Cell Biology International最新文献

{"title":"The Effect of Malonate as a Succinate Dehydrogenase Inhibitor on Myocardial Ischemia/Reperfusion Injury.","authors":"Amir Modarresi Chahardehi, Reza Arefnezhad, Sajjad Rafei, Alireza Arzhangzadeh, Reza Nasiri, Fatemeh Rezaei-Tazangi, Marziye Ranjbar Tavakoli","doi":"10.1002/cbin.70079","DOIUrl":"https://doi.org/10.1002/cbin.70079","url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion injury (MIRI) continues to provide a serious therapeutic challenge, substantially influencing myocardial infarct size and negative cardiovascular outcomes. Recent research underscores the critical significance of succinate accumulation and its rapid oxidation during reperfusion, initiating the generation of reactive oxygen species (ROS) and mitochondrial impairment. Malonate, a competitive inhibitor of succinate dehydrogenase (SDH), has attracted interest as a cardioprotective drug by reducing ROS production and cellular damage during the first reperfusion. Malonate preferentially accumulates in ischemic tissues via monocarboxylate transporter 1 (MCT1), driven by the acidic conditions of ischemia. This specific dosing prevents SDH, which in turn reduces succinate oxidation and ROS production, protecting mitochondrial integrity and heart function. The effects of malonate on infarct size reduction, left ventricular ejection fraction enhancement, and pro-inflammatory and fibrotic marker mitigation have been demonstrated in preclinical research conducted on animal models. Additionally, acidified malonate formulations improve therapeutic selectivity, providing significant cardioprotection at lower dosages. Notwithstanding encouraging experimental results, clinical validation is crucial to ascertain malonate's translational potential for the treatment of acute myocardial infarction (MI) and post-reperfusion heart failure. This review discusses the pathophysiology of MIRI, the function of SDH, and the mechanism of action of malonate, highlighting its potential as a targeted intervention for MIRI.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Embryo Production Method and Culture Medium on Embryonic Development in Red-Rumped Agouti.","authors":"Lhara Ricarliany Medeiros de Oliveira, Leonardo Vitorino Costa de Aquino, Luana Grasiele Pereira Bezerra, Moacir Franco de Oliveira, Alexandre Rodrigues Silva, Alexsandra Fernandes Pereira","doi":"10.1002/cbin.70080","DOIUrl":"https://doi.org/10.1002/cbin.70080","url":null,"abstract":"<p><p>Advances in Assisted Reproductive Technologies (ARTs) help overcome reproductive barriers. However, a comprehensive understanding of embryonic development is crucial for their success. In vitro fertilization (IVF) and artificial oocyte activation (AOA) are embryo production methods commonly used. Previous studies have reported low developmental success with these methods, possibly due to the culture medium used. Therefore, we aimed to optimize ARTs in red-rumped agouti by evaluating the influence of production method and culture medium on embryonic development. Oocytes were matured in vitro and divided into two groups: IVF with capacited spermatozoa or AOA with strontium chloride and cytochalasin B. Presumed zygotes were cultured in either KSOM or SOF medium after a 6-h incubation. Morphology, oocyte-sperm interaction, developmental kinetics, and oxidative stress levels were assessed. IVF-derived structures exhibited a higher rate of normal morphology compared to AOA-derived structures (p < 0.05). Embryo kinetics analysis showed that AOA-KSOM and IVF-KSOM groups had a higher number of cleaved structures than the SOF groups (p < 0.05) on Day 2. On Day 5, the IVF-KSOM group presented the highest percentage of cleavage/total zygotes and the highest percentage of structures with eight or more cells (p < 0.05). Morula formation was significantly higher in IVF-KSOM and AOA-KSOM (p < 0.05), highlighting KSOM's effectiveness. Notably, only the IVF-KSOM group produced blastocyst (p < 0.05). Oxidative stress assessment showed no differences between groups (p > 0.05). These findings confirm that IVF-KSOM is the most effective methodology for developing red-rumped agouti embryos, offering valuable insights into the reproductive biology of this species and aiding in the refinement of protocols for closely related rodents.