Medical Oncology最新文献

{"title":"Bioactive compounds in Raphanus sativus: mechanisms of apoptosis, anti-angiogenesis, cell cycle arrest and beyond in cancer prevention and treatment.","authors":"Tooba Naveed, Shaukat Ali, Muhammad Summer","doi":"10.1007/s12032-025-02894-z","DOIUrl":"https://doi.org/10.1007/s12032-025-02894-z","url":null,"abstract":"<p><p>Raphanus sativus or radish is rich in bioactive compounds such as phenolic, antioxidant enzymes, carbohydrates, glucosinolates, terpenes, coumarins, alkaloids, flavonoids (anthocyanin), amino acids, carotenoids, organic acids, and isothiocyanates that have antioxidant and chemopreventive properties. The prominent compounds present in radish are glucosinolates, isothiocyanates, sulforaphane, flavonoids, phenethyl isothiocyanates, etc., that through various mechanisms play an important role in the prevention and treatment of various cancers such as, liver, prostate, colon, oral, lung, cervical, breast, blood, and gastric cancers. The major mechanisms involved are alterations in biotransformation enzymes, such as Phase I and Phase II enzymes, which could help the body detoxify or remove xenobiotics; apoptotic induction caused by secondary glucosinolate metabolites; anti-tumorigenesis through preventing angiogenesis, invasion, migration, and metastasis of cancer cells; using cell cycle arrest to limit the development of cancer cells; anti-proliferation; and antioxidant potential and modulation of epigenetic. These bioactive compounds also exhibit anti-tumor mechanisms that target various cancer cell lines. This review highlights the mechanistic role of various bioactive compounds present in Raphanus sativus for the treatment and prevention of various cancers and also explains their role in various cancer cell lines.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"328"},"PeriodicalIF":2.8,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619021","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":"Resveratrol in oral cancer: a systematic review of preclinical studies on its anticancer mechanisms and therapeutic potential.","authors":"Bingru Li, Omer Qutaiba B Allela, Wadhah Hasan Alkhazali, Nasir Vadia, S Renuka Jyothi, Rajashree Panigrahi, Ashish Singh Chauhan, Surbhi Singh, Malika Akhrorova, Hayder Naji Sameer, Ahmed Yaseen, Zainab H Athab, Mohaned Adil","doi":"10.1007/s12032-025-02903-1","DOIUrl":"10.1007/s12032-025-02903-1","url":null,"abstract":"<p><strong>Objective: </strong>Oral cancer remains a major global health challenge due to its aggressive nature, high recurrence rates, and limited treatment options. Resveratrol (RV), a naturally occurring polyphenol, has demonstrated promising anticancer properties in various malignancies, including oral cancer. This systematic review aimed to evaluate preclinical evidence on RV's therapeutic effects in oral cancer, focusing on its mechanisms of apoptosis induction, metastasis inhibition, autophagy regulation, and immune modulation.</p><p><strong>Methods: </strong>A systematic review was conducted following PRISMA guidelines, with a comprehensive search in Google Scholar, PubMed, Embase, Scopus, and Web of Science for preclinical studies published up to March 2, 2025. Both in vitro and in vivo studies investigating RV's effects on oral cancer were included based on predefined inclusion and exclusion criteria. Data extraction was performed independently by multiple researchers, with discrepancies resolved through consensus. Key mechanisms of RV's anticancer activity, including apoptosis, metastasis suppression, autophagy, and immune regulation, were analyzed.</p><p><strong>Results: </strong>Out of 346 studies screened, 19 (four in vivo and 15 in vitro) met the eligibility criteria. RV exhibited potent anticancer effects in a dose- and time-dependent manner, significantly reducing oral cancer cell viability and tumor growth in animal models. Mechanistically, RV induced apoptosis through caspase-3, -7, and -9 activation and modulation of pro-apoptotic (Bax, Bak) and anti-apoptotic (Bcl-2, Bcl-XL) proteins. RV also inhibited key oncogenic pathways, including Akt/mTOR and JAK2/STAT3, thereby suppressing tumor proliferation and immune evasion. Additionally, RV impaired metastatic progression by downregulating EMT-related transcription factors (TWIST, SLUG, and Zeb1) and reducing angiogenic markers such as VEGF and MMPs. Notably, RV induced autophagy in a dose- and time-dependent manner, as evidenced by increased LC3-II, Beclin1, and p62 expression. In cisplatin-resistant oral cancer models, RV promoted both apoptotic and autophagic cell death, suggesting its potential as an adjuvant therapy.