Medical OncologyPub Date : 2025-02-23DOI: 10.1007/s12032-025-02633-4
Mohamed J Saadh, Wajida Ataallah Khidr, Karar H Alfarttoosi, Ashok Kumar Bishoyi, Subbulakshmi Ganesan, Aman Shankhyan, S Gayathri, Jasur Rizaev, Waam Mohammed Taher, Mariem Alwan, Mahmood Jasem Jawad, Ali M Ali Al-Nuaimi
{"title":"Metal nanoparticles as a promising therapeutic approach for prostate cancer diagnosis and therapy: a comprehensive review.","authors":"Mohamed J Saadh, Wajida Ataallah Khidr, Karar H Alfarttoosi, Ashok Kumar Bishoyi, Subbulakshmi Ganesan, Aman Shankhyan, S Gayathri, Jasur Rizaev, Waam Mohammed Taher, Mariem Alwan, Mahmood Jasem Jawad, Ali M Ali Al-Nuaimi","doi":"10.1007/s12032-025-02633-4","DOIUrl":"10.1007/s12032-025-02633-4","url":null,"abstract":"<p><p>Prostate cancer is a leading cause of mortality among men worldwide, particularly in the USA and European nations, with an estimated 1.9 million new cases and over 580,000 deaths annually, according to recent global statistics. The treatment of prostate tumors presents significant clinical challenges, due to the disease's high metastatic potential, specifically to vital organs, such as the liver, lungs, bones, and brain. The intrinsic heterogeneity of prostate cancer cells, characterized by diverse genetic, molecular, and phenotypic profiles, complicates conventional therapeutic strategies, highlighting the need for advanced diagnostic and treatment modalities. Nanoparticles play a critical role in oncology field due to their unique physicochemical properties, including high surface area-to-volume ratio and the ability to be functionalized with targeting ligands. Metallic-based nanoparticles exhibits significant potential for applications in field of nanomedicine, drug delivery systems, gene silencing methods, radiotherapy enhancement, cancer diagnostics, and targeted therapeutic interventions. Metal nanoparticles have substantially improved the sensitivity and specificity of major imaging modalities and have demonstrated remarkable efficacy as biosensors for the detection of prostate cancer-specific biomarkers. This review article provides an in-depth analysis of the utilization of metal nanomaterials in prostate cancer, focusing on their roles in enhancing therapeutic efficacy, advancing diagnostic precision, and supporting the development of novel treatment strategies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"83"},"PeriodicalIF":2.8,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483681","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":"STM2457 impairs the proliferation of esophageal squamous cell carcinoma by activating DNA damage response through ATM-Chk2 axis.","authors":"Chuanli Gao, Hui Yang, Jiao Cheng, Shuang He, Yong Yang, Lei Xu, Qiang Ma, Xiaolan Guo, Xiaowu Zhong","doi":"10.1007/s12032-025-02634-3","DOIUrl":"10.1007/s12032-025-02634-3","url":null,"abstract":"<p><p>METTL3 has been proven to play an important role in the proliferation of Esophageal squamous cell carcinoma (ESCC). In this study, we focused on investigating the therapeutic role and molecular mechanism of STM2457 in ESCC, which is a novel small-molecule inhibitor of METTL3. The effect of STM2457 on ESCC was evaluated using ESCC cell lines by the cell viability measurement, cloning formation assay, scratching assay, transwell assay, and flow cytometry techniques. Furthermore, the molecular mechanism study was employed to evaluate by RT-qPCR, Western blotting, proteomics analysis, comet assay, etc. Additionally, the anticancer effect of STM2457 was carried out by nude mice tumor xenograft in vivo. This study showed STM2457 could significantly inhibit the proliferation and migration of Eca109 and KYSE150 cells, which promoted G0/G1 phase arrest and apoptosis in a dose-dependent manners in vitro. Moreover, proteomics analysis suggested the important role of ATM in action mechanism of STM2457. Further studies showed that STM2457 may activate DNA damage response and the expression of ATM, p-ATM, p-Chk2, and γ-H2AX protein in ATM-Chk2 pathway. Intriguingly, ATM inhibitor CGK-733 and knocking down ATM significantly reduced the expression of ATM in Eca109 and KYSE150 cells treated with STM2457. Importantly, STM2457 significantly upregulated the expression of ATM and γ-H2AX protein and inhibited the growth of ESCC in vivo. Finally, STM2457 combined with PTX could also significantly inhibit the proliferation and migration ability of Eca109 and KYSE150 cells by targeting the ATM-mediated DDR pathway. In tumor-bearing nude mice model, STM2457 combined with Paclitaxel can inhibit the growth of ESCC and increased the expression of ATM and γ-H2AX protein. These findings revealed ATM-Chk2 pathway is a promising therapeutic target for STM2457 to effectively inhibit the proliferation of ESCC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"82"},"PeriodicalIF":2.8,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476088","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}
