Recent studies have highlighted the significant role of 5-hydroxymethylcytosine (5hmC) in carcinogenesis. However, the specific role of 5hmC in osteosarcoma (OS) remains largely unexplored. The-re-fore, this study aimed to investigate the function of 5hmC and TET3 in OS. In this study, we found a decreased total level of 5hmC in OS tissues. The expression of the TET3 protein was also decreased in OS. Importantly, the decreased levels of TET3 were associated with a decreased disease-free survival (DFS) rate in patients. To investigate the role of TET3 and 5hmC in OS, we manipulated the levels of TET3 in MG-63 cells. Silencing TET3 in these cells resulted in a twofold increase in proliferation. Additio-nally, the level of 5hmC decreased in these cells. Con-versely, over-expression of TET3 in MG-63 cells led to the expected inhibition of proliferation and invasion, accompanied by an increase in 5hmC levels. In conclusion, both 5hmC and TET3 protein levels were decreased in OS. Additionally, the over-expression of TET3 inhibited the proliferation of MG-63 cells, while the suppression of TET3 had the opposite effect. These findings suggest that decreased levels of 5hmC and TET3 may serve as potential markers for OS.

• MeSH
• 5-methylcytosin * analogy a deriváty   metabolismus   MeSH
• demetylace DNA * MeSH
• dioxygenasy * metabolismus   MeSH
• epigeneze genetická * MeSH
• lidé MeSH
• nádorové buněčné linie MeSH
• nádory kostí genetika   metabolismus   patologie   MeSH
• osteosarkom genetika   metabolismus   patologie   MeSH
• proliferace buněk * MeSH
• protoonkogenní proteiny metabolismus   genetika   MeSH
• regulace genové exprese u nádorů MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

Circular RNAs (circRNAs) have played an essential role in cancer development. This study aimed to illustrate the impact and potential mechanism of circRACGAP1 action in NSCLC development. The expression patterns of circRACGAP1, miR-1296, and CDK2 in NSCLC tissues and cell lines were analysed by RT-qPCR. The function of circRACGAP1 in NSCLC cell proliferation and apoptosis was investigated using the CCK-8 assay, flow cytometry, TUNEL staining, and Western blot. The interaction among circRACGAP1, miR-1296, and CDK2 was clarified by dual-luciferase reporter assay while the correlation was confirmed by the Pearson correlation coefficient. The expression of circRACGAP1 and CDK2 was up-regulated in NSCLC tissues, while the expression of miR-1296 was down-regulated. Cell function studies further revealed that circRACGAP1 could promote NSCLC cell proliferation, accelerate the cell cycle process, up-regulate B-cell lymphoma 2 (Bcl2) expression, and down-regulate Bcl2-associated X (Bax) expression. miR-1296 was identified as a downstream target to reverse circRACGAP1-mediated cell proliferation. miR-1296 directly targeted the 3'-UTR of CDK2 to regulate proliferation and apoptosis of NSCLC cells. Additionally, the dual-luciferase reporter assay and Pearson correlation coefficient analysis proved that circRACGAP1 acted in NSCLC cells by negatively regulating miR-1296 expression and positively regulating CDK2 expression. In summary, our study revealed that circRACGAP1 promoted NSCLC cell proliferation by regulating the miR-1296/CDK2 pathway, providing potential diagnostic and therapeutic targets for NSCLC.

• MeSH
• apoptóza * genetika   MeSH
• cyklin-dependentní kinasa 2 * metabolismus   genetika   MeSH
• kruhová RNA * genetika   metabolismus   MeSH
• lidé MeSH
• mikro RNA * genetika   metabolismus   MeSH
• nádorové buněčné linie MeSH
• nádory plic * genetika   patologie   metabolismus   MeSH
• nemalobuněčný karcinom plic * genetika   patologie   metabolismus   MeSH
• proliferace buněk * genetika   MeSH
• proteiny aktivující GTPasu genetika   metabolismus   MeSH
• regulace genové exprese u nádorů MeSH
• signální transdukce genetika   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

