Cancers, Год журнала: 2024, Номер 16(23), С. 4048 - 4048
Опубликована: Дек. 2, 2024
Lung cancer, a malignant neoplasm originating from the epithelial cells of lung, is characterized by its aggressive growth and poor prognosis, making it leading cause cancer-related mortality globally [...].
Язык: Английский
Life, Год журнала: 2025, Номер 15(1), С. 126 - 126
Опубликована: Янв. 18, 2025
Post-translational modifications (PTMs) of proteins dynamically build the buffering and adapting interface between oncogenic mutations environmental stressors, on one hand, cancer cell structure, functioning, behavior. Aberrant PTMs can be considered as enabling characteristics long they orchestrate all malignant variability in proteome cells, cancer-associated tumor microenvironment (TME). On other enhance anticancer mechanisms tumoral ecosystem or sustain beneficial effects oncologic therapies through degradation inactivation carcinogenic or/and activation tumor-suppressor proteins. In this review, we summarized analyzed a wide spectrum involved regulatory that drive tumorigenesis, genetic instability, epigenetic reprogramming, events metastatic cascade, cytoskeleton extracellular matrix (ECM) remodeling, angiogenesis, immune response, tumor-associated microbiome, metabolism rewiring most important hallmarks cancer. All develop due to proteins, which modulate gene transcription, intracellular signaling, protein size, activity, stability localization, trafficking, secretion, half-life, protein–protein interactions (PPIs). associated with exploited better understand underlying molecular heterogeneous chameleonic disease, find new biomarkers progression prognosis, personalize oncotherapies, discover targets for drug development.
Язык: Английский
Процитировано
2
Cancer Cell International, Год журнала: 2025, Номер 25(1)
Опубликована: Фев. 12, 2025
Язык: Английский
Процитировано
1
Acta Pharmaceutica Sinica B, Год журнала: 2025, Номер 15(2), С. 737 - 756
Опубликована: Янв. 1, 2025
Antibody-drug conjugates (ADCs) are antitumor drugs composed of monoclonal antibodies and cytotoxic payload covalently coupled by a linker. Currently, 15 ADCs have been clinically approved worldwide. More than 100 clinical trials at different phases underway to investigate the newly developed ADCs. represent one fastest growing classes targeted in oncology drug development. It takes advantage specific targeting tumor-specific antigen deliver chemotherapeutic precisely tumor cells, thereby producing promising efficacy favorable adverse effect profiles. However, emergence resistance has severely hindered In this review, we introduce structure mechanism ADCs, describe development summarized latest research about mechanisms ADC resistance, discussed strategies overcome predicted biomarkers for treatment response ADC, aiming contribute future.
Язык: Английский
Процитировано
0
Ecotoxicology and Environmental Safety, Год журнала: 2025, Номер 290, С. 117587 - 117587
Опубликована: Янв. 1, 2025
Chlorpyrifos (CPF) is a broad-spectrum organophosphate chloride (OP) insecticide widely used in domestic use and open field. However, there currently no relevant research revealing the toxic effects of CPF exposure on skin, then it necessary to comprehensively understand mechanisms. The results showed that skin tissue structure function mice were significantly disrupted after exposure. Furthermore, PPI network analysis molecular docking experiments pinpointed core targets such as Bcl2, EGFR, Caspase-3, TNF-α, IL-1β, VEGF. Additionally, through KEGG analysis, VEGF apoptosis signaling pathways identified pivotal implicated CPF-induced toxicity. These subsequently confirmed animal experimentation. In conclusion, our study suggests primarily induces damage by disrupting function, mediated proliferation processes cells, alongside aberrant angiogenesis heightened inflammatory response. insights are expected advance development preventive therapeutic strategies aimed at mitigating adverse skin.
Язык: Английский
Процитировано
0
European Journal of Medicinal Chemistry, Год журнала: 2025, Номер 286, С. 117291 - 117291
Опубликована: Янв. 19, 2025
Язык: Английский
Процитировано
0
Cancer Drug Resistance, Год журнала: 2025, Номер unknown
Опубликована: Янв. 25, 2025
Small-molecule BRAF inhibitors (e.g., vemurafenib and dabrafenib) MEK (MAPK/ERK) kinases trametinib) have distinctly improved the survival of patients suffering from BRAF-mutant cancers such as melanomas. However, emergence resistance to inhibitor-based melanoma therapy, well reduced sensitivity other CRC, poses a considerable clinical problem. For instance, reactivation MAPK/ERK signaling hampering cell death induction mechanisms was responsible for inhibitor resistance, which can be correlated with distinct post-translational epigenetic processes. Histone deacetylases (HDACs) are prominent drug targets some HDAC already been clinically approved therapy various blood cancers. In addition, several HDACs were identified, also play crucial role in Consequently, inhibition described promising approach overcome resistance. This review summarizes influence (Zn2+-dependent NAD+-dependent sirtuins) on based upregulated prevention tumor death. Moreover, it outlines reasonable HDAC-based strategies circumvent BRAF-associated downregulated mechanisms.
