m) untersucht. Im Mittelpunkt stand die Frage, ob sich die sehr unterschiedlichen Vegetationseinheiten entlang dieses Transektes gegenseitig beeinflussen, d.h. ob die Sukzession auf der in der Mitte des Transektes liegenden Ackerbrache einen negativen Einfluß auf die naturnähere Vegetation der angrenzenden Trocken- und Halbtrockenrasen hat. Hierzu wurde die Vegetationsentwicklung 4 Jahre beobachtet. Der Hauptteil der Diasporen verbleibt auf den jeweiligen Flächen, in der direkten Nähe der Mutterpflanze. Nur wenige Diasporen werden weiter transportiert und gelangen in angrenzende Pflanzenbestände. Während sichauf der Brache einige wenige Arten der Trocken- und Halbtrockenrasen etablieren konnten, gelang dies umgekehrt den Ruderalarten nur auf anderen tiefergründigen Standorten. In den flachgründigen Trockenrasen überlebten aufkommende Ruderalarten nicht. Die extremen Standortsverhältnisse (Flachgründigkeit und Trockenheit des Bodens) sichern die Stabilität dieser Biotope.
Function of p21 (Cip1/Waf1/CDKN1A) in migration and invasion of cancer and trophoblastic cells
(2019)
Tumor progression and pregnancy have several features in common. Tumor cells and placental trophoblasts share many signaling pathways involved in migration and invasion. Preeclampsia, associated with impaired differentiation and migration of trophoblastic cells, is an unpredictable and unpreventable disease leading to maternal and perinatal mortality and morbidity. Like in tumor cells, most pathways, in which p21 is involved, are deregulated in trophoblasts of preeclamptic placentas. The aim of the present study was to enlighten p21’s role in tumorigenic choriocarcinoma and trophoblastic cell lines. We show that knockdown of p21 induces defects in chromosome movement during mitosis, though hardly affecting proliferation and cell cycle distribution. Moreover, suppression of p21 compromises the migration and invasion capability of various trophoblastic and cancer cell lines mediated by, at least partially, a reduction of the extracellular signal-regulated kinase 3, identified using transcriptome-wide profiling, real-time PCR, and Western blot. Further analyses show that downregulation of p21 is associated with reduced matrix metalloproteinase 2 and tissue inhibitor of metalloproteinases 2. This work evinces that p21 is involved in chromosome movement during mitosis as well as in the motility and invasion capacity of trophoblastic and cancer cell lines.
Background: Although mechanistic target of rapamycin (mTOR) inhibitors, such as temsirolimus, show promise in treating bladder cancer, acquired resistance often hampers efficacy. This study evaluates mechanisms leading to resistance. Methods: Cell growth, proliferation, cell cycle phases, and cell cycle regulating proteins were compared in temsirolimus resistant (res) and sensitive (parental—par) RT112 and UMUC3 bladder cancer cells. To evaluate invasive behavior, adhesion to vascular endothelium or to immobilized extracellular matrix proteins and chemotactic activity were examined. Integrin α and β subtypes were analyzed and blocking was done to evaluate physiologic integrin relevance. Results: Growth of RT112res could no longer be restrained by temsirolimus and was even enhanced in UMUC3res, accompanied by accumulation in the S- and G2/M-phase. Proteins of the cdk-cyclin and Akt-mTOR axis increased, whereas p19, p27, p53, and p73 decreased in resistant cells treated with low-dosed temsirolimus. Chemotactic activity of RT112res/UMUC3res was elevated following temsirolimus re-exposure, along with significant integrin α2, α3, and β1 alterations. Blocking revealed a functional switch of the integrins, driving the resistant cells from being adhesive to being highly motile. Conclusion: Temsirolimus resistance is associated with reactivation of bladder cancer growth and invasive behavior. The α2, α3, and β1 integrins could be attractive treatment targets to hinder temsirolimus resistance.