</p><p><strong>Conclusion: </strong>This systematic review underscored the potential of RV as a promising anticancer agent for oral cancer. Through apoptosis induction, metastasis suppression, autophagy modulation, and immune regulation, RV demonstrated broad-spectrum anticancer effects. However, its low bioavailability remains a significant challenge. Future research should focus on optimizing drug delivery strategies, such as nanoparticle formulations and combination therapies, to enhance RV's therapeutic efficacy and facilitate clinical translation.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"329"},"PeriodicalIF":2.8,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626689","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":"LINC01410 in cancer: a comprehensive review of its oncogenic role, regulatory mechanisms, and clinical implications.","authors":"Saman Morovat, Pejman Morovat, Ashkan Kalantary-Charvadeh, Marzieh Mojbafan, Shahram Teimourian","doi":"10.1007/s12032-025-02889-w","DOIUrl":"https://doi.org/10.1007/s12032-025-02889-w","url":null,"abstract":"<p><p>LINC01410 is classified as a long non-coding RNA (lncRNA) that plays a pivotal role in cancer biology. Non-coding RNAs, including lncRNAs, have been recognized for their significant regulatory functions in various cellular processes, making them crucial for understanding the mechanisms underlying cancer development and progression. This review aims to synthesize the current knowledge of LINC01410's contributions to cancer development, and progression across different tumor types, highlighting its potential roles as a biomarker and therapeutic target. A comprehensive literature review was performed, encompassing experimental, clinical, and bioinformatics studies that examined LINC01410's expression profiles and functional roles in various cancers. Studies were selected based on their relevance to LINC01410's involvement in oncogenic processes and their methodological rigor. LINC01410 exhibits differential expression in several cancers, often correlates with tumor aggressiveness and patient prognosis. Mechanistically, LINC01410 acts as a competing endogenous RNA, regulating gene expression by sequestering microRNAs, which in turn modulates the expression of target mRNAs. This lncRNA has been implicated in promoting cancer cell proliferation, invasion, lymphangiogenesis, and chemoradiotherapy resistance underscoring its multifaceted roles in tumor biology. The exploration of LINC01410 has important implications in cancer diagnosis and therapy, positioning it as a potential biomarker for disease progression and a therapeutic target for intervention strategies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"325"},"PeriodicalIF":2.8,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619023","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":"N-ethyl-N-nitrosourea (ENU) alters cytokine expression in the bone marrow modifying the marrow microenvironment to develop leukemia.","authors":"Priyatosh Nath, Chaitali Sarkar, Prosun Tribedi, Debasish Maiti","doi":"10.1007/s12032-025-02882-3","DOIUrl":"https://doi.org/10.1007/s12032-025-02882-3","url":null,"abstract":"<p><p>Cytokines in the bone marrow (BM) microenvironment play a pivotal role in regulating hematopoiesis. In hematological disease including leukemia, altered levels of BM cytokines highlight the significance of its signaling in leukemogenesis. Elucidating the dynamics of cytokine expression and signaling in the BM is thus essential for uncovering new therapeutic targets and improving treatment outcomes. This study hypothesizes that chronic changes in cytokine expression within the BM drive the development of leukemia. To test this hypothesis, we designed a longitudinal animal experiment wherein mice were injected with the carcinogen N-ethyl-N-nitrosourea (ENU) and subsequently sacrificed at 10 distinct and even time points spanning 2-20 weeks after ENU exposure. Comparative analysis of BM samples from ENU-injected and normal mice revealed significant alterations in cytokine expression, oxidative stress, and key proteins involved in DNA synthesis and cell cycle regulation. The dynamic changes in the expression of studied cytokines, oxidative stress balance, and proteins like PCNA and NF-κB indicate modulation of the marrow microenvironment. These changes, which vary with exposure time, might impact the cellular processes in hematopoietic stem cells (HSCs) to give rise to leukemia. This study investigated the dynamic expression of hematopoietic and inflammatory genes, hinting at the critical role of deregulated cytokine expression in leukemia induction. The outcomes of this study will inform future research aimed at elucidating cytokine interactions in leukemogenesis.