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Combination of Exogenous Klotho Combined With Telmisartan Ameliorated Diabetic Cardiomyopathy via an Antifibrotic Mechanism.","authors":"Mansi Vinodkumar Trivedi, Hemant R Jadhav, Anil Bhanudas Gaikwad","doi":"10.1002/cbin.70078","DOIUrl":"https://doi.org/10.1002/cbin.70078","url":null,"abstract":"<p><p>Diabetic cardiomyopathy (DCM) is a progressive heart disorder associated with diabetes mellitus, leading to structural and functional cardiac abnormalities. The mechanisms responsible include renin-angiotensin-aldosterone (RAAS) activation, inflammation, apoptosis, and metabolic disturbances. Despite well-established epidemiological links, treatments for DCM are elusive. This study evaluated the efficacy of a novel combination of recombinant Klotho (KL) and the angiotensin receptor blocker telmisartan (TEL) in treating DCM, as well as investigating potential mechanisms involved. DCM was induced with a single dose of streptozotocin (55 mg/kg, i.p.), followed by a 4-week induction period. For treatment, rats were assigned to five groups: Normal control (NC), Diabetic control (DC), DC + KL (0.01 mg/kg, S.C.), DC + TEL (10 mg/kg, p.o.), and KL + TEL combination. Plasma biochemistry assessed cardiac damage (LDH, CK-MB) and stress markers (ANP, BNP). Electrocardiogram (ECG) measured heart parameters, including heart rate (HR), QTc, JT interval, RR interval, and T_peak-T_end intervals. Histological analysis (H&E, Masson's trichrome, and Picrosirius red) was performed to assess myocardial structure and fibrosis. Lastly, immunohistochemistry analysis was performed to check the expression of transforming growth factor-β1 (TGF-β1), pSMAD 2/3, matrix metalloproteinase 9 (MMP9), and PRKN. KL and TEL combination treatment significantly reduced cardiac damage markers, reduced ECG abnormalities, including QT_c, improved HR while suppressing pro-fibrotic signaling, enhancing mitophagy, and decreasing fibroblast proliferation. The involvement of pathways involving TGF-β1, pSMAD-2/3, MMP9, and pFOXO3a conferred protection to the heart in experimental in-vivo settings. These findings suggest that the combination of KL and TEL effectively mitigates key pathological features of DCM, highlighting its potential as a targeted treatment strategy.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of TcFLA-1BP and TcGP72 Deletion on the Infectivity and Survival of Trypanosoma cruzi in Cell Cultures.","authors":"Normanda Souza-Melo, Giovanna Henriques de Souza, Wanderley de Souza","doi":"10.1002/cbin.70076","DOIUrl":"10.1002/cbin.70076","url":null,"abstract":"<p><p>Chagas disease, caused by the protozoan Trypanosoma cruzi, is a neglected tropical disease with limited treatment options and no available vaccine. Understanding the role of proteins in the parasite's biological cycle is critical for advancing vaccine development and optimizing therapies. The flagellar attachment zone (FAZ) proteins play a pivotal role in motility, pathogenicity, and cell division in trypanosomatids, but their functions in T. cruzi are not as well-characterized as in Trypanosoma brucei and Leishmania spp. This study investigates the orthologous TcGP72 and TcFLA-1BP proteins in T. cruzi, focusing on their roles in the infective forms of the parasite. Our findings demonstrate that TcFLA-1BP is important for efficient host cell infection in vitro, indicating its critical role in the parasite's infectivity. Conversely, TcGP72 is nonessential for the infection process, but significantly contributes to cytoskeletal remodeling during the parasite's life cycle. These results provide new insights into the distinct functional roles of FAZ proteins in T. cruzi. Furthermore, the study underscores the importance of TcGP72 in maintaining cellular architecture, reinforcing the relevance of FAZ proteins in the parasite's pathogenesis and structural integrity.