Publications by authors named "Rumjanek F"
Article Synopsis
- Breast cancer is a prevalent cancer among women and is linked to genetic mutations that cause uncontrolled growth of breast cells, leading to increased energy needs for tumor cells.
- Inorganic phosphate (Pi) is crucial for cancer cell growth, and ectoenzymes on the cell membrane help release Pi from phosphorylated molecules, assisting in the energy acquisition needed by tumors.
- A study on MDA-MB-231 breast cancer cells revealed that their ectophosphatase activity is higher in acidic conditions and can be inhibited by sodium orthovanadate, which also hampers key processes like cell proliferation and migration, important in cancer progression.
Article Synopsis
- The text indicates that it serves as a correction to a previously published article, specifically DOI: 10.3389/fonc.2019.01430.
- The correction may address errors or omissions found in the original study.
- It emphasizes the importance of accurate scientific communication for research integrity.
Article Synopsis
- Tumor cells, particularly metastatic ones, show altered metabolism, releasing more heat compared to non-metastatic cells, as analyzed through isothermal microcalorimetry.
- In experiments, components such as mitochondrial extracts and inhibitors of actin filaments or specific genes influenced the heat release patterns of these cancer cells.
- The presence of uncoupling protein 2 in metastatic cells and the impact of lipid metabolism on heat release suggest that this thermogenic activity could serve as a measurable indicator of cancer metastasis.
Article Synopsis
- The study investigates the role of a proton (H)-dependent inorganic phosphate (Pi) transporter in breast cancer cells (MDA-MB-231) and how it functions in the acidic tumor microenvironment, which is characterized by high Pi levels.
- MDA-MB-231 cells show significantly higher H-dependent Pi transport than other breast cell lines, exhibiting linear transport kinetics and low affinity for Pi at acidic pH.
- The research findings suggest that the H-dependent Pi transporter provides tumor cells with an alternative uptake pathway for Pi when sodium (Na)-dependent transport is saturated, potentially supporting tumor growth and energy demands.
Article Synopsis
- The text indicates a correction to a previously published article, specifically DOI: 10.3389/fonc.2018.00090.!
- The correction likely addresses errors or inaccuracies found in the original publication, which is common in academic research.!
- Understanding these corrections is important for researchers and readers to ensure the accuracy and reliability of the information presented in the article.!
Article Synopsis
- The mechanisms behind tumorigenesis and metastasis remain poorly understood, with evidence suggesting malignancy arises not just from mutations but from heterogeneous tumor cell populations facing selective pressures.
- The authors propose that transcription factors, particularly those with intrinsically disordered domains (IDRs), can have varied functions that may drive oncogenesis and metastasis independently of mutations.
- A study on oral cancer cells indicated that metastatic cells contained osmolytes—small molecules that stabilize proteins and may alter transcription factor conformations—suggesting a link between osmolyte levels and increased metastatic potential.
Article Synopsis
- * Tumor cells often show up-regulated inorganic phosphate transporters, such as NaPi-IIb and PiT-1, which may promote tumor growth and could be used in clinical diagnostics.
- * Recent advancements in molecular biology have revealed that these transporters are also involved in tumor mechanisms like proliferation, drug resistance, and associations with oncogenes.
Article Synopsis
- Cancer treatment has improved with targeted therapy, but drug resistance, particularly the multidrug resistance (MDR) phenotype, continues to hinder success.
- This MDR phenotype enhances resistance to various drugs by promoting metabolic changes that increase energy and nutrient demands in cancer cells.
- The review explores the connection between metabolism and MDR, highlighting the role of glycolytic enzymes, especially glyceraldehyde-3-phosphate dehydrogenase, in contributing to resistance and potentially serving as new treatment targets.
Article Synopsis
- Tumor cells adapt to various stresses, developing distinct metabolic profiles that reflect their levels of metastatic potential, particularly in tongue squamous cell carcinoma lines.* -
- The study utilized nuclear magnetic resonance (NMR) spectroscopy and fluorescence lifetime imaging microscopy (FLIM) to analyze metabolites and energy metabolism in different cancer cell lines, finding variations in NAD(P)H concentrations and energy strategies.* -
- Findings suggest that lipid metabolism, indicated by the accumulation of specific fatty acids and malonate, is linked to increased invasiveness in metastatic cells, highlighting a connection between metabolic pathways and cancer progression.*
Article Synopsis
- Recent studies indicate that levels of inorganic phosphate (Pi) are higher in the breast cancer environment than in normal tissues, and breast cancer cells show increased expression of the NaPi-IIb carrier, potentially influencing cancer growth.