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"324"},"PeriodicalIF":2.8,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619024","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":"Protective role of ursolic acid against cisplatin-induced oxidative stress and ferroptosis in the liver of Swiss albino mice.","authors":"Sandra Kannampuzha, Abilash Valsala Gopalakrishnan","doi":"10.1007/s12032-025-02854-7","DOIUrl":"https://doi.org/10.1007/s12032-025-02854-7","url":null,"abstract":"<p><p>Cisplatin is a widely used anticancer drug, but its therapeutic use is often limited by systemic toxicities, including hepatotoxicity. Ursolic acid, a natural pentacyclic triterpenoid with antioxidant properties, may help reduce such toxic effects. Recent studies have implicated the role of ferroptosis in cisplatin-induced tissue damage. This study investigates the protective role of ursolic acid against cisplatin-induced liver damage in Swiss albino mice, with a focus on ferroptosis and the expression of TFR1 as well as caspase-3. Mice were divided into five groups (n = 6): Control (DMSO), Cisplatin alone (10 mg/kg), Cis + UA1 (10 mg/kg + 10 mg/kg), Cis + UA2 (10 mg/kg + 40 mg/kg), and UA alone (40 mg/kg). The mice were sacrificed after treatment, and the liver tissues were assessed for biochemical markers (ALT, AST, ALP), oxidative stress (ROS, antioxidant capacity), iron content, and histopathological changes. Immunohistochemical analysis of TFR1 was performed to confirm the involvement of ferroptosis. The expression pattern of caspase-3, which is a crucial executioner of apoptosis, was also evaluated. It was observed that cisplatin intake gradually reduced the body weight and increased the levels of hepatic enzymes. Cisplatin treatment also led to significant increases in ROS levels, iron accumulation, and notable histopathological damage in liver tissue. Mice with ursolic acid treatment demonstrated reduced ROS levels and liver enzymes and also presented with the restoration of antioxidant capacity and improved tissue structure. The expression of the ferroptosis marker TFR1 was also altered in the combination groups along with reduced caspase-3 expression suggesting the attenuation of apoptotic and implication of ferroptosis. This supports the protective role of ursolic acid. These results show that ursolic acid can be an excellent candidate to mitigate the systemic toxic effects of cisplatin and act as an adjuvant in combination with chemotherapies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"327"},"PeriodicalIF":2.8,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619025","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":"Effects of 3-Bromo-2-oxopropionic acid and LiCl treatment combined with electroporation on apoptotic and metabolic responses in DLD-1 colon cancer cells.","authors":"Güney Gürsoy, Zehra Çiçek","doi":"10.1007/s12032-025-02898-9","DOIUrl":"https://doi.org/10.1007/s12032-025-02898-9","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Colon cancer is particularly increasing in incidence in developed countries, and it ranks first in terms of morbidity and mortality worldwide. As in other types of cancer, metabolic changes and cellular death mechanisms play a critical role in cancer treatment. Cancer cells prefer glycolysis for energy production even in the presence of oxygen; this phenomenon is known as the Warburg effect. Glycolysis, which is essentially an anaerobic process, provides metabolic adaptation by preventing mitochondrial oxidative phosphorylation in cancer cells. Electroporation (EP) is a method that increases the uptake of drugs into the cell by creating temporary pores in the cell membrane. 3-Bromo-2-oxopropionic acid and Lithium chloride (LiCl) are agents that may show anticancer potential through different mechanisms. The aim of this study was to investigate the potential anticancer effects of the EP-assisted combination of 3-Bromo-2-oxopropionic acid and LiCl agents in DLD-1 colon cancer cells and to evaluate how these effects occur at the level of cell viability, apoptotic activity and metabolic markers. In the study, cell viability was evaluated by WST-8 tetrazolium based colorimetric method. Within the scope of analysis of apoptotic activity and metabolic responses; caspase-3, Phosphatidylinositol 3-kinase (PI3K) and Glucose transporter-1 (GLUT-1) levels were determined by ELISA method. While no change in cell viability was observed at 10 and 20 µM doses of 3-Bromo-2-oxopropionic acid, a significant decrease was detected in its combination with EP. IC&lt;sub&gt;50&lt;/sub&gt; value was determined as 37.99 ± 2.34 µM in a single application and as 27.33 ± 1.99 µM in its combination with EP. While low doses of LiCl (5 and 10 mM) did not affect cell viability, a significant decrease was detected at doses of 50, 75 and 100 mM. In its combination with EP, a significant loss of viability was observed even at low doses and the