Advances in cancer biology - metastasis最新文献

{"title":"Roles of the WNT/β-catenin signaling pathway in the metastasis and recurrence of NSCLC","authors":"Yi Liu ,&nbsp;JiaYing Ma ,&nbsp;Jitian Zhang ,&nbsp;Qi Sun","doi":"10.1016/j.adcanc.2025.100162","DOIUrl":"10.1016/j.adcanc.2025.100162","url":null,"abstract":"<div><div>Lung cancer is the leading cause of cancer-related death globally and the most common cause of brain metastasis. Non-small cell lung cancer (NSCLC) accounts for approximately 80 % of all lung cancers. High metastasis and recurrence rates are important factors contributing to the poor prognosis of patients with NSCLC. The canonical WNT signaling pathway, as a highly conserved signal transduction pathway, not only directly affects the metastasis and recurrence of NSCLC, but also participates in it by regulating the stemness and epithelial-mesenchymal transition (EMT) process of lung cancer cells, or by interacting with other signaling pathways. In this review, we summarize the direct or indirect functions and mechanisms of roles of the WNT/β-catenin signaling pathway (including WNT ligands, β-catenin, glycogen synthase kinase 3Β, adenomatous polyposis coli, axis inhibition protein, dishevelled, frizzled serpentine receptor, Dickkopf-related protein, lymphoid enhancer-binding factor/T cell-specific factor, and S-phase kinase associated protein 1–cullin–F-box E3 ligase) in NSCLC metastasis and recurrence. Additionally, we explore the potential of inhibitors of this pathway in preventing NSCLC metastasis and recurrence.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"15 ","pages":"Article 100162"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145617246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular pathology of microRNA-103a as a probable diagnostic and therapeutic tumor marker","authors":"Iman Akhlaghipour ,&nbsp;Negin Taghehchian ,&nbsp;Meysam Moghbeli","doi":"10.1016/j.adcanc.2025.100150","DOIUrl":"10.1016/j.adcanc.2025.100150","url":null,"abstract":"<div><div>Late diagnosis has a key role in therapeutic failure and tumor relapse. Therefore, assessment of the molecular tumor biology can help to introduce novel early diagnostic markers. MicroRNAs (miRNAs) have important roles in regulation of tumor cell proliferation, invasion, drug resistance, and angiogenesis. Due to the high stability of miRNAs in paraffin-embedded tissues and body fluids, they can be also used as the non-invasive markers for cancer screening and early diagnosis. According to numerous reports about the role of miR-103a in various cancers, in the present review we investigated the molecular biology of miR-103a during tumor progression. It has been reported that miR-103a has a dual function as an oncogene and tumor suppressor in various cancers. MiR-103a exerts its role in tumor progression by regulation of signaling pathways, apoptosis, cell cycle, cell metabolism, and transcription factors. This review paves the way in introducing miR-103a as a diagnostic and therapeutic marker among cancer patients following the animal studies and clinical trials.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"15 ","pages":"Article 100150"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144879453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Niosomes containing enciprazine hydrochloride have been shown to efficiently inhibit the proliferation and induce apoptosis in colorectal cancer cells” [Advan. Cancer Biol. Metastasis 12 (2024) 100128]","authors":"Hosain Nasirian ,&nbsp;Saeedeh TarvijEslami ,&nbsp;Hedieh Ghourchian ,&nbsp;Marjaneh Ebrahimi ,&nbsp;Tohid Piri-Gharaghie ,&nbsp;Ghazal Ghajari","doi":"10.1016/j.adcanc.2025.100156","DOIUrl":"10.1016/j.adcanc.2025.100156","url":null,"abstract":"","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"15 ","pages":"Article 100156"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disulfiram alone regulates the radiosensitivity of lung cancer through NF-κB pathway and regulates the immune microenvironment after radiotherapy by targeting PD-L1 through c-Myc","authors":"Yanfei Cui ,&nbsp;Minghua Zhang ,&nbsp;Sijia Zhang ,&nbsp;Yanli Cai ,&nbsp;Yangang Qu ,&nbsp;Lihua Luo","doi":"10.1016/j.adcanc.2025.100149","DOIUrl":"10.1016/j.adcanc.2025.100149","url":null,"abstract":"<div><h3>Background</h3><div>Lung cancer often develops resistance to radiotherapy (RT), which undermines its therapeutic efficacy. Disulfiram (DSF), a drug commonly used in the treatment of alcohol use disorders, has shown potential in inducing anti-tumor effects. However, its impact on radioresistance in lung cancer and its effects on the tumor immune microenvironment have not been fully elucidated.