Medical Oncology最新文献

{"title":"Contribution of tumor microenvironment (TME) to tumor apoptosis, angiogenesis, metastasis, and drug resistance.","authors":"Yanhong Xiao, Mahan Hassani, Melina Barahouei Moghaddam, Ahmad Fazilat, Masoud Ojarudi, Mohammad Valilo","doi":"10.1007/s12032-025-02675-8","DOIUrl":"10.1007/s12032-025-02675-8","url":null,"abstract":"<p><p>The tumor microenvironment (TME) contains tumor cells, surrounding cells, and secreted factors. It provides a favorable environment for the maintenance of cancer stem cells (CSCs), the spread of cancer cells to metastatic sites, angiogenesis, and apoptosis, as well as the growth, proliferation, invasion, and drug resistance of cancer cells. Cancer cells rely on the activation of oncogenes, inactivation of tumor suppressors, and the support of a normal stroma for their growth, proliferation, and survival, all of which are provided by the TME. The TME is characterized by the presence of various cells, including cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), CD8 + cytotoxic T cells (CTLs), regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), mesenchymal stem cells (MSCs), endothelial cells, adipocytes, and neuroendocrine (NE) cells. The high expression of inflammatory cytokines, angiogenic factors, and anti-apoptotic factors, as well as drug resistance mechanisms in the TME, contributes to the poor therapeutic efficacy of anticancer drugs and tumor progression. Hence, this review describes the mechanisms through which the TME is involved in apoptosis, angiogenesis, metastasis, and drug resistance in tumor cells.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"108"},"PeriodicalIF":2.8,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143634264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"αKG-induced oxidative stress and mTOR inhibition as a therapeutic strategy for liver cancer.","authors":"Sung Kyung Choi, Myoung Jun Kim, Jueng Soo You","doi":"10.1007/s12032-025-02653-0","DOIUrl":"10.1007/s12032-025-02653-0","url":null,"abstract":"<p><p>Despite the availability of targeted therapies, liver cancer remains a severe health burden. The need for adjuvant therapy to improve treatment efficacy and prevent recurrence is emerging. Alpha-ketoglutarate (αKG) is an intermediate in the tricarboxylic acid cycle and a cofactor for various oxygenases. A critical role of this multifunctional metabolite has started to be revealed in physiological and pathological conditions. We found that αKG exerts various anti-tumor effects in liver cancer cells. Our kinetic transcriptome study suggested that increasing reactive oxygen species and inhibiting mTORC1 signaling underlies. Indeed, αKG treatment elevated oxidative stress and induced DNA damage, presumably caused by early downregulation of the antioxidant gene SLC7A11. Further, we validated impaired mTOR signaling and decreased cellular energy production. This unique mechanism underscores αKG's potential as a liver cancer therapy by harnessing oxidative stress and disrupting metabolic signaling. These findings could provide valuable insights into further exploration of αKG as a promising therapeutic agent in liver cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"105"},"PeriodicalIF":2.8,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11906577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the antiangiogenic effect of AMG232 in multiple myeloma coculture systems.","authors":"Zahra Pooraskari, Hossein Barri Ghazani, Reyhane Piri, Sina Habibi, Minoo Shahidi","doi":"10.1007/s12032-025-02659-8","DOIUrl":"10.1007/s12032-025-02659-8","url":null,"abstract":"<p><p>This study explored the efficacy of AMG232, a potent and selective MDM2 inhibitor, as an antiangiogenic agent in a multiple myeloma (MM) cell line (AMO-1) cocultured with endothelial cells (HUVECs) in vitro. HUVECs and AMO-1 cells were cocultured in transwell systems. Cell viability was assessed through an MTT assay after exposure to various concentrations of AMG232. Following treatment, gene expression changes were analyzed via quantitative real-time