- This research focused on the Pi transport in the MDA-MB-231 breast cancer cell line, examining how sodium concentration, pH, and metabolic inhibitors affect the transport process and its relationship with cell migration and adhesion.
- Findings revealed that Pi transport in these cancer cells is sodium-dependent and influenced by factors like pH and Pi concentration, suggesting that targeting Pi transport could be a viable therapeutic approach for breast cancer treatment.
Article Synopsis
- The study focuses on understanding the biochemistry of head and neck tumors to gain insights into their metastatic potential, which is linked to high mortality rates.* -
- Researchers conducted RNA-Seq analyses on 5 different oral cancer cell lines to identify differentially expressed genes (DEGs) and their contributions to tumor invasion and metastatic progression.* -
- Key findings include the identification of 26 consistently expressed genes throughout tumor progression, two novel metastatic markers (PIGG and SLC8B1), and several genes (MYH14, ANGPTL4, PPARD, ENPP1) that could be targeted for pharmacological interventions.*
Article Synopsis
- * Suppressing MAGE-A10 led to changes in cell shape, inhibited growth, and increased cell adhesion in the lines tested (LN1 and LN2).
- * The knockdown of MAGE-A10 reduced cell migration and invasion capabilities, while also influencing the expression of key adhesion molecules like E-cadherin and N-cadherin, suggesting a role in the epithelial-mesenchymal transition (EMT) process.
Article Synopsis
- Tumors have various cell types with different metabolic traits that adapt to available oxygen and nutrients, influencing their progression to metastasis.
- Research showed that metastatic cells (4C11+) have heightened mitochondrial function and increased energy production, linked to processes like glutamine breakdown and fatty acid oxidation.
- These findings suggest that specific metabolic characteristics, particularly involving mitochondrial activity, play a crucial role in the transition from non-tumorigenic to metastatic cell phenotypes.
Article Synopsis
- - Current studies on cancer metabolism rely heavily on genomic, transcriptomic, and proteomic data, but may overlook crucial factors like post-translational modifications that impact protein function and activity.
- - The assumption that changes in gene expression directly correlate with protein levels often fails, as there’s no consistent relationship between mRNA levels of metabolic enzymes/transcription factors and their actual protein activities.
- - To better understand cancer cell behavior, it is essential to focus on the functional analysis of proteins and their regulatory mechanisms rather than just gene and mRNA information, using both local and systemic approaches to study cellular processes.
Article Synopsis
- - Tumor cells exhibit unique energy metabolism compared to normal cells, and the study investigates how histone deacetylase inhibitors (HDACis) like sodium butyrate (NaB) and trichostatin A (TSA) influence this in various breast cancer cell lines.
- - Non-tumorigenic MCF-10A cells showed less sensitivity to NaB and TSA compared to aggressive tumor cells, with T-47D cells being the most affected, indicating that cancer aggressiveness correlates with susceptibility to these treatments.
- - The treatments altered metabolic activities, such as reducing glycolysis in certain cell lines and increasing oxygen consumption, suggesting that epigenetic changes through protein acetylation impact energy metabolism
Significant efforts have been made for the development of new anticancer drugs (protein kinase or proteasome inhibitors, monoclonal humanized antibodies) with presumably low or negligible side effects and high specificity. However, an in-depth analysis of the side effects of several currently used canonical (platin-based drugs, taxanes, anthracyclines, etoposides, antimetabolites) and new generation anticancer drugs as the first line of clinical treatment reveals significant perturbation of glycolysis and oxidative phosphorylation. Canonical and new generation drug side effects include decreased (1) intracellular ATP levels, (2) glycolytic/mitochondrial enzyme/transporter activities and/or (3) mitochondrial electrical membrane potentials.
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- Mitochondria have become increasingly recognized for their crucial roles in cellular functions such as ATP production, maintaining redox balance, and facilitating apoptosis since the 19th century.
- In cancer cells, mitochondria shift from being faulty to potentially aiding in metastasis by supporting harmful cellular behaviors.
