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Regulacija ekspresije somatskih podtipova H1 u ljudskim staničnim linijama
No full textHistone H1 or linker histone is involved in the regulation of chromatin
structure (4). Histone H1 is part of a multigene family encoding eleven
subtypes, seven somatic subtypes, and four germ-line specific subtypes (1).
The complement of histone H1 is defined as the subtype composition and
their proportions in a cell on a given condition. H1 complement is variable
and several studies have reported that is altered in disease, in particular in
cancer (2). Therefore, more studies must be performed in order to
understand its functions in diseases. In this study the global aim is to
understand regulation of the expression of somatic subtypes in human cell
lines. Our first objective was to study the role of m6A in the regulation of
the mRNA and protein levels of histone H1 subtypes. We used cycloleucine
to inhibit METTL3, m6A methyltransferase. We tested several doses finding
that in high doses of inhibitor prevent the ability of cells to replicate in the
same hour period as untreated cells and effect of cycloleucine is dosedependent in both cell lines. In HEK293T cycloleucine had shown different
effects on the cell cycle depending on the dose and the time of treatment.
In contrast, in HeLa the distribution of the cell cycle phases was not affected
at 24h in any dose. H1 subtypes were differentially affected. At the mRNA
level, HeLa cell line showed alteration of mRNA levels that occur in most of
the H1 genes and controls at all doses tested, including the lowest dose. At
the protein level, changes observed (increase or decrease) are in agreement
with changes observed in the mRNA, except for H1.4. Considering the
magnitude of the change, there is no correspondence between mRNA and
protein levels. In general, the effects are different among subtypes
supporting the idea that m6A plays a subtype specific role in H1 regulation.
Our second objective was to study the regulation of H1 protein levels by the
proteasome in HeLa and HEK293T. We used to inhibitors MG132 and
bortezomib. We confirmed that the proteasome is involved in the
degradation of H1 subtypes in a subtype- and cell-type specific manner.Histon H1 ili vezni histon sudjeluje u regulaciji strukture kromatina (4).
Histon H1 dio je multigenske obitelji koja kodira jedanaest podtipova,
sedam somatskih podtipova i četiri podtipa specifična za zametnu liniju (1).
Komplement histona H1 definiran je kao sastav podtipa i njihov udio u
stanici u danom stanju. H1 komplement je varijabilan i nekoliko je studija
objavilo da se mijenja tijekom bolesti, posebice kod raka (2). Stoga je
potrebno provesti više studija kako bi se razumjele njegove funkcije u
bolestima. U ovoj studiji globalni cilj je razumjeti regulaciju ekspresije
somatskih podtipova u ljudskim staničnim linijama. Naš prvi cilj bio je
proučiti ulogu m6A u regulaciji razine mRNA i proteina podtipova histona
H1. Koristili smo cikloleucin za inhibiciju METTL3, m6A metiltransferaze.
Testirali smo nekoliko doza otkrivši da visoke doze inhibitora sprječavaju
sposobnost stanica da se repliciraju u istom vremenskom razdoblju kao i
netretirane stanice, a učinak cikloleucina ovisi o dozi u obje stanične linije.
U HEK293T cikloleucin je pokazao različite učinke na stanični ciklus ovisno
o dozi i vremenu liječenja. Nasuprot tome, u HeLa distribucija faza
staničnog ciklusa nije bila promijenjena u 24 sata ni u jednoj dozi. Podtipovi
H1 različito su pogođeni. Na razini mRNA, stanična linija HeLa pokazala je
promjenu razina mRNA koja se javlja u većini H1 gena i kontrola pri svim
testiranim dozama, uključujući najnižu dozu. Na razini proteina, uočene
promjene (povećanje ili smanjenje) u skladu su s promjenama uočenim u
mRNA, osim za H1.4. S obzirom na veličinu promjene, ne postoji
podudarnost između razine mRNA i proteina. Općenito, učinci su različiti
među podtipovima što podržava ideju da m6A igra specifičnu ulogu podtipa
u regulaciji H1. Naš drugi cilj bio je proučiti regulaciju razine H1 proteina
pomoću proteasoma u HeLa i HEK293T. Koristili smo inhibitore MG132 i
bortezomib. Potvrdili smo da je proteasom uključen u razgradnju podtipova
H1 na način specifičan za podtip i tip stanice
Computational and experimental therapeutic efficacy analysis of andrographolide phospholipid complex self-assembled nanoparticles against Neuro2a cells
No full textBackground: Neuroblastoma is one of the most common malignancies in childhood, accounts for approximately 7% of all malignancies. Andrographolide (AN) inhibits cancer cells progression via multiple pathways like cell cycle arrest, mitochondrial apoptosis, NF-κβ inhibition, and antiangiogenesis mechanism. Despite multiple advantages, application of AN is very limited due to its low aqueous solubility (6.39 ±0.47 μg/mL), high lipophilicity (log P ~ 2.632 ±0.135), and reduced stability owing to pH sensitive lactone ring.