Medical OncologyPub Date : 2025-02-21DOI: 10.1007/s12032-025-02629-0
Garen S Sellers, McKade A Poirier, Trenton G Mayberry, Braydon C Cowan, Mark R Wakefield, Yujiang Fang
{"title":"From conventional to cutting edge: an exploration of osteosarcoma treatments.","authors":"Garen S Sellers, McKade A Poirier, Trenton G Mayberry, Braydon C Cowan, Mark R Wakefield, Yujiang Fang","doi":"10.1007/s12032-025-02629-0","DOIUrl":"10.1007/s12032-025-02629-0","url":null,"abstract":"<p><p>Osteosarcoma is a highly aggressive cancer in children and young adults that has a remarkably high mortality rate upon metastasis. Current standard treatments have remained largely unchanged for nearly five decades, focusing on a combination of chemotherapy with high-dose methotrexate, doxorubicin, and cisplatin, complemented by aggressive surgical resections. Despite this lack of change, recent advancements in medical research have spurred hope for more effective and less invasive approaches to managing osteosarcoma. In this review, we provide an overview of existing therapeutic modalities, including chemotherapy regimens tailored to tumor stage and patient response, radiation therapies aimed at local tumor control, and advanced surgical techniques such as limb-sparing procedures. Additionally, we explore two promising future treatments that are currently under investigation for osteosarcoma cases: targeted therapies utilizing nanomaterials like graphene oxide and innovative oncolytic viruses. This review highlights potential breakthroughs in treatment options while identifying areas that warrant further investigation in the management of osteosarcoma. Considering the limited advancements in treatment over the past decades, identifying and highlighting novel and effective therapies is vital for improving patient outcomes and survival rates.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"81"},"PeriodicalIF":2.8,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468502","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}
Medical OncologyPub Date : 2025-02-20DOI: 10.1007/s12032-025-02630-7
Md Anwarul Haque, Thanasis Poullikkas, F M Al-Amin Kaisar, Shariful Haque, Mst Hajera Khatun, Al Mamun, Alam Khan
{"title":"PHLPP1 depletion promotes tumorigenesis and stemness in triple-negative breast cancer cells through AKT signaling.","authors":"Md Anwarul Haque, Thanasis Poullikkas, F M Al-Amin Kaisar, Shariful Haque, Mst Hajera Khatun, Al Mamun, Alam Khan","doi":"10.1007/s12032-025-02630-7","DOIUrl":"10.1007/s12032-025-02630-7","url":null,"abstract":"<p><p>Breast cancer, particularly triple-negative breast cancer (TNBC), is a major cause of women's mortality, and effective treatment options are still lacking due to the absence of known mechanisms and biomarkers. Therefore, unveiling novel molecular mechanisms to identify potential biomarkers is urgently needed to ensure an effective TNBC treatment. In this study, we investigated the role of PHLPP1, a tumor suppressor gene, in the tumorigenesis and induction of cancer stem cells in TNBC using publicly available data and experimental protocols. Our study found that lower levels of PHLPP1 contributed negatively to patient overall survival. In addition, loss of PHLPP1 increased breast cancer cell proliferation, long-term colony regrowth ability, and the number of migrated and invaded cells. Consequently, we designed a stable PHLPP1 knockdown (KD) cell line to understand its impact through its stemness potential. As expected, PHLPP1 KD dramatically upregulated breast cancer stemness markers (NANOG, OCT4, and SOX2) expression and significantly increased cancer stem cell frequencies in TNBC cells. Mechanistically, PHLPP1 loss enhanced AKT phosphorylation at Ser473, thus activating AKT signaling, leading to larger tumor formation in vivo and elevated stemness expression. This study concludes that PHLPP1 has the capability to reduce the expression of cancer stemness genes by negatively regulating the AKT signaling pathway. Therefore, these findings may pave the way for discoveries in the context of cancer stemness and future strategies for developing effective treatment options for TNBC patients.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"80"},"PeriodicalIF":2.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468519","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}