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression Interplay Between Cathepsin B and Its Natural Inhibitor Stefin A in Cancer and Embryonic Cell Lines.","authors":"Anastasia O Syrocheva, Konstantin I Ivanov, Victor S Laktyushkin, Neonila V Gorokhovets, Alessandro Parodi, Andrey A Zamyatnin","doi":"10.1002/cbin.70077","DOIUrl":"https://doi.org/10.1002/cbin.70077","url":null,"abstract":"<p><p>Cathepsin B (CTSB) is a lysosomal protease that also operates outside the acidic environment of lysosomes. In healthy cells, CTSB plays a crucial role in processes such as apoptosis, autophagy, and the maintenance of cellular homeostasis. However, in cancer, it contributes significantly to disease progression by promoting invasion and metastasis. This study introduces a novel exploration of the relationship between CTSB and its natural inhibitor, Stefin A (STFA), renal cancer cells. For the first time, we demonstrated the precise regulatory influence of CTSB on STFA expression by investigating their expression in noncancerous embryonic renal cells (Hek293T), renal cancer cells (769p), and nonrenal cancer cells (Du145). This study highlights the intricate interplay between CTSB and its inhibitor, offering new insights into the CTSB/STFA balance that occurs in kidney cancer biology. In this study, we simultaneously examined the mRNA and protein expression of CTSB and STFA in various cancer cell lines by employing CTSB gain-of-function, loss-of-function, and biochemical inhibition approaches to understand the contributions of CTSB expression and activity in influencing STFA levels and their reciprocal subcellular localization. We found that cancer cells exhibited impaired regulation of CTSB and STFA gene expression. In particular, our results indicate that exogenous expression of CTSB significantly alters STFA levels, suggesting a feedback mechanism influenced by CTSB's enzymatic activity. Importantly, the relationship between CTSB and STFA is preserved at the protein level, indicating complex regulatory mechanisms mitigating transcriptional misbalances at the translational level. This study provides insight into the interplay between CTSB and STFA in cancer cells and compares it to their behavior in embryonic cells, highlighting how aberrant CTSB expression can influence its inhibitor and advancing our understanding of this balance in tumor progression.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Total Flavonoids of Hedyotis Diffusa Willd Suppresses Prostate Cancer Progression by Promoting AR Ubiquitination and Degradation via the PIAS4/STAT3 Pathway.","authors":"Rui Feng, Zhongxing Li, Yuejun Jia, Yali Ji, Meitian Guo, Xing Wang","doi":"10.1002/cbin.70070","DOIUrl":"https://doi.org/10.1002/cbin.70070","url":null,"abstract":"<p><p>Total flavonoids of Hedyotis diffusa Willd (TFHDW) is an active compound extracted from Hedyotis diffusa Willd (HDW), one of the most well-known herbs possessing antitumor effects. In this study, the potential antitumor effects of TFHDW were investigated in vitro in mouse prostate cancer cells RM1 and human prostate cancer cells LNCaP and in vivo using a xenograft tumor model involving injection of RM1 cells. Upon TFHDW treatment, RM1 and LNCaP cells exhibited augmented protein expression of the protein inhibitor of activated STAT (PIAS4) and diminished activity of signal transducer and activator of transcription 3 (STAT3), along with impaired proliferative, migratory, and invasive capacities. Ectopic STAT3 expression or PIAS4 silencing in RM1 and LNCaP cells partly annulled the inhibition effect of TFHDW treatment on cell malignant phenotypes. Mechanistic studies revealed that TFHDW elevated transcriptional activity of damage-specific DNA-binding protein 2 via PIAS4/STAT3, consequently enhancing ubiquitination and degradation of androgen receptor (AR) protein. By this, TFHDW alleviated the growth of prostate cancer in vitro and in vivo. Altogether, our work uncovers new insights into the link between TFHDW and the PIAS4/STAT3/AR axis in prostate cancer. These findings may provide a novel therapeutic option for targeting the PIAS4/STAT3/AR axis in prostate cancer.