DNA ligase 1 (LIG1) plays a key role in DNA synthesis and DNA damage repair pathways. LIG1 has been shown to be up-regulated in human non-small cell lung cancer (NSCLC); however, its role and molecular regulatory mechanism in NSCLC cell proliferation are still not fully understand. In this study, we aimed to explore the role of LIG1 and post-transcripional regulators in NSCLC. Utilizing bioinformatic tools and qRT-PCR, our investigation substantiated the up-regulation of LIG1 within NSCLC cell lines and tumour tissues. Remarkably, individuals exhibiting elevated levels of LIG1 had diminished survival rates. Functionally, the depletion of LIG1 inhibited cell proliferation and migration, contrasting with the increased proliferation and migration upon LIG1 over-expression. Prediction from the TargetScanHuman database and results of dual luciferase reporter assays indicated that miR-325 could directly bind to and negatively regulate LIG1. Moreover, our findings demonstrated that the mimicry of miR-325 decreased cell viability, whereas its inhibition correspondingly increased viability, indicative of the tumour-suppressive role of miR-325 through the down-regulation of LIG1. Collectively, our findings show that LIG1 could promote tumour progression and knockdown of LIG1 could exert suppressive effects on NSCLC. As the post-transcriptional factor of LIG1, miR-325 could negatively regulate the expression of LIG1 to inhibit tumour progression in vitro. These findings suggest that LIG1 and miR-325 might be potential therapeutic targets for NSCLC treatment.

• MeSH
• DNA-ligasa ATP * metabolismus   genetika   MeSH
• lidé MeSH
• mikro RNA * genetika   metabolismus   MeSH
• nádorové buněčné linie MeSH
• nádory plic * patologie   genetika   metabolismus   MeSH
• nemalobuněčný karcinom plic * genetika   patologie   metabolismus   MeSH
• pohyb buněk * MeSH
• proliferace buněk * MeSH
• regulace genové exprese u nádorů MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

Lysosomes are crucial in the tumour immune microenvironment, which is essential for the survival and homeostasis in multiple myeloma (MM). Here, we aimed to identify lysosome-related genes for the prognosis of MM and predicted their regulatory mechanisms. Gene expression profiles of MM from the GSE2658 and GSE57317 datasets were analysed. Lysosome-related differentially expressed genes (DEGs) were identified and used for molecular subtyping of MM patients. A prognostic model was constructed using univariate Cox regression and LASSO regression analyses. The relationship between prognostic genes, immune cell types, and autophagy pathways was assessed through correlation analysis. RT-qPCR was performed to validate the expression of prognostic genes in MM cells. A total of 9,954 DEGs were identified between high and low immune score groups, with 213 intersecting with lysosomal genes. Molecular subtyping revealed two distinct MM subtypes with significant differences in immune cell types and autophagy pathway activities. Five lysosome-related DEGs (CORO1A, ELANE, PSAP, RNASE2, and SNAPIN) were identified as significant prognostic markers. The prognostic model showed moderate predictive accuracy with AUC values up to 0.723. Prognostic genes demonstrated significant correlations with various immune cell types and autophagy pathways. Additionally, CORO1A, PSAP and RNASE2 expression was up-regulated in MM cells, while ELANE and SNAPIN were down-regulated. Five lysosomal genes in MM were identified, and a new risk model for prognosis was developed using these genes. This research could lead to discovering important gene markers for the treatment and prognosis of MM.

• MeSH
• autofagie genetika   MeSH
• lidé MeSH
• lyzozomy * metabolismus   genetika   MeSH
• mnohočetný myelom * genetika   imunologie   MeSH
• nádorové biomarkery genetika   MeSH
• nádorové mikroprostředí genetika   imunologie   MeSH
• prognóza MeSH
• regulace genové exprese u nádorů MeSH
• stanovení celkové genové exprese MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

