Chemical Engineering Journal, Journal Year: 2024, Volume and Issue: unknown, P. 158134 - 158134
Published: Nov. 1, 2024
Language: Английский
Cell Biology International, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 28, 2025
Breast cancer is a multifaceted and prevalent malignancy, impacting considerable proportion of women globally. Numerous signaling pathways intricately regulate cellular functions such as growth, proliferation, survival. Among the various regulators, lncRNAs have emerged significant players despite their inability to encode proteins. An expanding body literature underscores pivotal roles play in biology, particularly context breast cancer. Autophagy, process dedicated degradation recycling components, now recognized crucial factor initiation progression. The interplay between lncRNAs, pathways, autophagy pathophysiology remains an active area investigation. Researchers identified specific that are dysregulated patients, influencing modulation key pathways. Using experimental methodologies bioinformatics approaches, multiple been elucidated, providing deeper insights into contributions pathogenesis metastatic processes. In summary, pathophysiological landscape characterized by complex interactions involving lncRNA-mediated autophagy. This understanding paves way for identifying novel therapeutic targets, prognostic markers, diagnostic ultimately contributing improved treatment outcomes management.
Language: Английский
Citations
1
Phytomedicine, Journal Year: 2025, Volume and Issue: 137, P. 156377 - 156377
Published: Jan. 6, 2025
Language: Английский
Citations
0
International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(7), P. 3438 - 3438
Published: April 7, 2025
Approximately 70-80% of breast cancers are estrogen receptor-positive (ER+), with 65% these cases also being progesterone (ER+PR+). In most ER+ advanced cancer, endocrine therapy (ET) serves as the first-line treatment, utilizing various drugs that inhibit ER signaling. These include tamoxifen, a selective receptor modulator (SERM); fulvestrant, degrader (SERD); and aromatase inhibitors (AIs), which block synthesis. However, intrinsic or acquired hormone resistance eventually develops, leading to disease progression. The combination ET cyclin-dependent kinase 4 6 (CDK4/6is) has been shown significantly increase progression-free survival (PFS) and, in some cases, overall (OS). CDK4/6is works by arresting cell cycle G1 phase, preventing DNA synthesis, enhancing efficacy ET. This review highlights key mechanisms ET, whether used alone biological agents, well emerging therapeutic strategies aimed at overcoming resistance. Addressing remains work progress, near future, better patient selection for different approaches is expected through identification more precise genetic markers. particular, liquid biopsy may provide real-time portrait disease, offering insights into driving cancer
Language: Английский
Citations
0
Biomedicines, Journal Year: 2025, Volume and Issue: 13(4), P. 982 - 982
Published: April 17, 2025
Background/Objectives: Prenatal hypoxia (PH) is a leading cause of nervous system disorders in early childhood and subsequently leads to decline the cognitive mnemonic functions central (such as memory impairment, reduced learning ability, information processing). It also increases anxiety risk brain adulthood. Compensatory–adaptive mechanisms mother–placenta–fetus system, which enhance fetus’s CNS resilience, are known, including activation endogenous neuroprotection response hypoxic injury through pharmacological modulation HSP70. Methods: To evaluate effect HSP70 modulators—Cerebrocurin, Angiolin, Tamoxifen, Glutaredoxin, Thiotriazoline, HSF-1 (heat shock factor 1 protein), well Mildronate Mexidol—on motor skills, exploratory behaviors, psycho-emotional activities, learning, memories offspring after PH. Experimental PH was induced by daily intraperitoneal injections sodium nitrite solution into pregnant female rats from 16th 21st day pregnancy at dose 50 mg/kg. The newborns received Angiolin (50 mg/kg), Thiotriazoline Mexidol (100 Cerebrocurin (150 µL/kg), L-arginine (200 Glutaredoxin µg/kg), or mg/kg) for 30 days. At month, were tested open field test, 2 months, they trained working spatial radial maze. Results: Modeling led persistent impairments activity, behavior, decrease cognitive–mnestic CNS. found that had most pronounced effects on indicators activity status 1-month-old animals They exhibited significant cognitive-enhancing memory-supporting during training evaluation skill retention maze 2-month-old Conclusions: first time, we obtained experimental data modulators following intrauterine hypoxia. Based results this study, identified agents promising neuroprotective perinatal
Language: Английский
Citations
0
Antioxidants and Redox Signaling, Journal Year: 2025, Volume and Issue: unknown
Published: May 19, 2025
Background: Ferroptosis is a nonapoptotic type of cell death characterized by an increase in lipid reactive oxygen species (ROS). Acute myeloid leukemia (AML)-derived bone marrow mesenchymal stem cells (AML-BMSCs) support the progression and drug resistance AML secreting various bioactive substances, including exosomes. However, role BMSCs regulating metabolism ferroptosis remains unexplored. Results: Exosomes secreted AML-BMSCs increased expression miR-196a-5p cells. MiR-196a-5p promoted proliferation cells, reduced ROS ferroptosis, was associated with poor prognosis patients. Mechanistically, inhibited level neural precursor expressed developmentally down-regulated 4-like (NEDD4L). Co-immunoprecipitation (CO-IP) analysis showed that NEDD4L bound to long-chain acyl-CoA synthetase (ACSL)3 ubiquitin-mediated degradation ACSL3 protein. In addition, we also demonstrated highly Ras-associated binding protein 7A (RAB7A), which exosomal release. Importantly, cytarabine (Ara-C) activated RAB7A secretion miR-196a-5p, weakened ubiquitination NEDD4L, leading inhibition Ara-C AML. Innovation: This first time exosomes (BMSCs-exos) have been linked thereby expanding our understanding mechanism High levels inhibiting NEDD4L-mediated ACSL3. Conclusion: study identified new network through BMSCs-exos regulate We combined provide ideas for research targeting exosome ferroptosis. Antioxid. Redox Signal. 00, 000-000.