Objectives and results: In present investigation, a molecular complex of AN with soya-L-α-phosphatidyl choline (SPC) was synthesized as ANSPC and characterized by FT-IR and1H NMR spectroscopy. Spectral and molecular simulation techniques confirmed the intermolecular interactions between the 14-OH group of AN and the N+(CH3)3 part of SPC. In addition, molecular dynamics (MD) simulation was used to determine the degree of interaction between various proteins such as TNF-α, caspase-3, and Bcl-2. Later, ANSPC complex was transformed in to self-assembled soft nanoparticles of size 201.8 ±1.48 nm with PDI of 0.092 ± 0.004 and zeta potential of 21.7 ± 0.85 mV. The IC50 of free AN (8.319 μg/mL) and the self-assembled soft ANSPC nano-particles (3.406 μg/mL ~ 1.2 μg of AN) against Neuro2a cells was estimated with significant (P <0.05) difference. Interestingly, the self-assembled soft ANSPC nanoparticles showed better endocytosis compared to free AN in Neuro2a cells. In vitro biological assays confirmed that self-assembled soft ANSPC nanoparticles induces apoptosis in Neuro2a cells by declining the MMP (Δψm) and increasing the ROS generation.
Conclusion: Self-assembled soft ANSPC nanoparticles warrant further in-depth antitumor study in xenograft model of neuroblastoma to establish the anticancer potential
Psoriasis - pathogenesis and treatment
No full textPsorijaza je kronična upalna bolest kože, karakterizirana abnormalnom proliferacijom keratinocita u gorenjem sloju kože. Ona je multigenska i imunološki posredovana bolest koja uključuje složene interakcije između prirođenog i stečenog imunološkog sustava, a u kojoj glavnu ulogu ima osovina interleukina (IL)-23/Th17 stanica. Genetski čimbenici u kombinaciji s okolišnim čimbenicima kao što su pretilost, stres, pušenje i infekcije, također doprinose razvoju i pogoršanju bolesti. Postoji nekoliko tipova psorijaze, od kojih je najčešći tip plak psorijaza koja je karakterizirana crvenkastim plakovima popraćenim srebrnastobijelim ljuskicama. Dijagnoza psorijaze temelji se na kliničkoj slici i povijesti bolesti u obitelji, no u rijetkim slučajevima može se provesti i biopsija. Za procjenu ozbiljnosti bolesti i utjecaja na kvalitetu života pacijenata koriste se Indeks područja i težine psorijaze (PASI) i Dermatološki indeks kvalitete života (DLQI). Osim procjene, ovi kriteriji također omogućuju i praćenje napretka bolesti te prilagodbu terapije prema potrebama pacijenata. Liječenje psorijaze razlikuje se ovisno o težini bolesti. Blagi oblici bolesti tretiraju se topikalnim terapijama i fototerapijom, dok se teži oblici, između ostalog, tretiraju biološkim agensima koji su pokazali velik napredak u liječenju psorijaze. Iako su postojeće terapije učinkovite, one uzrokuju niz nuspojava zbog čega postoji stalna potreba za razvojem novih i poboljšanih metoda liječenja. Budući pristupi bolesti uključuju razvoj biomarkera i primjenu Multi-Omics tehnologije za bolje razumijevanje i praćenje bolesti te inovacije u administraciji lijekova kao što su mikroigle i topikalni nanonosači. Psorijaza ima značajan utjecaj na kvalitetu života pacijenata te je povezana s komorbiditetima kao što su depresija, psorijatični artritis i kardiovaskularne bolesti zbog čega se zahtijeva holistički i multidisciplinarni pristup liječenja pacijenata te nove učinkovitije terapije.Psoriasis is a chronic inflammatory skin disease, characterised by abnormal proliferation of keratinocytes in the upper layer of the skin. It is a multigenic and immune-mediated disease that involves complex interactions between the innate and adaptive immune systems, in which the IL-23/Th17 axis plays a major role. Genetic factors combined with environmental factors such as obesity, stress, smoking and infections also contribute to the development and worsening of the disease. There are several types of psoriasis, but the most common type is plaque psoriasis, characterised by reddish plaques