</div></div><div><h3>Methods</h3><div>Clonogenic assays, Rad51 foci formation, and a nude mouse model were employed to assess the impact of DSF on lung cancer radiosensitivity. Immune profiling was conducted using flow cytometry, and downstream mechanisms were investigated using RT-qPCR and Western blotting. The therapeutic effects of the combination of DSF, RT, and anti-PD-L1 antibody were further validated in a C57BL/6 mouse tumor model.</div></div><div><h3>Results</h3><div>DSF increased radiosensitivity in lung cancer cells, enhanced CD8⁺ T cell infiltration, and upregulated PD-L1 expression through c-Myc. The combination of DSF, RT, and anti-PD-L1 antibody resulted in the most significant anti-tumor effects.</div></div><div><h3>Conclusions</h3><div>DSF effectively mitigates radioresistance in lung cancer and enhances the efficacy of radioimmunotherapy, offering a promising therapeutic strategy for improving treatment outcomes.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"15 ","pages":"Article 100149"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144843008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated dysregulation of RNF43 and associated lncRNAs reveals transcriptional remodeling in colorectal carcinoma","authors":"Alireza Soleimani ,&nbsp;Amir Sadeghi ,&nbsp;Zahra Fazeli ,&nbsp;Solat Eslami ,&nbsp;Mohammad Rahmanian ,&nbsp;Binazir Khanabadi ,&nbsp;Soudeh Ghafouri-Fard ,&nbsp;Mir Davood Omrani","doi":"10.1016/j.adcanc.2025.100155","DOIUrl":"10.1016/j.adcanc.2025.100155","url":null,"abstract":"<div><div>The Wnt signaling cascade is crucial for diverse biological processes, including cell cycle regulation, inflammation, embryonic development, and tumorigenesis. The present study investigates the expression of TSPOAP1-AS1, TMEM147-AS1, and FOXP4-AS1 lncRNAs, along with RNF43, all of which are associated with the Wnt/β-catenin signaling pathway, in colorectal cancer (CRC) samples compared to adjacent normal tissues (ANTs). RNF43 was significantly overexpressed in CRC samples, with a median 2.34-fold increase relative to normal tissues (P value = 0.04). In contrast, the lncRNA TSPOAP1-AS1 was markedly down-regulated in tumors, showing a median 0.42-fold reduction (P value = 0.03). The remaining two lncRNAs—TMEM147-AS1 and FOXP4-AS1—were also significantly elevated, exhibiting median fold-changes of 2.94-fold (P value &lt; 0.0001) and 2.02-fold (P value = 0.003), respectively. All four transcripts achieved exceptionally high specificity (97.5–100 %) but only moderate sensitivity (29.3–56.1 %) for discrimination of CRC samples from ANTS, reflecting their stringent discrimination of ANTs at the expense of missing a subset of tumors. Taken together, our results revealed a coordinated dysregulation of Wnt-related genes in CRC, i.e. loss of TSPOAP1-AS1 alongside gain of RNF43, TMEM147-AS1, and FOXP4-AS1 expression, highlighting their potential as complementary biomarkers.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"15 ","pages":"Article 100155"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145264971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evolution of the AGMK1-9T7 GLI1+ progenitor cells to become tumor cells and potentially cancer-stem cells","authors":"Andrew M. Lewis Jr. ,&nbsp;Gideon Foseh ,&nbsp;Keith Peden ,&nbsp;Adovi Akue ,&nbsp;Mark KuKuruga ,&nbsp;Daniel Rotroff ,&nbsp;Gladys Lewis ,&nbsp;Ilya Mazo","doi":"10.1016/j.adcanc.2025.100151","DOIUrl":"10.1016/j.adcanc.2025.100151","url":null,"abstract":"<div><div>We have investigated the expression of selected genes and miRNAs that have been found to be associated with human cancer-stem cells for their involvement in the neoplastic evolution of our AGMK1-9T7 cell line from a non-tumorigenic status at passage (p)13 to a tumorigenic/metastatic status at p40 to p43. Among these genes are CD90, CD44, CD24, PODXL, ALDH1A, ALDHA2, and ALDHA3 genes, as well as 17 other genes and 38 miRNAs. While CD90 and CD24 were not expressed by any passages of AGMK1-9T7 cells, CD44 was expressed in cells at p13, p23, p33, and p43. The expression of PODXL was first detected as weakly expressed at p33 but was highly expressed by p43. Of the 17 genes that have been associated with human cancer-stem-cell functions that we examined across this spectrum of neoplasia, 5 were