Language: Английский
Citations
0
Clinical and Experimental Medicine, Journal Year: 2024, Volume and Issue: 24(1)
Published: July 3, 2024
Despite being characterized by high malignancy, morbidity, and low survival rates, the underlying mechanism of hepatocellular carcinoma (HCC) has not been fully elucidated. Ferroptosis, a non-apoptotic form regulated cell death, possesses distinct morphological, biochemical, genetic characteristics compared to other types death. Dysregulated actions within molecular network that regulates ferroptosis have identified as significant contributors progression HCC. Long non-coding RNAs (lncRNAs) emerged influential diverse cellular processes, regulating gene function expression through multiple mechanistic pathways. An increasing body evidence indicates deregulated lncRNAs are implicated in malignant events such proliferation, growth, invasion, metabolism influencing Therefore, elucidating inherent role modulatory functions on HCC might promote development novel therapeutic interventions for this disease. This review provides succinct overview roles ferroptosis-related treatment, aiming drive promising targets biomarkers patients.
Language: Английский
Citations
2
PeerJ, Journal Year: 2024, Volume and Issue: 12, P. e17933 - e17933
Published: Aug. 26, 2024
LncRNA is a type of transcript with length exceeding 200 nucleotides, which was once considered junk no biological function during the transcription process. In recent years, lncRNA has been shown to act as an important regulatory factor at multiple levels gene expression, affecting various programmed cell death modes including ferroptosis. Ferroptosis, new form death, characterized by deficiency cysteine or inactivation glutathione peroxidase, leading depletion glutathione, aggregation iron ions, and lipid peroxidation. These processes are influenced many physiological processes, such Nrf2 pathway, autophagy, p53 pathway so on. An increasing number studies have that can block expression specific molecules through decoy effect, guide proteins function, promote interactions between scaffolds. action regulate key factors in metabolism, antioxidant metabolism epigenetic genetic regulation, thereby regulating process this review, we snapshotted mechanism ferroptosis example, emphasizing regulation on these pathways, helping fully understand evolution fate.
Language: Английский
Citations
1
International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 287, P. 138589 - 138589
Published: Dec. 9, 2024
Breast cancer (BC) is one of the common female cancers and it characterized by considerable problems regarding its development therapy. Long non-coding RNAs (lncRNAs) have been identified as significant modulators in BC development, especially, tumorigenicity chemoresistance. We therefore endeavor to present an up-to-date understanding lncRNAs their impact on progression treatment, concerning molecular processes, treatment options, use a therapeutic opportunity. LncRNAs are novel regulators genes that cause resistance directly functioning both coding patients, but little known about mechanisms actions. Thus, additional study required deeper modes action possible roles disease. This aims investigate functions BC, with particular attention role tumorigenesis, drug mechanisms, targets. will help identify targets improve effectiveness treatment.
Language: Английский
Citations
1
Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15
Published: Nov. 27, 2024
Breast cancer poses a serious threat to women's health globally. Current radiotherapy and chemotherapy regimens can induce drug-resistance effects in tissues, such as anti-apoptosis, anti-pyroptosis, anti-necroptosis, leading poor clinical outcomes the treatment of breast cancer. Ferroptosis is novel programmed cell death modality characterized by iron overload, excessive generation reactive oxygen species, membrane lipid peroxidation. The occurrence ferroptosis results from imbalance between intracellular peroxidation mechanisms (executive system) antioxidant (defensive system), specifically involving metabolism pathways, amino acid pathways. In recent years, it has been found that associated with progression various diseases, including tumors, hypertension, diabetes, Alzheimer's disease. Studies have confirmed triggering cells significantly inhibit proliferation invasion, improve sensitivity chemotherapy, making induction potential strategy for This paper reviews development concept ferroptosis, (including signaling pathways GSH-GPX4, FSP1-CoQ1, DHODH-CoQ10, GCH1-BH4) disease, latest research progress, summarizes on disease within framework metabolism, biology, biology. key regulatory factors well important concepts significant open questions field related natural compounds, are introduced. It hoped future will make further breakthroughs use treating cells. Meanwhile, compounds may also become new direction drug targeting treatment. provides theoretical basis opens up pathway drugs prevention
Language: Английский
Citations
0
Chemical Engineering Journal, Journal Year: 2024, Volume and Issue: unknown, P. 158134 - 158134
Published: Nov. 1, 2024
Language: Английский
Citations
0