Folia Biologica celebrates 70 years of continuous publication of research papers. The first volume was published in Prague in 1954 on behalf of the Institute of Molecular Genetics of the Czechoslovak Academy of Sciences (since 1990 the Academy of Sciences of the Czech Republic) under the subtitle "International edition of the journal Czechoslovakian Biology". Born in the dark days of the Cold War, Folia Biologica provided a thin but important link between the politically controlled science behind the Iron Curtain in the former Czechoslovakia and that of the free Western world. Initially, the journal focused on research papers in the fields of experimental medicine, immunology, virology, and experimental zoology. Since 1961 (Volume 7), Folia Biologica has been indexed in the Web of Science database. The first issue of Volume 7 was introduced by a review article by Peter Brian Medawar (1915-1987), winner of the 1960 Nobel Prize in Physiology or Medicine "for the discovery of acquired immunological tolerance", which is reprinted in this anniversary issue [1].In the late 1960s, during the political relaxation that culminated in the Prague Spring, cooperation with free Western science intensified and enabled a lively scientific dialogue between Czechoslovak and foreign biological scientists, namely immunologists, molecular biologists, and virologists, as illustrated by a series of original research articles from Folia Biologica by Georg Davis Snell (1903-1996) and Jean Dausset (1916-2009), who were awarded the Nobel Prize in Physiology and Medicine in 1980 "for their discoveries concerning genetically determined structures on the cell surface that regulate immunological reactions", which led to the discovery of the major histocompatibility system (MHC) [2-7]. Another powerful example is an article in Folia Biologica by François Jacob (1920-2013), who was awarded the Nobel Prize in 1965 for discoveries that helped elucidate the transcriptional control of enzyme levels [8].Despite the years of political repression during the "normalization" period following the invasion of the Warsaw Pact troops into Czechoslovakia in 1968, the scientists and editors of Folia Biologica from the Academy of Sciences were able to maintain vibrant contacts with the world's leading scientists. In 1981, the journal changed its subtitle to "Journal of Cellular and Molecular Biology". In 1983, Folia Biologica published the article by Renato Dulbecco (1914-2012), who was awarded the Nobel Prize in 1975 for "discoveries concerning the interaction between tumor viruses and the genetic material of the cell"[9].With further orientation towards human molecular medicine, the journal entered the era after the Velvet Revolution in 1989, which represented the desired end of political control over national science. The interest of Czechoslovak and Czech scientists in publishing in Folia Biologica began to decline at the end of the 1990s, when they had at their disposal the full range of scientific journals from all over the world. Since volume 63 (January 2006), Folia Biologica has been published by the First Faculty of Medicine, Charles University, Prague, in a fully open access model.With the new decade that begins with this issue, the journal has undergone a series of improvements, including the strengthening of the editorial board, the assignment of a DOI (Digital Object Identifier) number to each article, the improvement of the cover layout and graphics, the innovation of the website, and a more precise definition of the journal's aim. Folia Biologica now publishes articles describing original research aimed at elucidating a wide range of issues in biomedicine, especially in oncology and human molecular genetics. In addition, the journal focuses on the cellular and molecular mechanisms of disease and provides studies on all organisms, cells and tissues that serve as biological and disease models, as well as clinical and translational research studies. Further improvements towards sustainable and rapid publication will be accomplished by introducing an online-only publication model planned for 2025.To celebrate the 70th anniversary of Folia Biologica, we begin the anniversary volume with the reprint of Sir Peter Brian Medawar's review. To commemorate the continuing history of the journal, and to thank our predecessors and contributors, we present the title pages, table of contents, and editorial boards of Folia Biologica by decade, illustrating the changes in research focus, human knowledge, and the evolution of the journal.We would like to thank all authors, reviewers, editorial board members, editors and managing editors involved in the journal production in the past decades, namely Ivan Málek, Milan Hašek, Alena Langerová, Josef Říman, Jan Bubeník, Jan Svoboda, Emanual Nečas, Karel Smetana Jr. and Zdeněk Kostrouch, for their commitment and dedication to Folia Biologica.We wish our journal many more decades of scientifically interesting articles, publishing open-minded science by excellent authors for the pleasure of satisfied readers!

• MeSH
• dějiny 20. století MeSH
• dějiny 21. století MeSH
• lidé MeSH
• periodika jako téma * dějiny   MeSH
• výročí a významné události MeSH
• Check Tag
• dějiny 20. století MeSH
• dějiny 21. století MeSH
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• historické články MeSH
• úvodníky MeSH
• Geografické názvy
• Česká republika MeSH
• Československo MeSH

Chlamydia psittaci pneumonia (CPP) is a lung disease caused by the infection with the Chla-mydia psittaci bacterium, which can lead to severe acute respiratory distress syndrome and systemic symptoms. This study explored the specific mechanisms underlying the impact of reactive oxygen species (ROS) on the Th17/Treg balance in CPP. The levels of ROS and the differentiation ratio of Th17/Treg in the peripheral blood of healthy individuals and CPP patients were measured using ELISA and flow cytometry, respectively. The association between the ROS levels and Th17/Treg was assessed using Pearson correlation analysis. The ROS levels and the Th17/Treg ratio were measured in CD4+ T cells following H2O2 treatment and NLRP3 inhibition. The effects of H2O2 treatment and NLRP3 inhibition on the NLRP3/IL-1β/caspase-1 pathway were observed using immunoblotting. Compared to the healthy group, the CPP group exhibited increased levels of ROS in the peripheral blood, an elevated ratio of Th17 differentiation, and a decreased ratio of Treg differentiation. ROS levels were positively correlated with the Th17 cell proportion but negatively correlated with the Treg cell proportion. The ROS levels and NLRP3/IL-1β/caspase-1 expression were up-regulated in CD4+ T cells after H2O2 treatment. Furthermore, there was an increase in Th17 differentiation and a decrease in Treg differentiation. Conversely, the NLRP3/IL-1β/caspase-1 pathway inhibition reversed the effects of H2O2 treatment, with no significant change in the ROS levels. ROS regulates the Th17/Treg balance in CPP, possibly through the NLRP3/IL-1β/caspase-1 pathway. This study provides a new perspective on the development of immunotherapy for CPP.

