Cancer Cell International最新文献

{"title":"Interferon signaling and STING pathway in head and neck cancers: unlocking immune secrets and therapeutic frontiers.","authors":"Kosar Zolfaghari, Mohammad Yazdi, Shaghayegh Mohammadioun, Fatemeh Tajafrooz, Hesam Malekfarnood, Kiarash Saleki, Nima Rezaei","doi":"10.1186/s12935-025-03963-z","DOIUrl":"10.1186/s12935-025-03963-z","url":null,"abstract":"<p><p>Head and neck squamous cell carcinomas (HNSCCs) rank seventh among the most prevalent malignancies globally. The immune response in cancer conditions governs the course of the disease and clinical outlook. Interferons (IFNs) are a key part of the innate immune system and are essential in modulating the tumor microenvironment (TME). Additionally, IFNs could influence proliferation and affect differentiation, emigration, and death of cancer cells. The cGAS-stimulator of interferon genes (STING) signaling identifies cytosolic DNA and triggers an immune response. Aberrant induction of the cGAS-STING signaling may lead to excess and sustained release of type-I IFN, leading to imbalanced aggregation in various tissues or organs. It is noteworthy that STING signaling has shown a dual role, both promoting tumor resistance and antitumor immunity. Moreover, STING agonists have been investigated in recent studies; however, challenges such as toxicity should be addressed. IFNs have also been used as monotherapy or adjuvant treatment before chemotherapy to increase efficacy against HNSCC tumors. The present review briefly describes IFN signaling with a focus on the STING pathway, and discusses its role in modulating immunotherapy and chemotherapy effects in HNSCC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"324"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Niosome-loaded silibinin and methotrexate for synergistic breast cancer combination chemotherapy: in silico and in vitro study.","authors":"Aysan Salemi, Masoumeh Kaveh Zenjanab, Mohammad Amin Adili Aghdam, Niloofar Sahragardan, Rana Jahanban Esfahlan","doi":"10.1186/s12935-025-03977-7","DOIUrl":"10.1186/s12935-025-03977-7","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Breast cancer, a leading cause of cancer-related deaths in women, faces significant treatment challenges due to drug resistance. Methotrexate (MTX), an effective chemotherapy medication for various malignancies, often encounters resistance in breast cancer, reducing its efficacy. This resistance underscores the urgent need for novel therapeutic strategies. Nano-drug delivery systems (NDDSs), such as niosomes, offer a promising solution. These systems can encapsulate both hydrophobic and hydrophilic drugs, enabling reduced dosages and enhanced delivery. By overcoming drug resistance, NDDSs pave the way for more effective combination chemotherapy in breast cancer treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;In this study, two pharmacological agents, (i) methotrexate (MTX) as a hydrophilic drug and (ii) silibinin (SiL) as a hydrophobic drug, were simultaneously loaded into the hydrophilic and lipophilic part of niosome, respectively. Niosomes were synthesized by the thin film layer hydration method and characterized by zeta sizer, FTIR, and TEM. Also, MTT assay, DAPI, dead/alive and F-actin/DAPI staining, and spheroid cell culture were used to analyze nanoparticle biocompatibility, cell viability, apoptosis, cell adhesion density, and anti-tumor response, respectively, in 2D and 3D cultured MDA-MB-231 mammospheres. Additionally, an in-silico network analysis was conducted to investigate the interaction of MTX and SiL with human proteins, especially those that contribute to breast cancer pathways.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Ideal niosomes with spherical morphology, ~ 87 nm size and ~-15 mV zeta potential, and high biocompatibility were successfully synthesized. The combination of MTX and SiL exhibited significant synergistic effects, as evidenced by the Fa value of 0.5 for NiO@MTXSiL at a concentration of 3.84 µg/mL. This value is markedly lower compared to those observed for MTXSiL (11.78 µg/mL), SiL (26.24 µg/mL), and MTX (18.48 µg/mL). Importantly, in the TNBC microtumor model, lower doses of NiO@MTXSiL achieved an almost complete anti-tumor drug response, leaving only ~ 6% residual tumor cells. Moreover, our computational analysis identified seven human proteins (i.e. BRCA1, CCND1, CDK4, CDK6, CDKN1A, Rb1, and Tp53) as breast cancer key players in the MTX and SiL interaction network with human proteins. Of these, Tp53 emerges as the most crucial protein, serving as a hub-bottleneck node, a common direct neighbor of MTX and SiL, and a key player in four breast cancer subtypes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;The designed nano-niosome, NiO@MTXSiL, is safe, stable, and has an optimal size and surface charge. It offers high drug loading capacity for co-delivering hydrophobic and hydrophilic chemotherapeutics with different anti-cancer