up-regulated &gt;2 log2 fold and 8 were down-regulated &gt;2 log2 fold. The expression of the ALDH1A genes, which have been associated with cancer-stem cells, was investigated by the ALDEFLUOR assay in AGMK1-9T7 cells from p13 to p43. Using RT-qPCR, the ALDH1A2 gene was found to be up-regulated in cells from p13 to p43. Twenty-six of the 38 miRNAs reported to be associated with human cancer-stem cells were expressed by the AGMK1-9T7 cells at different passages. From these data, we propose that the AGMK1-9T7 cells are evolving from their non-tumorigenic state to become tumor cells and potentially cancer-stem cells by p43. We suggest that this <em>in vitro</em> system might provide a model to investigate the role of these processes in neoplastic development in humans.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"15 ","pages":"Article 100151"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145157162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hybrid EMT and inflammation: the deadly alliance","authors":"Rohit Gundamaraju ,&nbsp;Vidhya Tangeda ,&nbsp;Harshini Raja ,&nbsp;Chandrashekar Goud ,&nbsp;Hima Sree Buddiraju ,&nbsp;Vishnu Pulavarthy","doi":"10.1016/j.adcanc.2025.100160","DOIUrl":"10.1016/j.adcanc.2025.100160","url":null,"abstract":"<div><div>Tumors have unbounded components fitted which execute widespread pathophysiologies. It has been noted that tumor associated inflammation attributes to metastatic endpoints making it an aggressive phenotype. The inflammatory cells and system are set to have a cross talk with tumor cells in the microenvironment varying with the cancer. Likewise, EMT process might also trigger inflammation by the cancer cells. On the other hand, hybrid EMT possesses characteristics of both epithelial and mesenchymal nature which are said to possess unique stemness and express therapeutic resistance. A deeper understanding of the immune events in the tumor microenvironment is necessary to gain better understanding. Further, interpreting how cancer cells are attuning to stress and harsh environments is instrumental in learning about the concept of hybrid EMT. The current review focusses on the interrelationship between inflammation and how might aid in the hybrid EMT phenotype or the regulatory inflammatory factors bolstering hybrid EMT.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"15 ","pages":"Article 100160"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145465150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aneuploidy in Hepatocellular Carcinoma: Risk factors, mechanisms, and clinical relevance","authors":"Marwa Zahra ,&nbsp;Hassan Mohamed El-Said Azzazy","doi":"10.1016/j.adcanc.2025.100144","DOIUrl":"10.1016/j.adcanc.2025.100144","url":null,"abstract":"<div><div>Mechanisms of aneuploidy set the stage for cancer. Aneuploidy, an aberration in chromosome number in a cell, occurs naturally during cellular development in certain tissues. However, aneuploidy is omnipresent in cancer as cancer cells express complex karyotypes with chromosome numbers that deviate from the norm. Aneuploidy is a hallmark in Hepatocellular Carcinoma (HCC), as it is linked to poor prognosis due to genetic and epigenetic aberrations. Mechanisms contributing to aneuploidy in HCC include chromosomal instability, telomere shortening, which promotes genomic instability in early tumor development, and telomere stabilization, which enhances tumor cell survival by preventing excessive telomere attrition in later stages. Multiple chromosomal alterations are linked to the progression of invasive tumors in HCC. Therefore, understanding the association between aneuploidy and HCC is critical because it could unravel the role of genetic and molecular alterations in HCC. This review sheds light on the risk factors associated with aneuploidy in HCC to aid the development of future therapeutic and diagnostic approaches for management of HCC.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"15 ","pages":"Article 100144"},"PeriodicalIF":2.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144694292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the apoptotic and antimetastatic effect of daphnetin-containing nano niosomes on MCF-7 cells","authors":"Saeed Homaeii,&nbsp;Mahsa Kavousi,&nbsp;Elahe Ali Asgari","doi":"10.1016/j.adcanc.2025.100139","DOIUrl":"10.1016/j.adcanc.2025.100139","url":null,"abstract":"<div><div>Breast cancer is the most common cancer in the world and the second leading cause of cancer-related deaths in women worldwide. Although great progress has been made in elucidating the molecular features and underlying pathogenesis of breast tumors and various therapeutic strategies have been applied for individualized treatment, some types of breast cancer patients with aggressive features have a poor prognosis in terms of treatment. Nanotechnology is increasingly used in biology and medicine, including as a tool for diagnosing, treating and targeting tumors. The aim of this study is therefore to develop a drug delivery system based on niosomes loaded with daphnetin, a phytochemical coumarin. To confirm the synthesis of the loaded nano niosome, their physical and chemical properties were examined using SEM, FTIR and DLS. In this study, the toxic effect of daphnetin-loaded nanoparticles on the MCF-7 cell line was measured using the MTT assay. The expression level of apoptotic genes <em>Bax</em> and <em>Caspase 3</em>; and metastatic genes <em>MMP2</em> and <em>ITGA5</em> were quantitatively evaluated using the Real-time PCR method, and the division and metastatic potential of cancer cells were qualitatively evaluated by performing the scratch (repair) method. Finally, the effect of the investigated compounds on the amount of apoptosis and necrosis and the induced cell cycle was evaluated using the flow cytometry method.</div><div>The results of the SEM study showed that the synthesized nanoparticles had a spherical morphology and a diameter of less than 200 nm. The zeta potential was determined to be 39.1 mV using a DLS device. The results of the FTIR study also showed successful interactions between niosome and daphnetin. According to the flow cytometry results, the frequency of early apoptosis and delayed apoptosis was significantly higher in the cells treated with the IC₅₀ concentration of daphnetin-loaded nanoparticles than in the group treated with daphnetin and free niosome. The expression of apoptotic genes was also increased in the group treated with the IC₅₀ concentration of the loaded nanoparticles and the expression of antimetastatic genes was decreased. The results of the cell migration assay (scratch test) also show that treatment with the IC₅₀ concentration of the loaded nanoparticles can effectively control cell migration. Therefore, they can be considered as chemotherapeutic agents against breast cancer.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"14 ","pages":"Article 100139"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143816727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The targeted delivery of anti-metastasis oligonucleotide in breast cancer cells by the nanoliposomes conjugated with RGD ligand","authors":"Farahanaz Kavian Manesh ,&nbsp;Ali Jebali ,&nbsp;Flora Forouzesh","doi":"10.1016/j.adcanc.2025.100140","DOIUrl":"10.1016/j.adcanc.2025.100140","url":null,"abstract":"<div><div>To decrease the <em>ETV4</em> gene, which is important in metastasis, the nanoliposome containing ETV4 antisense oligonucleotide conjugated with Arginylglycylaspartic acid (RGD) ligand was used in the study. The nanoliposome containing ETV4 antisense oligonucleotide conjugated with RGD ligand was synthesized and characterized by AFM, DLS, and FTIR. Then, MDA-MB-231, MCF-7, and MCF-10A cell lines were treated with different concentrations of nanoliposomes containing antisense ETV4 oligonucleotide conjugated with RGD, nanoliposomes without antisense ETV4 oligonucleotide, and antisense ETV4 oligonucleotide for 24 h. Finally, an MTT assay was used to evaluate cell viability, Real-time PCR was employed to assess the <em>ETV4</em> mRNA expression, and western blotting was applied to evaluate the expression of ETV4 protein. Here, the characterization data revealed that the nanoliposome containing antisense ETV4 oligonucleotide conjugated with RGD had a spherical shape with a size range of 50–120 nm and zeta potential of −18mV to +7 mV. This study showed that although nanoliposomes containing antisense ETV4 oligonucleotide conjugated with RGD could effectively decrease the cell viability of MDA-MB-231 and MCF-7 cells, they could not dcrease cell viability of MCF-10A, indicating the effect of RGD ligand. Also, this novel carrier could decrease both mRNA and protein of <em>the ETV4</em> gene in a dose dependent manner.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"14 ","pages":"Article 100140"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143895474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}