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Testosterone Enhances Wound Healing and Stress Resistance in A549 Lung Adenocarcinoma Cells via Actin Remodeling and AQP3 Upregulation.","authors":"Mi Nam Lee, Seong-Eung Cha, Hyunwoo Lim, Eung-Sam Kim","doi":"10.1002/cbin.70075","DOIUrl":"https://doi.org/10.1002/cbin.70075","url":null,"abstract":"<p><p>The role of androgens in lung function is contentious, yet their effects on type II alveolar epithelial cells (AECII)-derived lung cancer models remain underexplored. This study reveals that androgens provide survival advantages to A549 cells, a male lung adenocarcinoma AECII cell line, by promoting wound healing and enhancing stress resilience. We demonstrated that testosterone and dihydrotestosterone (DHT) significantly upregulate aquaporin 3 (AQP3) through androgen receptor (AR) accumulation and ERK pathway activation, thereby mitigating cell death under oxidative stress induced by hydrogen peroxide and cyclic cell-stretching. Testosterone facilitated cellular wound healing by promoting actin cytoskeleton remodeling and focal adhesion complex formation, reliant on AR rather than AQP3. Under air-liquid interface culture conditions, testosterone consistently induced AQP3 upregulation, enhanced actin remodeling, and facilitated cellular wound healing responses. Validation of these findings was achieved through gene expression analyses, protein level assessments, cell imaging, and in vitro wound healing assays. The underlying molecular mechanisms of androgen action were elucidated using AQP3- and AR-specific siRNAs and pharmacological inhibitors. These findings underscore the urgent need to investigate the role of sex hormones in lung cancer and other androgen-responsive epithelial models, focusing on their influence on cancer cell survival and motility.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression Patterns of Deubiquitinating Enzymes in Paclitaxel-Treated Lung Cancer Cells.","authors":"Hwa-Yeong Kim, Hae-Seul Choi, Kwang-Hyun Baek","doi":"10.1002/cbin.70072","DOIUrl":"https://doi.org/10.1002/cbin.70072","url":null,"abstract":"<p><p>Lung cancer remains a leading cause of cancer-related mortality, underscoring the urgent need for more effective therapeutic strategies, particularly due to the frequent development of drug resistance. Paclitaxel, a widely used chemotherapeutic agent for non-small cell lung cancer (NSCLC), often faces resistance that limits its clinical efficacy. Therefore, identifying molecular markers that modulate paclitaxel responsiveness is critical. The ubiquitin-proteasome system (UPS), which regulates protein homeostasis, plays a role in cancer progression, apoptosis, and drug resistance, with deubiquitinating enzymes (DUBs), serving as key regulators. Recent studies suggest that targeting specific DUBs may enhance drug sensitivity. This study aimed to investigate the expression patterns of DUB genes in response to paclitaxel treatment. Multiplex RT-PCR and RT-qPCR analysis revealed that USP1, USP5, USP28, and USP34 were downregulated, whereas USP10 and USP36 were upregulated in paclitaxel-treated A549 cells. Western blot analysis confirmed changes in protein levels consistent with mRNA expression for all DUBs except USP10 and USP36, which displayed discordant patterns. Furthermore, paclitaxel-induced apoptosis was verified by altered levels of apoptotic and antiapoptotic proteins including PARP, caspase-3, Bax, Bcl-2, Bcl-XL, and p53. The identification of these DUB genes highlights their potential as biomarkers for predicting drug responsiveness and prognosis during paclitaxel treatment, thereby proposing a new direction for improving the therapeutic efficacy of paclitaxel in NSCLC.