mechanisms, improving anti-tumor response and overcoming MDR. It shows higher cytotoxicity against MDA-MB-231 breast cancer cells compared to free drugs, making it a promising candi","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"336"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495823/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-translational modifications in anaplastic thyroid carcinoma: biological mechanisms and therapeutic potential.","authors":"Linkun Zhong, Huizheng Li, Jianhang Miao, Kuo Zhang, Ling Cui, Zhaohua Wang","doi":"10.1186/s12935-025-03971-z","DOIUrl":"10.1186/s12935-025-03971-z","url":null,"abstract":"<p><p>Anaplastic thyroid carcinoma (ATC) remains one of the most lethal tumors, exhibiting a high recurrence rate, mortality rate and resistance to treatment. Post-translational modifications (PTMs) influence protein function by altering protein structure and play a crucial role in key signal transduction events related to tumor transformation and carcinogenesis, mainly including phosphorylation, ubiquitination, acetylation, and glycosylation. We highlight that dysregulation of PTM-mediated cascades in core proteins or signaling pathways serves as key factors in ATC progression. Phosphorylation, acetylation, and ubiquitination, along with the activation of various pathways, are associated with the proliferation, invasion, and metastasis of ATC. The first two PTMs significantly contribute to both targeted drug synthesis and the development of treatment resistance. Additionally, glycosylation is linked to the de-differentiation of ATC and offers an approach for new therapeutic strategies. Moreover, we discuss the potential of PTMs as biomarkers and therapeutic targets for ATC. Different PTMs play a crucial role in the application of various therapeutic approaches, particularly in the context of targeted drugs. These modifications underlie the molecular mechanisms for the selection of corresponding drugs and contribute to resistance. This review aims to provide a comprehensive understanding of the biological processes by which multiple PTMs co-regulate ATC by exploring the interplay of PTMs and their impact on ATC progression. Besides, there are still some gaps and unresolved issues in this field. By integrating different insights, we emphasize the progress in tools for early intervention to improve the prognosis of patients with ATC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"334"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495765/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrahydropalmatine has analgesic role in mouse model of bone cancer pain by inactivating the TNF-α/uPA/PAR2/TRPV1 pathway in dorsal root ganglia.","authors":"Guangda Zheng, Linghan Meng, Lu Shang, Juanxia Ren, Dongtao Li, Yanju Bao","doi":"10.1186/s12935-025-03972-y","DOIUrl":"10.1186/s12935-025-03972-y","url":null,"abstract":"<p><strong>Background: </strong>Treatment of bone cancer pain (BCP) remains a challenge. The current paper was to research the analgesic effect of Tetrahydropalmatine (THP) on BCP and the related mechanisms.</p><p><strong>Methods: </strong>Mouse model of BCP was constructed by injecting E0771 breast cancer cells into the tibia. Behavioral test was performed to research the effect of THP on pain nociception of BCP mice. Tibia and dorsal root ganglia (DRG) damage was evaluated by HE and Nissl staining. The construction of BCP cell models was conducted by co-culture DRG neurons with E0771 breast cancer cells. The effect of THP on the viability and apoptosis of BCP cell models was monitored by CCK-8 and Tunel assays. TNF-α/uPA/PAR2/TRPV1 pathway activity in DRG was detected by qRT-PCR and Western blot. Pomalidomide (PMA), exogenous TNF-α protein and Capsaicin were utilized to treat BCP mouse model and cell models to explore whether THP exerted analgesic effect via inactivating the TNF-α/uPA/PAR2/TRPV1 pathway.</p><p><strong>Results: </strong>THP attenuated pain nociception, relieved tibia destruction, and mitigated inflammation, neuronal death and neuronal excitotoxicity in DRG of BCP mice. It enhanced the viability, but suppressed the apoptosis of BCP cell models. The activated TNF-α/uPA/PAR2/TRPV1 pathway in BCP mouse model and cell models was abrogated by THP treatment. PMA and THP had additive effect, which combination attenuated pain nociception, tibia and DRG damage of BCP mice, and apoptosis of BCP cell models. The pain relief and the TNF-α/uPA/PAR2/TRPV1 pathway inactivation induced by THP in BCP mice was abolished by exogenous TNF-α protein or Capsaicin.</p><p><strong>Conclusion: </strong>THP exerted the analgesic role in BCP might be through inactivating the TNF-α/uPA/PAR2/TRPV1 pathway in DRG. It may be an effective drug for relieving BCP in patients.