accompanied by silvery-white scales. The diagnosis of psoriasis is based on the clinical picture and family history of the disease, but in rare cases, a biopsy can also be performed. The Psoriasis Area and Severity Index (PASI) and the
Dermatological Quality of Life Index (DQLI) are used to assess the severity of the disease and its impact on the patient's quality of life. These criteria are also used for monitoring the progress of the disease and adjusting the therapy according to the needs of the patients. Treatment of psoriasis varies depending on the severity of the disease. Mild forms of the disease are treated with topical therapies and phototherapy, while more severe forms are treated with biological agents that have shown great progress in the treatment of psoriasis. Although existing therapies are effective, they cause several side effects, which is why there is a constant need to develop new and improved treatment methods. Future approaches include the development of biomarkers and the application of Multi-Omics technology for better understanding and monitoring of the disease. Drug delivery innovations such as microneedles and topical nanocarriers are also being introduced. Psoriasis has a significant impact on the quality of life of patients and is associated with comorbidities such as depression, psoriatic arthritis and cardiovascular diseases, which require a holistic and multidisciplinary approach to the treatment of patients and new more effective treatments
Chronic pain – sex and age differences in pain threshold
No full textKronična bol je patološka pojava koja pogađa milijune diljem svijeta postavljajući jedinstvene izazove u dijagnozi i liječenju. Kroničnu bol karakterizira nelagoda odnosno, bol koja traje i nakon tipičnog razdoblja odravljenja kao posljedica dugotrajnih malignih mehanizama. Iako utječe na pojedince svih dobi i spolova, istraživanja ukazuju na značajne varijacije u tome kako se bol doživljava u različitim demografskim skupinama. Bol je vrlo složen i individualiziran fenomen na čiju modulaciju utječu biološki, psihološki i sociokulturni faktori. Razumijevanje dobno - spolnih razlika u pragovima moglo bi pokazati „tko je osjetljiviji na bol, žene ili muškarci, starija ili mlađa populacija”. Klinička aplikacija ovih podataka je ključna iz nekoliko razloga kao što su prilagođavanje strategija liječenja, potencijalni razvoj novih analgetika koji će se specijalizirati na specifične mehanizme bolnog puta te eliminacija rodnih predrasuda tijekom postavljanja analgeze i propisivanja tretmana.Chronic pain is a pathological condition which affects millions worldwide, posing unique challenges in diagnosis and treatment. Chronic pain is characterized by discomfort or pain that persists even after a typical period of healing and is a result of chronic pathological mechanisms. Although it affects individuals of all ages and genders, research indicates significant variation in how pain is experienced by different demographic groups. Pain is a very complex and individualized phenomenon whose modulation is influenced by biological, psychological and sociocultural factors. Understanding age-sex differences in thresholds could show "who is more sensitive to pain, women or men, older or younger populations". The clinical application of these data is crucial for several reasons, the adjustment of treatment strategies, the potential development of new analgesics that will specialize in specific mechanisms of the pain pathway and the elimination of gender biases during the setting of analgesia and the prescription of treatment.