PCR. Wound healing and tube formation assays were also conducted to quantify the effects on cell migration and angiogenesis. AMG232 showed dose-dependent cytotoxicity in AMO-1 cells (IC₅₀ = 386.1 nM), whereas HUVECs were moderately sensitive (IC₅₀= 942.1 nM). In coculture, both cell types displayed increased resistance to AMG232, indicating a protective cell-cell interaction. Treatment with 250-nM AMG232 significantly downregulated the mRNA expression of angiogenic factors-including VEGF-A, VEGFR-2, MMP-2, IL-6, and HIF-1α-in both AMO-1 cells and HUVECs (P < 0.05). Wound healing assays revealed that AMG232 markedly inhibited HUVEC migration, with significantly reduced wound closure rates at 24 and 48 h compared with the controls (P < 0.01). Tube formation assays further revealed that AMG232 substantially decreased angiogenesis in HUVECs, as evidenced by reductions in junction number, mesh number, and total tube length (P < 0.01). Our research revealed that AMG232 effectively inhibited angiogenesis and exhibited cytotoxic effects on MM cells by downregulating key angiogenic factors and impairing endothelial cell functions. These results suggest that AMG232 has significant potential as a therapeutic agent for targeting angiogenesis in MM treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"107"},"PeriodicalIF":2.8,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual targeting of CXC chemokine receptor 4 and multidrug resistance protein 1 by ZIN056 effectively combat daunorubicin resistance in acute myeloid leukemia cells.","authors":"Mohammad Abohassan, Mesfer Mohammad Al Shahrani, Sarah Khaled AlOuda, Prasanna Rajagopalan","doi":"10.1007/s12032-025-02656-x","DOIUrl":"10.1007/s12032-025-02656-x","url":null,"abstract":"<p><p>Drug resistance, associated with the overexpression of CXC chemokine receptor CXCR4 and multidrug resistance protein 1 (MDR1) remains a significant barrier to effective therapy in Acute Myeloid Leukemia (AML). Targeting both CXCR4 and MDR1 could potentially enhance treatment efficacy in resistance. In silico computational screening of the Zinc natural product library using Discovery Studio Visualizer, Protein-Ligand Interaction Profiler, GROMACS, and GMX_MMPBSA techniques were used. THP-1, and SKM-1 cells were used for in vitro analysis. Flow cytometry was employed for target analysis and apoptosis enumerations. The virtual screening identified ZIN056 with favorable binding affinities of - 10.6 kcal/mol and - 9.1 kcal/mol for CXCR4 and MDR1, respectively. MD simulations demonstrated stable binding interactions, with Root Mean Square Deviation values around 0.2 nm for both proteins. The ΔG binding calculations further confirmed values of - 30.09 kcal/mol for CXCR4 and - 34.47 kcal/mol for MDR1, indicating energetically favorable binding. The compound inhibited the THP-1 and SKM-1 cell proliferation with GI₅₀ values of 250.6 nM, and 346.7 nM, respectively. ZIN056 decreased CXCR-4 expression and MDR1-induced positive population (MDR1⁺) in THP-1 and SKM-1 cells. ZIN056 inhibited the proliferation of the regular and MDR1⁺ AML cells, while Daunorubicin exhibited a tenfold resistance in controlling MDR1⁺ AML cell proliferation. ZIN056-induced apoptosis in MDR1 + AML cells, whereas Daunorubicin failed to promote apoptosis in these cells. The findings suggest that dual targeting of CXCR4 and MDR1 using ZIN056 may offer a promising strategy to overcome drug resistance in AML and provide a foundation for further development of dual inhibitors for AML patients.