IC&lt;sub&gt;50&lt;/sub&gt; value decreased from 98.92 ± 0.64 mM to 81.88 ± 1.64 mM. A decrease in IC&lt;sub&gt;50&lt;/sub&gt; doses is observed in the treatment with the combination of both 3-Bromo-2-oxopropionic acid and LiCl with EP. The combined treatment enables the same lethal effect on cancer cells with lower drug doses. Caspase-3 activity increased significantly in combined applications with EP. While 3-Bromo-2-oxopropionic acid alone did not change the level of PI3K, it caused a significant increase in its combination with EP. While LiCl caused an increase in the level of PI3K at low doses, a decrease was detected in its combination with EP. Regular partial increases in GLUT-1 level were determined in a dose-dependent manner in 3-Bromo-2-oxopropionic acid treatment alone. A similar increase was determined at 20 and 30 µM doses combined with EP, while a decrease occurred at 40 µM. While no significant increase was detected in GLUT-1 levels compared to the control group in 10 mM LiCl treatment alone and in combination with EP, a significant increase was detected in","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"326"},"PeriodicalIF":2.8,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619022","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":"The role of radiotheranostics in personalized treatment for breast cancer.","authors":"Dheeraj Sharma, Shriyansh Srivastava, Naga Rani Kagithala, Kalpana Pravin Rahate, Sathvik Belagodu Sridhar","doi":"10.1007/s12032-025-02825-y","DOIUrl":"https://doi.org/10.1007/s12032-025-02825-y","url":null,"abstract":"<p><p>Radiotheranostics merges diagnostic imaging and targeted radionuclide therapy to allow treatment of breast cancer to be tailored individually. It employs radiopharmaceuticals and molecular imaging modalities such as PET and SPECT for accurate characterization and treatment of the tumor. The review presents the mechanisms, clinical uses, and future potential of radiotheranostics in breast cancer. The review focuses on the potential of nuclear medicine in driving personalized treatment through biomarker-guided strategies. We discussed recent literature on well-established biomarkers like HER2, ER, and PR as well as novel targets like TROP-2. Theranostic agents like ^177Lu-DOTA-trastuzumab and novel innovations with alpha-emitters as well as dual-targeting nanoparticles are noted. Radiotheranostic agents have enhanced results, most importantly, in HER2-positive patients with metastatic or advanced breast cancer. Therapeutic promise also is brought by recent advances to hard-to-treat subtypes, such as triple-negative breast cancer. While radiotheranostics holds great promise, its wider use in the clinic is hampered by factors like heterogeneity of biomarkers, dosimetry accuracy, and regulatory limitations. Research continues to affirm its revolutionary role in the administration of tailor-made treatment regimens to breast cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"322"},"PeriodicalIF":2.8,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608740","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":"Anatolian propolis extracts enhance cisplatin efficacy in ovarian cancer through AKT/mTOR pathway modulation and demonstrate antibacterial and antibiofilm activities.","authors":"Esra Erdoğan, Berna Özdem, Özge Öztürk Çimentepe, İbrahim Tekedereli","doi":"10.1007/s12032-025-02888-x","DOIUrl":"https://doi.org/10.1007/s12032-025-02888-x","url":null,"abstract":"<p><p>Propolis, a natural resinous substance rich in bioactive compounds, has been traditionally used for its therapeutic properties. This study investigates the cytotoxic and anticancer effects of Anatolian propolis on ovarian cancer cells, focusing on its modulation of the AKT/mTOR pathway and its ability to enhance cisplatin efficacy. Its antimicrobial and antibiofilm properties were also assessed, addressing infection risks in immunocompromised cancer patients. In epithelial ovarian cancer (A2780) cell line, apoptosis, cell cycle progression, and cell viability were evaluated using flow cytometric analysis, propidium iodide/annexin V staining, and MTS assay, respectively. The signaling pathways were analyzed using Western blotting. The IC₅₀ value of propolis was determined as 0.342 ± 0.180 mg/mL in the A2780 cell line and 1.11 ± 0.31 mg/mL in the MCF-10A cell line. Apoptosis in the cells was evaluated using annexin V/PI staining and Caspase-3 expression via flow cytometry after treatment with varying concentrations of propolis and cisplatin. The combination of propolis at IC₅₀ and cisplatin at IC₂₅ demonstrated the highest apoptotic activity. Propolis treatment upregulated pro-apoptotic Bax while downregulating survival proteins (Bcl-2, mTOR/p-mTOR, and AKT/p-AKT) in A2780 cells, demonstrating AKT/mTOR pathway-mediated anticancer activity. Propolis exhibited potent antibacterial and antibiofilm activity against clinically relevant pathogens including MRSA and MDR E. coli, confirming its antimicrobial potential. Anatolian propolis demonstrates anticancer activity by modulating the AKT/mTOR pathway and enhancing cisplatin efficacy. Its antibacterial and antibiofilm properties further highlight its potential as a dual-function therapeutic agent, especially in cancer contexts where secondary infections are a common complication.