Medical OncologyPub Date : 2025-02-19DOI: 10.1007/s12032-025-02625-4
Nazlı Çil, Elif Önder, Ayşe Nur Damar, Seyedmahdi Tabatabaei, Ümit Çabuş, Gülçin Abban Mete
{"title":"In vitro cytotoxic and apoptotic effects of boric acid on endometrial adenocarcinoma cell lines (HEC-1B and Ischikawa).","authors":"Nazlı Çil, Elif Önder, Ayşe Nur Damar, Seyedmahdi Tabatabaei, Ümit Çabuş, Gülçin Abban Mete","doi":"10.1007/s12032-025-02625-4","DOIUrl":"10.1007/s12032-025-02625-4","url":null,"abstract":"<p><p>Endometrial carcinoma, the most common malignancy of the female genital tract, remains challenging to treat despite early-stage dominance. Surgical interventions and irradiation are insufficient for advanced endometrial cancer. Our aim was to investigate to explore the in vitro cytotoxicity and apoptotic effects of boric acid (BA) on endometrial adenocarcinoma cell lines (Ishikawa and HEC-1B cell lines), providing experimental evidence for the potential application of boric acid as an anticancer drug. Time- and dose-dependent cell viability was determined with the XTT cell proliferation test. Differences in mRNA levels were determined by RT-PCR using cDNAs and SYBR green assay. Colony formation and the effect of BA on wound healing were evaluated. Immunocytochemistry and TUNEL tests were performed to evaluate apoptosis. BA increased the expression of Caspase 3 and Bax in HEC-1B and Ischikawa cell lines. It was determined that BA significantly decreased the number of colonies in both cell lines (p < 0.05). In HEC-1B and Ishikawa cell lines, there was an increase in cell migration in the control group at 16 and 24 h. The apoptotic index was higher in the BA group, although it was not statistically significant. According to immunohistochemistry results, Caspase 3 and Bax expression in HEC-1B and Ishikawa cell lines were statistically increased in BA group. The expression of Bcl-2 was decreased statistically with BA treatment in both cell lines (p = 0.0001). BA treatment inhibited cell migration and colony formation, which are important for carcinogenesis, in endometrial adenocarcinoma cell lines. This inhibition was shown to occur through the apoptotic pathway.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"79"},"PeriodicalIF":2.8,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11839787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458591","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}
Medical OncologyPub Date : 2025-02-18DOI: 10.1007/s12032-025-02627-2
Apurwa Mishra, Trupti N Patel
{"title":"Locking the gates of immortality: targeting alternative lengthening of telomeres (ALT) pathways.","authors":"Apurwa Mishra, Trupti N Patel","doi":"10.1007/s12032-025-02627-2","DOIUrl":"10.1007/s12032-025-02627-2","url":null,"abstract":"<p><p>Telomere maintenance is essential for the unlimited proliferation of cancer cells. While most cancers reactivate telomerase to preserve telomeres, approximately 10-15% utilize the alternative lengthening of telomeres (ALT), a telomerase-independent mechanism driven by homologous recombination. ALT is primarily observed in sarcomas and neuroepithelial tumors and it is characterized by hallmarks such as heterogeneous telomere lengths, the presence of ALT-associated PML bodies (APBs), extrachromosomal telomeric repeats (ECTRs), and elevated replication stress. This review has a threefold aim: (1) to examine the mechanisms of ALT activation, (2) to highlight existing therapeutic interventions targeting ALT components and telosomic complexes, and, (3) to pinpoint potential molecular targets for novel anticancer treatments. Therapeutic strategies focus on disrupting APBs, stabilizing G-quadruplex structures, and inhibiting replication stress proteins such as FANCM and SMARCAL1. Emerging evidence highlights the role of shelterin proteins like TRF1 and TRF2, chromatin remodeling factors such as ATRX and DAXX, and the dysregulated cGAS-STING pathway in facilitating ALT activity. Moreover, the inhibitory role of RAP1-SUN1 protein interactions in telomere recombination provides a novel therapeutic avenue. Recent advances have elucidated the intricate balance of replication stress, DNA damage response, and recombination in ALT regulation. These insights can help overcome challenges posed by ALT + cancers, including their ability to transition from telomerase-dependent states. Targeting ALT-specific vulnerabilities offers a promising direction for developing innovative therapies that exploit the unique biology of ALT-driven tumors.