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"106"},"PeriodicalIF":2.8,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combination therapy using parthenolide and doxorubicin induces apoptosis in Raji cells: insights into miR-27b and signaling pathway alterations.","authors":"Zahra Zare-Badie, Farahnaz Zare, Banafsheh Rastegari, Gholamhossein Tamaddon","doi":"10.1007/s12032-025-02673-w","DOIUrl":"10.1007/s12032-025-02673-w","url":null,"abstract":"<p><p>Burkitt lymphoma, a highly aggressive form of non-Hodgkin lymphoma, have significant treatment challenges, such as chemotherapy-related toxicity and the risk of relapse, especially in older adults. Treatment of Raji cells, a Burkitt lymphoma cell line, with parthenolide in combination to doxorubicin may enhance therapeutic efficacy. This study aimed to evaluate cell viability and apoptosis following treatment with these agents, and to investigate the underlying molecular mechanisms involving miR-27b and the MET/PI3K/AKT signaling pathway. Raji cells were treated with varying concentrations of parthenolide and doxorubicin for 48 and 72 h, cell viability was assessed using the MTT assay, and apoptosis was quantified using flow cytometry. Subsequently, we performed quantitative RT-PCR to evaluate the expression levels of miR-27b, MET, PI3K, and AKT. The half-maximum inhibitory concentration (IC₅₀) values of 976.1 nM for doxorubicin and 4.39 µM for parthenolide were determined at 48 h. The apoptosis rate increased from 7.6% in the untreated control to 44.5% and 49.2% for doxorubicin and parthenolide, respectively, reached to 81.2% at higher doses of parthenolide in combination (p < 0.001). miR-27b expression was significantly upregulated, particularly in the combination group (p < 0.001). MET and PI3K expression was significantly downregulated by the combination treatments (p < 0.05). In conclusion, combination of parthenolide and doxorubicin exert enhanced cytotoxic effects via increased apoptosis and modulation of miR-27b and the MET signaling pathway in Raji cells, regulatory relationship between miR-27b and the MET signaling pathway may contribute to the observed therapeutic benefits. Further research is required to clarify the molecular mechanisms and therapeutic applications of this combination strategy.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"99"},"PeriodicalIF":2.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advancements in genistein nanocarrier systems for effective cancer management.","authors":"Diya Arora, Vanshita, Hemant Bhati, Keshav Bansal","doi":"10.1007/s12032-025-02649-w","DOIUrl":"10.1007/s12032-025-02649-w","url":null,"abstract":"<p><p>Cancer continues to be a significant global health concern, consistently ranking as one of the leading causes of mortality across diverse populations and socio-economic contexts. Genistein, a soy-derived isoflavonoid, has gained significant attention for its diverse health benefits, particularly its potent anticancer activity. Emerging pre-clinical and clinical evidences highlights its ability to modulate key cellular processes, including apoptosis, autophagy, angiogenesis, metastasis, immune responses and cell cycle regulation. Despite its therapeutic potential, the clinical translation of genistein is limited by its poor pharmacokinetics, low aqueous solubility, and rapid metabolic degradation, resulting in suboptimal bioavailability. To address these limitations, various nanotechnology-based formulations have been developed, significantly improving the bioavailability, stability, and therapeutic efficacy of genistein. Functionalized nanocarriers further enhance its effectiveness by enabling targeted drug delivery, reducing off-target toxicities, and achieving sustained release at the tumor site. This review provides a comprehensive overview of advanced nanoformulations for genistein delivery emphasizing their efficacy against prevalent cancers such as breast, lung, and colon cancer. By exploring the interplay between genistein's therapeutic potential and innovative drug delivery systems, this review underscores the transformative impact of nanotechnology in overcoming the limitations of conventional cancer therapies and improving patience compliance.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"101"},"PeriodicalIF":2.