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The frequency of SLCO1B1 c.388A>G and SLCO1B1 c.521T>C polymorphisms in the Croatian population
No full textPharmacogenetics plays a critical role in personalizing medicine, particularly in optimizing drug efficacy and minimizing adverse effects. The SLCO1B1 gene, encoding the SLCO1B1 transporter, is important for the hepatic uptake of statins, influencing their pharmacokinetics and pharmacodynamics. This study investigates the frequency of SLCO1B1 c.388A>G and SLCO1B1 c.521T>C polymorphisms in the Croatian population. A total of 459 individuals of Croatian descent were genotyped using the TaqMan® method. The results revealed that the c.388A>G polymorphism is nearly evenly distributed, with allele frequencies of 52.96% for the wild-type (A) and 47.04% for the variant (G). In contrast, the c.521T>C polymorphism was less common, with a wild-type allele (T) frequency of 80.94% and a variant allele (C) frequency of 19.06%. These findings align with previous studies conducted in both Croatian and European populations. Further analysis explored the relationship between these polymorphisms and demographic factors such as gender, age, and year of birth. While the c.388A>G polymorphism showed no significant associations with these variables, the c.521T>C polymorphism demonstrated a notable gender difference in its distribution in the heterozygous genotype (521T/C). Additionally, a significant correlation was observed between the year of birth and the homozygous variant genotype (521C/C), suggesting potential generational shifts in allele frequencies. The identification of such genetic variants in the Croatian population underscores the importance of integrating pharmacogenetic testing into routine clinical practice. By tailoring statin therapy to an individual's genetic profile, healthcare providers can optimize treatment efficacy while minimizing the risk of adverse drug reactions. This approach not only enhances patient care but also has broader implications for public health, potentially leading to more effective and personalized treatment strategies in Croatia and beyond. As the understanding of pharmacogenomics continues to evolve, studies like this contribute to the growing body of evidence supporting the clinical utility of genetic testing in optimizing drug therapy and advancing personalized healthcare
Connection between gut microbiome and development of Parkinson's disease
No full textOd samih početaka svoje evolucije, čovjek je koegzistrirao s mikroorganizmima koji su s njime uspostavili komenzalni odnos te
metaboličkim procesima znatno utjecali na njegovu fiziologiju. Od svih sustava u ljudskome tijelu najbolje je istražena gastrointestinalna mikrobna populacija, za koju se smatra da je uključena u komunikacijsku os između crijeva i mozga. Ovaj pojam sve češći je fokus znanstvenika jer se smatra da njegova modulacija, uzrokovana disbalansom crijevne mikrobiote,
uvelike utječe na razvoj homeostatskih anomalija. U ovom kontekstu posebnu kategoriju izučavanja predstavljaju neurodegenerativne bolesti među kojima se ističe Parkinsonova. Riječ je o kroničnoj multifaktorijalnoj bolesti od koje u svijetu boluje više od 7 milijuna ljudi, proživljavajući teške simptome motoričkog i nemotoričkog tipa. Nemogućnost sprječavanja progresije dopaminergičnog neuronskog propadanja i trenutno nedovoljno poznavanje mehanizama patogeneze poticaj su za definiranje novih potencijalnih terapijskih meta i pristupa liječenja. U posljednjih dvadesetak godina, najutjecajnija hipoteza mikrobiomske uključenosti bazirana je na ideji da određeni patogen gastrointestinalnog trakta (ili njegovi toksični metaboliti/gradivne komponente) potiče povećanje permeabilnosti barijere crijeva i proces pogrešnoga smatanja proteina α-sinukleina, odnosno njegovu transmisiju vagusnim živcem do središnjeg živčanog sustava gdje se agregira, što je svojstveno patologiji Parkinsonove bolesti. Većina drugih hipoteza sugerira da kompozicijske promjene mikrobiote ili infekcije specifičnim patogenima dovode do uspostave neuroinflamacijskog stanja i okoliša, a terapije koje uključuju probiotike, prebiotike i transplantaciju fekalne mikrobiote primjeri su odmaka u dosadašnjem pristupu liječenja nadomještajem dopamina. Pronalasku univerzalnog rješenja koje bi dovelo do potpunog izlječenja ipak predstoji još dug put interdisciplinarne suradnje i validiranja novih pretpostavki.Ever since his evolutional beginnings, man has coexisted with microorganisms that established a commensal relationship with him and significantly influenced his physiology through metabolic processes. Of all the systems in the human body, the gastrointestinal microbial population is the most well-studied, and it is thought to be involved in the communication axis between the gut and the brain. The scientists’ focus on this concept has largely increased because it is believed that its modulation, caused by the imbalance of intestinal microbiota, greatly affects the development of