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"78"},"PeriodicalIF":2.8,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441360","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":"Ovarian cancer and its management through advanced drug delivery system.","authors":"Sujit Bose, Shubham Sharma, Atul Kumar, Yachana Mishra, Vijay Mishra","doi":"10.1007/s12032-025-02621-8","DOIUrl":"10.1007/s12032-025-02621-8","url":null,"abstract":"<p><p>Ovarian cancer is the deadliest gynecological cancer, often being diagnosed at a late-stage when the disease is already advanced. This makes it known as the ''silent killer'' due to its high mortality rate among women. The ovary itself is composed of three main types of cells epithelial cells, germ cells, and stromal cells. Over 90% of all occurrences of ovarian cancer are epithelial ovarian carcinoma. Ovarian cancer is responsible for 2.5% of cancer in women. The primary signs include stomach bloating, trouble eating or feeling full rapidly, fatigue, and discomfort during intercourse. The management of ovarian cancer is improved by advanced drug delivery systems because they increase therapeutic targeting, reduce side effects, and overcome drug resistance. Accurate distribution to cancer cells is made possible by methods such as ligand-functionalized nanomedicines, dual-targeted nano-drugs, drug conjugates, antibody-drug conjugates and peptide/folate drug conjugates. These technologies enhance individualized and successful ovarian cancer treatment outcomes by maximizing chemotherapy efficacy, extending drug release, and lowering toxicity.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"76"},"PeriodicalIF":2.8,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441291","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}
Medical OncologyPub Date : 2025-02-17DOI: 10.1007/s12032-025-02626-3
Tomas Zemanek, Lubos Danisovic, Andreas Nicodemou
{"title":"Exosomes and solid cancer therapy: where are we now?","authors":"Tomas Zemanek, Lubos Danisovic, Andreas Nicodemou","doi":"10.1007/s12032-025-02626-3","DOIUrl":"10.1007/s12032-025-02626-3","url":null,"abstract":"<p><p>Cancer immunotherapy has revolutionized oncology, offering new hope for patients with previously incurable cancers. However, solid tumors remain a significant challenge due to immune evasion, therapeutic resistance, and the immunosuppressive tumor microenvironment. Exosomes, a specialized subset of extracellular vesicles, have emerged as promising tools in cancer therapy owing to their unique role in intercellular communication and immune modulation. These vesicles transport antigens, major histocompatibility complex (MHC) molecules, and immune-modulatory cargo, positioning them as potential platforms for cancer vaccines, drug delivery systems, and combinatorial therapies. Advances in engineered exosomes have improved drug bioavailability, tumor targeting, and immune stimulation, showcasing their potential in personalized medicine. This review highlights their multifaceted role in the tumor microenvironment, and their mechanisms of action in solid cancer therapy. Additionally, we discuss emerging strategies to overcome clinical and technical hurdles, paving the way for novel and effective cancer treatments.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"77"},"PeriodicalIF":2.8,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11832697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441347","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":"Ciprofloxacin-encapsulated solid lipid nanoparticles: a comprehensive biochemical analysis of cytotoxic effects, proliferation inhibition, and apoptotic induction in KG1-a leukemia cells.","authors":"Salma Hussein Kadhim, Gholamreza Dehghan, Majid Mahdavi","doi":"10.1007/s12032-025-02619-2","DOIUrl":"10.1007/s12032-025-02619-2","url":null,"abstract":"<p><p>As a fundamental approach to the treatment of acute myeloid leukemia (AML), chemotherapeutic agents face significant