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PKM2 knockout facilitates the activation of the AMPK/KLF4/ACADVL pathway, leading to increased oxidative degradation of fatty acids in TNBC.","authors":"Linghan Zhang, Li Cheng, Yingchao Ma, Junlin Li, Yue Zhong, Xiuzhi Zhu, XiaoMin Leng, Fuhua Xie","doi":"10.1007/s12032-025-02671-y","DOIUrl":"10.1007/s12032-025-02671-y","url":null,"abstract":"<p><p>This study unveils PKM2 as a master metabolic coordinator in triple-negative breast cancer (TNBC), governing the glycolysis-lipolysis balance through the AMPK/KLF4/ACADVL axis. We demonstrate stage-specific PKM2 upregulation in TNBC, with CRISPR/Cas9 knockout inducing dual metabolic reprogramming-suppressed glycolysis and activated lipid catabolism. Mechanistically, PKM2 ablation triggers AMPK-dependent nuclear translocation of KLF4, which directly activates ACADVL (mitochondrial β-oxidation rate-limiting enzyme), explaining lipid droplet depletion. Therapeutically, synergistic lethality emerges from combining PKM2 knockout with ACADVL inhibition, suggesting metabolic redundancy disruption strategies. Unlike PKM2-SCAP-mediated lipogenesis reported elsewhere, our work establishes a KLF4-driven lipid catabolic pathway specific to TNBC. Crucially, this AMPK/KLF4/ACADVL network operates independently of BRCA status, proposing targeted therapy for chemoresistant non-BRCA mutant TNBC. Our findings redefine TNBC metabolic plasticity through transcriptional-metabolic crosstalk, offering combinatorial therapeutic paradigms against metabolic adaptation.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"102"},"PeriodicalIF":2.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal RNAs and EZH2: unraveling the molecular dialogue driving tumor progression.","authors":"Ahmed Hussein Zwamel, Abdulrahman T Ahmad, Farag M A Altalbawy, H Malathi, Amandeep Singh, Majid S Jabir, Zafar Aminov, Madan Lal, Abhinav Kumar, Sabrean F Jawad","doi":"10.1007/s12032-025-02648-x","DOIUrl":"10.1007/s12032-025-02648-x","url":null,"abstract":"<p><p>The EZH2 gene encodes an enzyme that is part of the epigenetic factor Polycomb Repressive Complex 2 (PRC2). In order to control gene expression, PRC2 mainly modifies chromatin structure. In this complex process, EZH2 methylates histone proteins, which in turn suppresses further RNA transcriptions. As a result, EZH2 dysregulations can occasionally induce abnormal gene expression patterns, which can aid in the development and progression of cancer. Non-coding RNAs significantly impact the expression of EZH2 through epigenetic mechanisms. Meanwhile, normal and cancerous cells frequently release vesicles into the extracellular matrix, also known as exosomes, that occasionally carry RNA molecules from their origin cells, including messenger RNAs, microRNAs, and other non-coding RNAs. Thus exosomes are granted the ability to regulate numerous physiological functions and act as crucial messengers between cells by influencing gene expression in the recipient cell. We conducted this review to focus on EZH2's substantial biological role and the mechanisms that regulate it, driven by the desire to understand the possible impact of exosomal RNAs on EZH2 expression.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"103"},"PeriodicalIF":2.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fisetin as a chemoprotective and chemotherapeutic agent: mechanistic insights and future directions in cancer therapy.","authors":"Rabab Fatima, Priyal Soni, Mousmee Sharma, Parteek Prasher, Rajesh Kaverikana, Shivaprasad Shetty Mangalpady, Javad Sharifi-Rad, Daniela Calina","doi":"10.1007/s12032-025-02664-x","DOIUrl":"10.1007/s12032-025-02664-x","url":null,"abstract":"<p><p>Cancer remains a leading cause of mortality globally, characterized by the uncontrolled proliferation of abnormal cells, invasion of healthy tissues, and potential metastasis. Natural compounds have become a focus in cancer research due to their potential therapeutic roles. Among these, fisetin, a dietary flavonoid, demonstrates notable anti-cancer properties through various molecular mechanisms. This review evaluates the chemoprotective and chemotherapeutic potential of fisetin, focusing on its mechanisms of action against cancer and its capacity to enhance cancer treatment. A systematic literature search was conducted across PubMed, Web of Science, and Scopus databases using keywords related