- The article suggests that the metabolic processes in mitochondria contribute to the development of cancer and that tumor cells may exploit these metabolic pathways as part of a non-adaptive evolutionary strategy.
Article Synopsis
- Methyl jasmonate (MJ) is a compound that boosts plant defense mechanisms and shows promise in fighting cancer cells without harming normal cells.
- It works by arresting the cell cycle, triggering cell death through various pathways, and disrupting cellular metabolism by affecting key proteins and mitochondrial functions.
- MJ also enhances stress signaling, inhibits inflammatory enzymes in cancer cells, prevents cell migration, and may improve the effectiveness of certain chemotherapy drugs, making it a potential outstanding treatment option.
Article Synopsis
- - Transthyretin (TTR) is a protein involved in several amyloid diseases, with more than 100 variants affecting its stability and promoting aggregation, particularly in cases like senile amyloidosis.
- - A Brazilian patient with severe cardiomyopathy carries a rare mutation (A19D) in the TTR gene, which was analyzed using computational modeling to assess its stability compared to known variants.
- - The study found that the A19D variant shows decreased stability and increased amyloidogenicity due to structural changes and unfavorable charges within the protein, marking it as the first non-V30M mutation reported in Brazil.
Article Synopsis
- - Tumor cells survive in harsh environments by altering gene regulation and metabolic pathways, notably relying on the Warburg effect, which promotes anaerobic glycolysis even in oxygen-rich conditions.
- - The review reevaluates Otto Warburg's theories, showing that mitochondria in tumor cells are not dysfunctional, but rather vital for tumor growth and spread, highlighting their role in pathways like glutaminolysis.
- - The text also discusses potential treatments targeting the unique biochemistry of tumor cells, including a case study on the effects of the drug 3BP (3-bromopyruvate) on glycolytic enzymes.
Article Synopsis
- A study analyzed how the supply of the metabolic precursor 2-oxoglutarate (2-OG) impacts lysine production in the yeast Saccharomyces cerevisiae when grown on high glucose.
- The researchers identified three groups of reactions involving 2-OG: the producer group (enzymes that create 2-OG) and two consumer groups (enzymes that convert 2-OG into lysine and glutamate).
- They found that increasing the activity of enzymes in the 2-OG producer group significantly controls lysine synthesis, indicating that enhancing these enzymes could be an effective way to boost lysine production.
Article Synopsis
- SMYB1 is a protein from the parasite Schistosoma mansoni that resembles other proteins in the Y-box binding protein family and can bind to DNA and RNA.
- It is found in the cytoplasm across different life stages of the parasite, indicating its role in mRNA metabolism.
- The study identifies SMYB1 interacting with a protein similar to Drosophila's SmD3, suggesting SMYB1 is involved in RNA processing functions like turnover, transport, and stabilization.
Nutrient deprivation and reactive oxygen species (ROS) play an important role in breast cancer mitochondrial adaptation. Adaptations to these conditions allow cells to survive in the stressful microenvironment of the tumor bed. This study is directed at defining the consequences of High Nitric Oxide (HNO) exposure to mitochondria in human breast cancer cells.
View Article and Find Full Text PDFMitochondria combine hydrogen and oxygen to produce heat and adenosine triphosphate (ATP). As a toxic by-product of oxidative phosphorylation (OXPHOS), mitochondria generate reactive oxygen species (ROS). These free radicals may cause damage to mitochondrial DNA (mtDNA) and other molecules in the cell.
View Article and Find Full Text PDFGenomic instability at the 13q31 locus and somatic mtDNA mutation in the D-loop site correlate with tumor aggressiveness in sporadic Brazilian breast cancer cases.
Gilson Costa dos Santos Andréa Carla de Souza Góes Humberto de Vitto Carla Cristina Moreira Elizabeth Avvad
Clinics (Sao Paulo)
October 2012
Article Synopsis
- The study investigated genomic instability in sporadic breast cancer cases in Brazil by analyzing nuclear and mitochondrial DNA alterations.
- Researchers examined 64 pairs of breast cancer and non-cancerous samples to identify short tandem repeats and mitochondrial mutations.
- Findings revealed that nuclear instability was present in half of the cancer tissues, with specific loci affected, and that somatic mitochondrial mutations were linked to tumor aggressiveness and certain genetic mutations.