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"328"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating bulk RNA-seq, scRNA-seq, and spatial transcriptomics data to identify novel post-translational modification-related molecular subtypes and therapeutic responses in hepatocellular carcinoma.","authors":"Shiling Chen, Yunjie Li, Jichang Hu, Heli Li, Chen Hu, Jinzhu Zhao, Hong Qian, Shuya Bai, Zhouping Tang, Yangyang Feng","doi":"10.1186/s12935-025-03964-y","DOIUrl":"10.1186/s12935-025-03964-y","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"330"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular targets and therapeutic implications of curcumin in hepatocellular carcinoma: a comprehensive literature review.","authors":"Mojtaba Esmaeli, Maryam Dehghanpour Dehabadi, Ali Ghanbari","doi":"10.1186/s12935-025-03988-4","DOIUrl":"10.1186/s12935-025-03988-4","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, with Limited treatment options and poor outcomes in advanced stages. Curcumin, a bioactive compound derived from Curcuma longa, has drawn significant attention for its anticancer, anti-inflammatory, antioxidant, and immunomodulatory properties. This systematic review evaluated 26 studies published between 2020 and 2025-including in vitro, in vivo, and one clinical investigation-to examine the molecular mechanisms and therapeutic potential of curcumin and its nanoformulations in HCC. Curcumin was found to modulate multiple signaling pathways such as PI3K/AKT/mTOR, JAK2/STAT3, MAPK, and Wnt/β-catenin, leading to enhanced apoptosis, reduced cell proliferation, suppression of angiogenesis, and immune system modulation. Additional findings highlighted its role in reversing drug resistance and promoting ferroptosis through ACSL4 upregulation. Nanoformulated curcumin-delivered via liposomes, micelles, bilosomes, and other carriers-demonstrated improved bioavailability, stability, and tumor-targeting capacity, enhancing therapeutic efficacy in preclinical models. However, the translation of these promising preclinical effects into clinical practice remains limited, with only a single human study available. While curcumin shows potential as a supportive or adjunctive agent in HCC therapy, further well-designed clinical trials are essential to validate its efficacy and optimize formulation strategies for patient use.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"335"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LCP1 upregulation via EGFR signaling promotes oral cancer progression through the JAK2/STAT3/IL-1β axis.","authors":"Chiao-Rou Liu, Chia-Yu Yang, Kai-Ping Chang, Xiu-Ya Chan, Chu-Mi Hung, Kuan-Ming Lai, Hao-Ping Liu, Chih-Ching Wu","doi":"10.1186/s12935-025-03970-0","DOIUrl":"10.1186/s12935-025-03970-0","url":null,"abstract":"<p><p>Oral cancer is the sixth leading cause of cancer-related mortality in Taiwan, with over 90% of cases being oral cavity squamous cell carcinomas (OSCCs). The high mortality rate of OSCC is largely attributed to metastasis and locoregional relapse, underscoring the need to identify key drivers of tumor progression. To uncover proteins involved in OSCC relapse, we conducted an iTRAQ-based proteomic profiling of OSCC tissues from 6 patients with primary tumors and 4 patients with relapsed tumors. Lymphocyte cytosolic protein 1 (LCP1) emerged as a candidate associated with OSCC progression, further supported by transcriptomic analysis from The Cancer Genome Atlas (TCGA). LCP1 showed a 2.4-fold upregulation in relapsed tumors and correlated with poor patient survival. Functional assays revealed that LCP1 expression promoted tumor growth in vivo and enhances proliferation, migration, invasion, and cisplatin resistance in vitro across four OSCC cell lines. Mechanistically, LCP1 expression and phosphorylation were induced by EGF via the EGFR/PI3K/AKT and EGFR/ERK signaling pathways. Additionally, LCP1 activated the JAK2/STAT3 axis to upregulate pro-interleukin-1β (IL-1β) expression and IL-1β secretion, thereby amplifying OSCC cell aggressiveness. In summary, this study provides novel insights into the oncogenic role of LCP1 in OSCC, linking EGFR-mediated signals and IL-1β production, and identifies LCP1 as a promising target for therapeutic intervention.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"329"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncovirus classification and insights into herpes simplex virus, Varicella-Zoster virus.","authors":"Amir Ghaemi, Sanaz Sadeh","doi":"10.1186/s12935-025-03983-9","DOIUrl":"10.1186/s12935-025-03983-9","url":null,"abstract":"<p><p>Even though the paper entitled: The role of oncolytic virotherapy and viral oncogenes in the cancer stem cells: a review of virus in cancer stem cells\" provides informative details regarding viral contribution in cancer biology, its classification of Herpes Simplex Virus (HSV) and Varicella-Zoster Virus (VZV) as oncoviruses is inaccurate.Current evidence demonstrates that while HSV and VZV may reactivate in immunocompromised cancer patients, there is no causative relationship between these two viruses and oncogenesis. It is necessary to make a distinction between cancer-inducing viruses and reactivated viruses due to immune suppression among cancer patients.