to fisetin and cancer. The review synthesizes findings from in vitro and in vivo studies examining fisetin's effects on signaling pathways, apoptosis induction, oxidative stress modulation, and synergistic potential with chemotherapeutic agents. Fisetin has shown the ability to suppress tumor growth and metastasis by modulating critical signaling pathways, including PI3K/Akt/mTOR, NF-κB, and MAPK. It induces apoptosis in cancer cells through mitochondrial and endoplasmic reticulum stress responses and demonstrates antioxidative properties by reducing reactive oxygen species. Additionally, fisetin enhances the efficacy of conventional chemotherapies, indicating its role as a potential adjuvant in cancer treatment. Fisetin presents a promising natural compound with diverse anti-cancer effects, impacting cell cycle arrest, apoptosis, and oxidative stress pathways. Further clinical studies are warranted to fully elucidate its therapeutic potential and to optimize its delivery for improved bioavailability in cancer patients.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"104"},"PeriodicalIF":2.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative approach to decipher pharmacological mechanism of Cinnamomum zeylanicum essential oil in prostate cancer.","authors":"Debajani Mohanty, Sucheesmita Padhee, Arpita Priyadarshini, Rout George Kerry, Biswabhusan Dash, Ambika Sahoo, Sudipta Jena, Pratap Chandra Panda, Haseeb Ahmad Khan, Sanghamitra Nayak, Asit Ray","doi":"10.1007/s12032-025-02665-w","DOIUrl":"10.1007/s12032-025-02665-w","url":null,"abstract":"<p><p>Prostate cancer has garnered much importance in recent years due to its rising incidence and mortality among men worldwide. The ineffectiveness of existing therapies and adverse events associated with conventional treatment have led patients to turn towards traditional medicine for the management of prostate cancer. Cinnamomum zeylanicum bark essential oil (CZEO) possesses promising anticancer properties, yet the exact mechanism of action of CZEO for the management of prostate cancer remains unclear. Therefore, the current study tried to elucidate the bioactive components and key potential targets through which CZEO may exert its anticancer effect for treating prostate cancer. Fifty-nine constituents were identified by GC-MS, of which 52 were drug-like constituents. A total of 2847 targets related to CZEO and 2283 targets related to prostate cancer were obtained from public databases and the GEO dataset. Twenty-three overlapping targets exist between CZEO and disease targets. Compound-disease-target network analysis revealed camphor, eugenol, methyl eugenol, trans farnesyl acetate and nerol as the core bioactive ingredients of CZEO. The topological screening of the PPI network revealed BCL2, TNF, NFKBIA, CREBBP and IL7R as potential hub targets. These hub targets were validated based on mRNA expression level, pathological stages, overall survival, immune infiltrate and genetic alteration analysis in prostate adenocarcinoma and normal patients. KEGG enrichment analysis proposed that CZEO exhibits its anticancer effect mainly by modulating the PI3-AKT and MAPK signalling pathway. Moreover, molecular docking and dynamics simulation studies revealed a good binding affinity of these core compounds with TNF, NFKBIA and BCL2. CZEO exhibited a remarkable anti-proliferative effect against PC-3 cells with an IC₅₀ value of 13.56 µg/mL. CZEO promoted apoptosis and cell cycle arrest in the G2/M phase in PC-3 cells. CZEO-induced apoptosis was due to loss of mitochondrial membrane potential, increase in reactive oxygen species levels and activation of caspases (caspase 3, caspase 8 and caspase 9). RT-qPCR analysis revealed that CZEO modulated the mRNA expression level of hub genes (BCL2, TNF, NFKBIA, CREBBP, and IL7R, caspase 3, caspase 8 and caspase 9). The present study provides a mechanistic approach of Cinnamomum zeylanicum essential oil against prostate cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"100"},"PeriodicalIF":2.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}