homeostatic anomalies. Vast portion of research is centered around neurodegenerative diseases, among which Parkinson's stands out. It is a chronic multifactorial disease with more than 7 million patients worldwide
experiencing severe motor and non-motor symptoms. The inability to prevent further dopaminergic neuronal loss and currently insufficient knowledge of the pathogenesis mechanisms are motivational for defining new potential therapeutic targets and treatment approaches. In the last 20 years, the most influential hypothesis of microbiome involvement was based on the idea that a certain gastrointestinal pathogen (or its toxic metabolites/structural elements) causes a permeability increase in the intestinal barrier, as well as the misfolding of the protein α-synuclein, i.e. its transmission via the vagus nerve to the central nervous system where it aggregates, which is characteristic of the Parkinson's disease pathology. Other hypotheses mostly propose that compositional changes in the microbiota or infections with specific pathogens lead to the establishment of a neuroinflammatory state and environment. Although there are examples of progress in the treatment approach which currently mainly focuses on dopamine replacement (e.g. probiotics, prebiotics and fecal microbiota transplantation), much more interdisciplinary effort is needed in order to find a resolutive cure
Dataset of a project: "Preparation of lipid conjugates of pyridylporphyrins, their characterization and photodynamic activity"
No full textVirtual screening, structure based pharmacophore mapping, and molecular simulation studies of pyrido[2,3-d]pyrimidines as selective thymidylate synthase inhibitors
No full textHuman thymidylate synthase is the rate-limiting enzyme in the de novo synthesis of 2'-deoxythymidine-5'-monophosphate. dUMP (pyrimidine) and folate binding site hTS inhibitors showed resistance in colorectal cancer (CRC). In the present study, we have performed virtual screening of the pyrido[2,3-d]pyrimidine database, followed by binding free energy calculations, and pharmacophore mapping to design novel pyrido[2,3-d]pyrimidine derivatives to stabilize inactive confirmation of hTS. A library of 42 molecules was designed. Based on the molecular docking studies, four ligands (T36, T39, T40, and T13) were identified to have better interactions and docking scores with the catalytic sites [dUMP (pyrimidine) and folate binding sites] of hTS protein than standard drug, raltitrexed. To validate efficacy of the designed molecules, we performed molecular dynamics simulation studies at 1000 ns with principal component analysis and binding free energy calculations on the hTS protein, also drug likeness properties of all hits were in acceptable range. Compounds T36, T39, T40, and T13 interacted with the catalytic amino acid (Cys195), an essential amino acid for anticancer activity. The designed molecules stabilized the inactive conformation of hTS, resulting in the inhibition of hTS. The designed compounds will undergo synthesis and biological evaluation, which may yield selective, less toxic, and highly potent hTS inhibitors.Rezultati su dobiveni pomoću paketa za molekulsku dinamiku Amber 20
The role of microglia and astrocytes in glial scar formation
No full textSredišnji živčani sustav (SŽS) vrlo je osjetljiv na upalne procese, ozljede i traume. Obzirom da mu je regeneracija ograničena, ovaj je sustav razvio jedinstven odgovor na ozljedu, a čiji je temelj glijalni ožiljak. Glijalni ožiljak, kao heterogena struktura, građen je od više vrsta stanica, od kojih se ističu mikroglija i astrociti. Svojim specifičnim karakteristikama, ove stanice u zdravom SŽS-u održavaju homeostazu, dok u slučaju ozljede predvode njezinu ponovnu uspostavu. Mikroglija, smještena u samom parenhimu, glavni je imunosni čuvar ovog sustava, koji brojnim površinskim receptorima prepoznaje i najmanje promjene te brzo pokreće upalni odgovor. Specifični ameboidni oblik omogućuje joj obavljanje fagocitoze, ključne za održavanje ravnoteže SŽS-a. Astrociti, kao heterogene stanice obavljaju niz funkcija poput održavanja ionske homeostaze i krvnomoždane barijere (KMB), izgradnje neuronskih mreža, oblikovanja sinapsi te regulacije neurotransmitera. U slučaju ozljede SŽS-a, mikroglija i astrociti prolaze kroz niz morfoloških i funkcionalnih promjena koje rezultiraju formiranjem guste mreže astrocita oko lezije, kao i pojačanim mikroglijalnim uklanjanjem staničnog otpada. Dinamična komunikacija mikroglija i astrocita temelj je stabilnog i funkcionalnog ožiljka koji ograničava širenje upale i potiče regenerativni proces. Iako je glijalni ožiljak nužan za zaštitu zdravog tkiva, neke njegove komponente, poput kondroitin sulfat proteoglikana (CSPG) i kolagena I onemogućuju rast aksona i otežavaju oporavak SŽS-a. Otežana regeneracija pridonosi razvoju neurodegenerativnih bolesti, stoga je za razvoj novih terapija nužno razumjeti proces nastanka glijalnog ožiljka, s naglaskom na interakciju mikroglija i astrocita.The