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of Autophagy by Ursolic and Betulinic Acids: Distinct Cytotoxic and Membrane-Disruption in Malignant and Nonmalignant Cells.","authors":"Waleska Kerllen Martins, Tayana Mazin Tsubone, Chimara Emilia Nascimento Sanches, Cleidiane de Sousa Rocha, Ricardo Scarparo Navarro, Beatriz Simonsen Stolf, Susana Nogueira Diniz, Rosangela Itri, Mauricio S Baptista","doi":"10.1002/cbin.70073","DOIUrl":"https://doi.org/10.1002/cbin.70073","url":null,"abstract":"<p><p>Autophagy is a critical adaptive mechanism in tumor cells that promotes survival under stress, but when dysregulated, it may trigger programmed cell death. The pentacyclic triterpenoids betulinic acid (BA) and ursolic acid (UA) are structurally related compounds that modulate autophagy; however, comparative insights into their effects on nonmalignant and malignant cells, as well as model membranes, remain limited. Here, we investigated the distinct cellular outcomes induced by UA and BA in nonmalignant keratinocytes (HaCaT) and malignant cell lines (A549, HeLa, MCF7, MES-SA, PC3, SKMEL-25/28), as well as their interactions with mitochondrial membrane mimetics. At 20 μM, BA reduced HaCaT proliferation by 70%, while UA achieved only 30% inhibition. BA induced pronounced mitochondrial dysfunction (i.e., 60%), mitophagy activation, and autophagy-associated cell death linked to a lysosomal-mitochondrial stress axis. In contrast, UA induced lysosomal membrane permeabilization and the release of cathepsin B, resulting in ~50% cell death. In malignant cell lines, BA reduced viability to ~40%, whereas UA showed selective toxicity (53%-73% survival). Cotreatment with chloroquine enhanced UA's cytotoxicity by simulating BA-like lysosomal accumulation. Biophysical assays revealed differential membrane disruption profiles: BA permeabilized cardiolipin-rich membranes, while UA exerted milder surface-level effects. These findings illustrate how structurally similar triterpenoids exert divergent effects on cellular membranes, autophagic flux, and cell fate, offering a foundation for designing selective anticancer agents that target the lysosomal-mitochondrial axis.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring SLAMF5/CD84 in Cancer: Advancing the Frontiers of Tumor Immunology.","authors":"Safia Obaidur Rab, Ahmed Hussein Zwamel, Ashok Kumar Bishoyi, Suhas Ballal, Abhayveer Singh, Anita Devi, Girish Chandra Sharma, Pushpa Negi Bhakuni, Jasur Rizaev","doi":"10.1002/cbin.70074","DOIUrl":"https://doi.org/10.1002/cbin.70074","url":null,"abstract":"<p><p>The Signaling Lymphocytic Activation Molecule (SLAM) family receptors play essential roles in regulating immune cell activation, differentiation, and communication. SLAMF5, also known as CD84, has drawn increasing attention in cancer immunology due to its involvement in both tumor progression and immune modulation. This review explores the expression patterns, signaling mechanisms, and functional roles of SLAMF5/CD84 within the tumor microenvironment. SLAMF5/CD84 is expressed on multiple immune cell types and contributes to immune evasion by enhancing regulatory B cell function, promoting myeloid-derived suppressor cell expansion, and upregulating immune checkpoint molecules such as PD-L1. Its expression has been implicated in various hematologic malignancies and solid tumors, including chronic lymphocytic leukemia, multiple myeloma, and triple-negative breast cancer. Emerging therapeutic approaches targeting SLAMF5/CD84-such as monoclonal antibodies and CAR T-cell therapies-offer promising strategies to counteract immunosuppression and improve treatment outcomes. By highlighting recent findings and therapeutic developments, this review underscores the significance of SLAMF5/CD84 as both a prognostic biomarker and a novel target in cancer immunotherapy. Understanding SLAMF5/CD84's multifaceted roles in the tumor immune landscape could support the development of more effective and personalized cancer treatment strategies.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}