Язык: Английский
Процитировано
0
Foods, Год журнала: 2025, Номер 14(3), С. 381 - 381
Опубликована: Янв. 24, 2025
Gintonin, a non-saponin glycolipoprotein from Panax ginseng, acts as lysophosphatidic acid ligand. However, its anticancer effects, especially in melanoma, remain unclear. This study investigated the anti-proliferative effects and intracellular signaling mechanisms of gintonin-enriched fraction (GEF) ginseng human melanoma cell lines. In vitro, GEF treatment significantly inhibited proliferation, reduced clonogenic potential, delayed wound healing cells. Flow cytometry terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining showed that induced apoptosis, evidenced by increased apoptotic populations nuclear changes. also caused cycle arrest G1 phase for A375 cells G2/M A2058 It triggered via activation caspase-3, -9, poly (ADP-ribose) polymerase cleavage, downregulation B lymphoma-2 (Bcl-2). raised reactive oxygen species (ROS) levels mitochondrial stress, which were mitigated N-acetyl cysteine (NAC), an ROS inhibitor. vivo, suppressed tumor growth A375- A2058-xenografted mice without toxicity. These findings suggest has potential antitumor inducing apoptosis arrest, presenting promising therapeutic avenue.
Язык: Английский
Процитировано
0
Frontiers in Oncology, Год журнала: 2025, Номер 15
Опубликована: Янв. 30, 2025
Cell death mechanisms are broadly classified into accidental cell (ACD) and regulated (RCD). ACD such as necrosis, is an uncontrolled, process, while RCD tightly by specific signaling pathways molecular mechanisms. Tumor cells characterized their ability to evade sustain uncontrolled proliferation. The failure of programmed a key contributor tumor initiation, progression, resistance cancer therapies. Traditionally, research has focused primarily on apoptosis the dominant form in cancer. However, emerging evidence highlights importance other non-apoptotic forms RCD, pyroptosis, ferroptosis, necroptosis, parthanatos, tumorigenesis treatment response. These gaining attention for potential roles overcoming therapy resistance. In this review, we will discuss recent advances study malignant tumors explore therapeutic implications, offering insights new targets strategies.
Язык: Английский
Процитировано
0
International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(5), С. 1881 - 1881
Опубликована: Фев. 22, 2025
What is apoptosis? The Nomenclature Committee on Cell Death and numerous other pioneering cancer/p53 biologists use the terms "apoptosis" "cell death" interchangeably, disregard mind-numbing complexity heterogeneity that exists within a tumor (intratumor heterogeneity), contribution of polyploid giant cancer cells (PGCCs; root causes therapy resistance relapse) to this heterogeneity, then propose novel apoptosis-stimulating anticancer strategies. This shocking for following three reasons. First, clinical studies reported since 1990s have revealed increased apoptosis in solid tumors associated with diversity poor prognosis. Second, we known years dying (apoptotic) release panel secretions (e.g., via phoenix rising pathways) promote metastatic outgrowth. Third, over decade ago, it was demonstrated can recover from late stages (after formation apoptotic bodies) homeostatic process anastasis, resulting emergence aggressive variants. cell surface expression CD24 has recently been be preferentially enriched recovered (anastatic) exhibit tumorigenic properties. These related discoveries outlined herein call paradigm shift oncology focus strategies minimize occurrence treacherous tumor-repopulating events therapy-induced dormancy reactivation). They also raise an intriguing question: deregulated anastasis (rather than evasion apoptosis) hallmark cancer?
Язык: Английский
Процитировано
0
Blood Science, Год журнала: 2025, Номер 7(2), С. e00221 - e00221
Опубликована: Март 11, 2025
Hematological malignancies encompass a diverse range of blood-related cancers characterized by abnormal blood cell production. These cancers, classified the World Health Organization based on lineage, origin, and progression, provide more comprehensive framework for understanding cancer biology. This classification has significantly advanced research, particularly in genetic analyses diagnosis treatment. Despite recent clinical improvements, challenges, such as relapse, resistance, high mortality, remain unresolved. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), protein that induces apoptosis cells without affecting normal cells, emerged promising therapeutic target. However, its efficacy is limited factors, tumor heterogeneity resistance to TRAIL signaling. review examines mechanisms hematological malignancies, factors contributing current state preclinical highlighting potential strategies enhance TRAIL-based therapies cancers.
Язык: Английский
Процитировано
0