central nervous system (CNS) is highly sensitive to inflammatory processes, injuries, and trauma. Given its limited regenerative capacity, the CNS has developed a unique response to injury, whose major part is formation of a glial scar. The glial scar, a heterogeneous structure, contains multiple cell types, with microglia and astrocytes being particularly important. With their specific characteristics, these cells maintain homeostasis in a healthy CNS, while in case of injury they promote its recovery, which is limited. Microglia, located within the parenchyma, represent the primary immune guardians of this system. They detect the smallest changes through numerous surface receptors, quickly initiating an inflammatory response. Their specific amoeboid shape allows them to perform phagocytosis, which is crucial for maintaining CNS balance. Astrocytes, as heterogeneous cells, perform a variety of functions, including ionic homeostasis and the blood-brain barrier (BBB) maintenance, neural networks build up, synapses shaping, and neurotransmitters regulation. In the case of CNS injury, microglia and astrocytes undergo a series of morphological and functional changes, resulting in the formation of a dense astrocytic network around the lesion, as well as enhanced removal of cellular waste by microglia. The dynamic communication between microglia and astrocytes is fundamental to create a stable and functional scar that limits the spread of inflammation and promotes the regenerative process. Although the glial scar is essential for protecting healthy tissue, certain components, such as chondroitin sulfate proteoglycans (CSPGs) and collagen I, inhibit axonal growth and obstruct CNS recovery. Limited regeneration contributes to the development of neurodegenerative diseases; therefore, understanding the process of glial scar formation, with a focus on microglia-astrocyte interaction, is crucial for developing new therapies
Glioblastoma and neural stem cells: common characteristics
No full textOvaj rad istražuje usporedbu između neuralnih matičnih stanica (NMS) i glioblastoma (GBM), s posebnim naglaskom na razvoj novih terapijskih pristupa. NMS, koje su ključne za razvoj i regeneraciju mozga, posjeduju sposobnost samoobnove i diferencijacije u specijalizirane neuronske i glijalne stanice. Te sposobnosti su strogo regulirane, omogućujući fiziološku aktivnost mozga i njegovo obnavljanje nakon oštećenja. U usporedbi s NMS, GBM je maligni tumor kojeg karakterizira neometana proliferacija, invazivnost i otpornost na konvencionalne terapije. GBM koristi slične mehanizme samoobnove i diferencijacije kao NMS, no na disfunkcionalan način koji doprinosi njegovoj agresivnoj prirodi i sposobnosti širenja u okolna tkiva. Analizirani su različiti aspekti kako GBM održava svoje tumorske karakteristike u laboratorijskim uvjetima, uključujući genetske i epigenetske promjene koje utječu na njegov rast i invazivnost. Rad također razmatra nove terapijske pristupe koji se istražuju kako bi se poboljšala učinkovitost liječenja GBM. Naglasak je stavljen na prilagodbu postojećih terapeutskih strategija i razvoj inovativnih metoda koje se temelje na razumijevanju razlika između NMS i GBM. Ova usporedba omogućuje dublje razumijevanje mehanizama koji pridonose malignoj prirodi GBM i pruža temelje za buduća istraživanja i razvoj ciljanih terapija koje bi mogle unaprijediti liječenje ovog teškog oblika raka, čime bi se poboljšala prognoza za oboljele pacijente.This paper explores the comparison between neural stem cells (NSCs) and glioblastoma (GBM), focusing on the implications for developing new therapeutic approaches. NSCs, which are crucial for brain development and regeneration, possess the ability for self-renewal and differentiation into specialized neuronal and glial cells. These abilities are strictly regulated, enabling the physiological activity of the brain and its restoration after damage. In contrast to NSCs, GBM is a malignant tumor characterized by unrestricted proliferation, invasiveness, and resistance to conventional therapies. GBM utilizes similar mechanisms of self-renewal and differentiation as NSCs but in a dysfunctional manner that contributes to its aggressive nature and capacity to invade surrounding tissues. The work examines various aspects of how GBM maintains its tumor characteristics in laboratory settings, including genetic and epigenetic changes affecting its growth and invasiveness. New therapeutic approaches under investigation to improve the efficacy of GBM treatment will also be discussed. Emphasis is placed on adapting existing therapeutic strategies and developing innovative methods based on understanding the differences between NSCs and GBM. This comparison provides a deeper understanding of the mechanisms contributing to the malignant nature of GBM and offers groundwork for future research and the development of targeted therapies, potentially improving treatment outcomes and prognosis for patients with this challenging form of cancer