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"323"},"PeriodicalIF":2.8,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608738","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":"Exploring resveratrol's inhibitory potential on lung cancer stem cells: a scoping review of mechanistic pathways across cancer models.","authors":"Alisa Raihana Saiful Hakim, Chin Fei Chee, Tin Wui Wong, Noor Hayaty Abu Kasim, Nurrul Shaqinah Nasruddin, Farinawati Yazid","doi":"10.1007/s12032-025-02879-y","DOIUrl":"10.1007/s12032-025-02879-y","url":null,"abstract":"<p><p>Resveratrol is a natural compound with notable health benefits, such as anti-inflammatory, antioxidant, and chemopreventive properties. It has shown potential in inhibiting tumorigenesis and tumour progression via targeted therapy, specifically by targeting cancer stem cells (CSCs). CSCs are a small, self-renewing subpopulation within tumours that drive cancer progression and are marked by biomarker proteins such as CD133, CD44, Sox2, Nanog, Oct4, ABCG2 and ALDH1. Effective treatment requires direct targeting of these cells. Understanding the pathways that govern CSC formation and their response to resveratrol is crucial for optimizing therapy. While extensive research exists on resveratrol's effects in cancers like glioblastoma, breast, and colorectal, studies on its effects in lung cancer stem cells (LCSC) remain limited. This review aims to fill this gap by exploring resveratrol's impact on CSC across various cancers and hypothesizing its mechanisms in lung cancer stem cells (LCSC). By synthesizing findings from other cancer types, we aim to outline potential pathways resveratrol may target in lung CSC as well as to elucidate any interconnectedness between these signalling pathways.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"318"},"PeriodicalIF":2.8,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600861","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":"C-Phycocyanin induces apoptosis in oral squamous cell carcinoma KB cells via modulation of key molecular pathways.","authors":"Abbas Asoudeh-Fard, Mitra Salehi, Mohammadhossein Mirhashemi, Mojtaba Fathi, Azadeh Emami, Fatemeh Soltanmohammadi, Asghar Parsaei, Hossein Piri","doi":"10.1007/s12032-025-02886-z","DOIUrl":"https://doi.org/10.1007/s12032-025-02886-z","url":null,"abstract":"<p><p>Oral squamous cell carcinoma (OSCC) is an aggressive epithelial malignancy with limited therapeutic options and high recurrence rates. C-Phycocyanin, a phycobiliprotein derived from Spirulina platensis, exhibits promising anticancer properties by modulating various molecular pathways. This study aimed to investigate the cytotoxic and pro-apoptotic effects of C-Phycocyanin on human oral cancer cells (KB) and compare its safety profile on normal endothelial cells (HUVECs). Cell viability was assessed using the MTT assay in both KB and HUVEC cell lines following treatment with different concentrations of C-Phycocyanin. Apoptotic features were evaluated by DAPI nuclear staining and quantified using Annexin V/PI-based flow cytometry. The expression of apoptosis-related genes (P53, Bax, Bcl-2) and signaling molecules involved in the Akt/PTEN and MAPK (ERK2) pathways was analyzed by semi-quantitative RT-PCR. C-Phycocyanin significantly inhibited the viability of KB cells in a dose-dependent manner while exerting minimal cytotoxic effects on HUVEC cells. DAPI staining revealed nuclear fragmentation and chromatin condensation in KB cells. Flow cytometry confirmed apoptosis induction. RT-PCR analysis showed upregulation of P53 and Bax and downregulation of Bcl-2, suggesting activation of the intrinsic apoptotic pathway. In addition, C-Phycocyanin inhibited Akt and upregulated PTEN and MAPK (ERK2) pathway components. C-Phycocyanin effectively induces apoptosis in oral cancer cells by modulating key molecular pathways, with minimal toxicity on normal cells. These results support its potential as a natural and selective therapeutic agent for OSCC, meriting further in vivo validation.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 8","pages":"319"},"PeriodicalIF":2.8,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600860","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}