• MeSH
• buněčná diferenciace * účinky léků   MeSH
• buňky Th17 * imunologie   metabolismus   MeSH
• Chlamydophila psittaci * MeSH
• dospělí MeSH
• interleukin-1beta * metabolismus   MeSH
• kaspasa 1 * metabolismus   MeSH
• lidé středního věku MeSH
• lidé MeSH
• peroxid vodíku metabolismus   MeSH
• protein NLRP3 * metabolismus   MeSH
• psitakóza MeSH
• reaktivní formy kyslíku * metabolismus   MeSH
• regulační T-lymfocyty * imunologie   MeSH
• signální transdukce MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

Germline DNA testing using the next-gene-ration sequencing (NGS) technology has become the analytical standard for the diagnostics of hereditary diseases, including cancer. Its increasing use places high demands on correct sample identification, independent confirmation of prioritized variants, and their functional and clinical interpretation. To streamline these processes, we introduced parallel DNA and RNA capture-based NGS using identical capture panel CZECANCA, which is routinely used for DNA analysis of hereditary cancer predisposition. Here, we present the analytical workflow for RNA sample processing and its analytical and diagnostic performance. Parallel DNA/RNA analysis allowed credible sample identification by calculating the kinship coefficient. The RNA capture-based approach enriched transcriptional targets for the majority of clinically relevant cancer predisposition genes to a degree that allowed analysis of the effect of identified DNA variants on mRNA processing. By comparing the panel and whole-exome RNA enrichment, we demonstrated that the tissue-specific gene expression pattern is independent of the capture panel. Moreover, technical replicates confirmed high reproducibility of the tested RNA analysis. We concluded that parallel DNA/RNA NGS using the identical gene panel is a robust and cost-effective diagnostic strategy. In our setting, it allows routine analysis of 48 DNA/RNA pairs using NextSeq 500/550 Mid Output Kit v2.5 (150 cycles) in a single run with sufficient coverage to analyse 226 cancer predisposition and candidate ge-nes. This approach can replace laborious Sanger confirmatory sequencing, increase testing turnaround, reduce analysis costs, and improve interpretation of the impact of variants by analysing their effect on mRNA processing.

• MeSH
• DNA genetika   MeSH
• genetická predispozice k nemoci * MeSH
• lidé MeSH
• nádory genetika   diagnóza   MeSH
• reprodukovatelnost výsledků MeSH
• RNA genetika   MeSH
• sekvenční analýza DNA metody   MeSH
• sekvenční analýza RNA metody   MeSH
• vysoce účinné nukleotidové sekvenování * metody   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

Psoriasis is a chronic non-contagious autoimmune disease. Gallic acid is a natural compound with potential health benefits, including antioxidant, anticancer, antiviral and antibacterial properties. Nevertheless, the influence of gallic acid on psoriasis has not been fully determined. This investigation aimed to discover the effect of gallic acid on psoriasis. Thirty-one pairs of psoriatic skin tissues and healthy adult human skin tissues were collected. Human keratinocytes (HaCaT cells) were transfected with interleukin 17A (IL-17A) to create the psoriatic keratinocyte model. The content of bromodomain-containing protein 4 (BRD4) microRNA was assessed using qRT-PCR testing. The content of BRD4 was detected by Western blotting. Cell migration was evaluated by conducting a wound healing assay. Cell proliferation was determined using an EdU assay. Apoptosis was detected by the TUNEL assay. The contents of interferon gamma (IFN-γ), IL-6, IL-8 and IL-17 were detected by ELISA. BRD4 was up-regulated in psoriatic skin tissues and in the IL-17A group compared to the healthy adult human skin tissues and the control group. Silencing BRD4 inhibited cell migration, proliferation and inflammatory response but induced apoptosis in IL-17A-treated HaCaT cells. Conversely, BRD4 over-expression promoted cell migration, proliferation and inflammatory response but suppressed apoptosis in IL-17A-treated HaCaT cells. Gallic acid repressed cell migration, proliferation and inflammatory response but indu-ced apoptosis in HaCaT cells transfected with IL-17A by down-regulating BRD4. Gallic acid represses cell migration, proliferation and inflammatory response but induces apoptosis in IL-17A-transfected HaCaT cells by down-regulating BRD4.