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"331"},"PeriodicalIF":6.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12495670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Breast neoplasm epithelial-mesenchymal transition and cytokines: a systematic review.","authors":"Yian Chen, Haining Ding, Jiaqing Song, Xiufei Gao","doi":"10.1186/s12935-025-03973-x","DOIUrl":"10.1186/s12935-025-03973-x","url":null,"abstract":"<p><p>A crucial aspect of the association involving inflammation and the development of cancer is the ability of cancer cells to undergo a transition into mesenchymal cells. The process is referred to as epithelial-mesenchymal transition (EMT). Cytokines and chemokines, which are inflammatory agents found in the carcinoma microenvironment, induce epithelial-mesenchymal transition (EMT) changes in malignant cells. Evaluating the role of cytokines in EMT in breast carcinoma and investigating their potential therapeutic implications is the objective of this comprehensive research report. The following search criteria were applied to the Cochrane, Embase, PubMed, and Web of Science databases: \"cytokines,\" \"the cytokines,\" \"chemokines,\" \"EMT,\" \"epithelial-mesenchymal transition or transformation,\" \"breast tumor,\" \"breast carcinoma,\" and \"breast cancer.\" A body of research comprising 54 articles has demonstrated that a number of cytokines, including TNF-α, TGF-β, and IL-6, contribute to the promotion of EMT alterations in breast tumors. The epithelial markers E-cadherin and β-catenin were downregulated as a consequence of morphological changes induced by EMT; conversely, the mesenchymal markers N-cadherin, vimentin, and fibronectin were upregulated. The EMT transforming factors (EMT-TF) TWIST/ZEB/SNAI1/SNAI2 were upregulated. Pharmaceuticals with the capacity to specifically target cytokines or their epithelial-mesenchymal transition (EMT) signalling pathways have the potential to significantly reduce treatment resistance, impede the progression of cancer, and prevent the recurrence of breast cancer. Epithelial-mesenchymal transition (EMT) induced by cytokines is a factor in breast cancer progression and metastasis.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"323"},"PeriodicalIF":6.0,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12482044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcription factor MYB regulates glycolysis to promote the transfer and malignant progression of gastric cancer through the SSBP2/ISL1 axis.","authors":"Zhenni Sun, Mi Zhou, Yasai Yao, Xuehong Chen, Tao Qin, Yafei Han, Lu Yue, Ruyong Yao","doi":"10.1186/s12935-025-03985-7","DOIUrl":"10.1186/s12935-025-03985-7","url":null,"abstract":"<p><strong>Background: </strong>The transcription factor (TF) MYB is crucial to many biological processes. Single-stranded DNA binding protein 2 (SSBP2), insulin gene enhancer protein 1 (ISL1) and glycolysis participated in the development of gastric cancer (GC). This study aims to explore the regulatory mechanism of the MYB/SSBP2/ISL1 axis in the development of GC.</p><p><strong>Methods: </strong>The dataset GSE65801 of cancer tissue and paracancerous tissue samples from patients with GC was used to screen differential genes, identify GC-related key TFs and the target gene of TFs, and perform expression and survival correlation analysis. Subsequently, the expression was verified in GC tissues and cells by RT-qPCR, IHC and Western blot. CCK-8, cloning, Transwell, wound healing assay, flow cytometry and Kits testing detected the effects on cells. EMSA, Yeast one-hybrid, dual-luciferase assays, ChIP-seq analysis and ChIP-PCR analysis were used to verify transcription factor binding, and pull-down assay, CO-IP, and immunofluorescence (IF) were employed to confirm interaction. MYB action was further assessed by subcutaneous tumour experiments in nude mice.</p><p><strong>Results: </strong>MYB is the key differential expression TF in GC, and SSBP2 is a key target gene of MYB. MYB had a higher expression, but SSBP2 had a lower expression in GC patients' gastric cancer tissue. SSBP2 is a direct target of MYB in GC cells. SSBP2 was transcriptionally repressed by MYB. SSBP2 further negatively regulates ISL1 expression. MYB knockdown inhibited glycolysis, proliferation, invasion, and migration abilities in GC cells both in vivo and in vitro, but it was also reversed by SSBP2 knockdown. SSBP2 overexpression inhibits glycolysis, cell proliferation, invasion and migration abilities in GC cells, but it was reversed by ISL1 overexpression.</p><p><strong>Conclusion: </strong>MYB mediates glycolysis and malignant progression in GC cells through regulation of the SSBP2/ISL1 axis.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"322"},"PeriodicalIF":6.0,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12482532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}