clinical challenges, including poor solubility and low bioavailability. In this context, solid lipid nanoparticles (SLNs) have emerged as a promising drug delivery system in oncologic therapies, owing to their advantageous characteristics, such as enhanced physical stability and controlled drug-release profiles. This study focuses on the synthesis of ciprofloxacin (CP)-loaded SLNs, aiming to enhance the anticancer efficacy of CP, an antibiotic recognized for its potential anticancer properties, while simultaneously reducing its associated side effects. Characterization of blank SLN and CP-SLN was conducted using dynamic light scattering (DLS), atomic force microscopy (AFM), UV-Vis spectrophotometry, and Fourier transform infrared spectroscopy (FTIR). In vitro release was carried out using dialysis bag method in isotonic phosphate buffer (pH = 7.4). The anticancer and pro-apoptotic effects of the CP-SLN formulation were assessed through cell viability assays, Hoechst staining, and Annexin V/PI flow cytometry. Additionally, expression levels of Bax, Bcl2, and p53 were analyzed via Real-Time PCR. The synthesized CP-SLN formulation exhibited optimal characteristics, including a particle size of 340-360 nm, a polydispersity index (PDI) of 0.4, and an entrapment efficiency of 90%. The in vitro drug release showed an initial burst release in the time points 4-10 h. Both CP and the CP-SLN formulations demonstrated significant anti-proliferative and pro-apoptotic effects on KG1-a cells, as indicated by the upregulation of the Bax/Bcl2 ratio and p53, resulting in G0/G1 cell cycle arrest and apoptosis induction. The results suggest that encapsulating CP in SLN enhances its anticancer and pro-apoptotic effects in KG1-a stem-like leukemia cells. Thus, CP-SLN may serve as a promising formulation for leukemia treatment and could improve the efficacy of other therapeutic agents.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"75"},"PeriodicalIF":2.8,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143408452","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}
Medical OncologyPub Date : 2025-02-11DOI: 10.1007/s12032-025-02618-3
Tülin Burhanoğlu, Zehra Seda Halbutoğulları, Gulseren Turhal, Asuman Demiroglu-Zergeroglu
{"title":"Evaluation of the anticancer effects of hydroxycinnamic acid isomers on breast cancer stem cells.","authors":"Tülin Burhanoğlu, Zehra Seda Halbutoğulları, Gulseren Turhal, Asuman Demiroglu-Zergeroglu","doi":"10.1007/s12032-025-02618-3","DOIUrl":"10.1007/s12032-025-02618-3","url":null,"abstract":"<p><p>Research on breast cancer stem cells (BCSCs) is crucial for improving our understanding of their roles in tumor resistance, metastasis, and relapse. This study investigated the anti-cancer effects of two isomers of hydroxycinnamic acids (HCA): para-coumaric acid (PCA) and ortho-coumaric acid (OCA) on breast cancer stem cells (BCSCs). The isolated and characterized stem cells contained CD44 + /CD24 surface markers, exhibited high levels of aldehyde dehydrogenase activity, and were able to form mammospheres. The evaluation of HCAs on stem cell proliferation, cell cycle, and apoptosis was conducted by comparing them with MCF-7, the luminal breast cancer cell line. The viability and immunoblot analyses demonstrated that HCA applications resulted in a dose-dependent decrease in the number of viable cells and inhibited phosphorylation of Extracellular regulated kinases 1/2 (ERK1/2). These findings were supported by the detection of suppressed colony formation and delayed wound-healing in HCA-exposed cells. E-cadherin expression increased in OCA-treated cells. Additionally, the arrest of G1/S phase progression and the downregulation of Cyclin D1 expression exhibited that OCA and PCA-induced cytostatic effects in BSCS cells. After treatment, the increased Annexin-V/7-AAD staining, along with elevated expression of caspase-3/7 and a decreased Bcl-2/Bax ratio, indicated apoptosis mediated by the activation of Janus kinase (JNK) and p38 Mitogen-activated kinase (p38 MAPK). In conclusion, both OCA and PCA exhibit anti-carcinogenic potential on BCSCs; However, OCA has a stronger effect and is becoming a promising candidate for further research.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"73"},"PeriodicalIF":2.8,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11814044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391223","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}