• MeSH
• apoptóza * účinky léků   MeSH
• buněčné linie keratinocytů HaCaT MeSH
• buněčné linie MeSH
• dospělí MeSH
• interleukin-17 metabolismus   MeSH
• jaderné proteiny metabolismus   genetika   MeSH
• keratinocyty * účinky léků   metabolismus   MeSH
• kyselina gallová * farmakologie   MeSH
• lidé MeSH
• mikro RNA genetika   metabolismus   MeSH
• pohyb buněk * účinky léků   MeSH
• proliferace buněk * účinky léků   MeSH
• proteiny buněčného cyklu * metabolismus   genetika   MeSH
• proteiny obsahující bromodoménu MeSH
• psoriáza * metabolismus   patologie   farmakoterapie   MeSH
• regulace genové exprese účinky léků   MeSH
• transkripční faktory * metabolismus   MeSH
• zánět * patologie   MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

Effective treatment of patients with autism spectrum disorder (ASD) is still absent so far. Taurine exhibits therapeutic effects towards the autism-like behaviour in ASD model animals. Here, we determined the mechanism of taurine effect on hippocampal neurogenesis in genetically inbred BTBR T+ tf/J (BTBR) mice, a proposed model of ASD. In this ASD mouse model, we explored the effect of oral taurine supplementation on ASD-like behaviours in an open field test, elevated plus maze, marble burying test, self-grooming test, and three-chamber test. The mice were divided into four groups of normal controls (WT) and models (BTBR), who did or did not receive 6-week taurine supplementation in water (WT, WT+ Taurine, BTBR, and BTBR+Taurine). Neurogenesis-related effects were determined by Ki67 immunofluorescence staining. Western blot analysis was performed to detect the expression of phosphatase and tensin homologue deleted from chromosome 10 (PTEN)/mTOR/AKT pathway-associated proteins. Our results showed that taurine improved the autism-like behaviour, increased the proliferation of hippocampal cells, promoted PTEN expression, and reduced phosphorylation of mTOR and AKT in hippocampal tissue of the BTBR mice. In conclusion, taurine reduced the autism-like behaviour in partially inherited autism model mice, which may be associa-ted with improving the defective neural precursor cell proliferation and enhancing the PTEN-associated pathway in hippocampal tissue.

• MeSH
• autistická porucha * metabolismus   farmakoterapie   MeSH
• chování zvířat účinky léků   MeSH
• fosfohydroláza PTEN * metabolismus   MeSH
• hipokampus * metabolismus   účinky léků   MeSH
• modely nemocí na zvířatech MeSH
• myši MeSH
• neurogeneze * účinky léků   MeSH
• poruchy autistického spektra metabolismus   farmakoterapie   MeSH
• proliferace buněk účinky léků   MeSH
• protoonkogenní proteiny c-akt * metabolismus   MeSH
• signální transdukce * účinky léků   MeSH
• taurin * farmakologie   MeSH
• TOR serin-threoninkinasy * metabolismus   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Docosahexaenoic acid (DHA) is an omega-3 polyunsaturated fatty acid with promising anticancer potential. Anaemia is a frequent adverse effect of anticancer treatment caused in part by eryptosis and haemolysis. Thus, it is important to investigate the role of DHA in red blood cell (RBC) death. RBCs were treated with anticancer concentrations (10-100 μM) of DHA under different physiological conditions, and fluorescence-assisted cell sorting was employed to measure eryptotic markers. Cell membrane scrambling was detected by annexin-V-FITC labelling, cytoplasmic Ca2+ by Fluo4/AM, cell size by forward scatter (FSC), and oxidative stress by H2DCFDA. Haemolytic markers were also assayed by photometric methods. DHA caused significant phospholipid scrambling with Ca2+ accumulation, loss of cellular volume, and oxidative stress. These changes were associated with dacrocyte formation, as revealed by electron microscopy. Moreover, DHA exhibited a dual effect on membrane integrity: it was haemolytic under isotonic conditions and anti-haemolytic in hypotonic environments. Importantly, inhibition of Rac1 GTPase activity with NSC23766 significantly reduced DHA-mediated haemolysis, as did co-administration of either sucrose or polyethylene glycol 8,000. Conversely, the presence of 125 mM KCl and urea without extracellular Ca2+ significantly exacerbated DHA toxicity. In conclusion, this is the first report that identifies key biochemical mechanisms underlying the cytotoxic effects of DHA in RBCs, promoting further development and validation of DHA in anticancer therapy.

• MeSH
• eryptóza * účinky léků   MeSH
• erytrocyty účinky léků   metabolismus   MeSH
• hemolýza * účinky léků   MeSH
• kyseliny dokosahexaenové * farmakologie   MeSH
• lidé MeSH
• oxidační stres * účinky léků   MeSH
• signální transdukce účinky léků   MeSH
• vápník * metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH