Benign fibro-osseous lesions are characterized by the replacement of normal bone with cellular fibrous connective tissue with new bone formation. The published cytogenetic information on these tumors is limited to only few cases. Here, we report the cytogenetic and molecular genetic findings of a fibro-osseous tumor.

Renal cell carcinoma (RCC) is a typical malignant lesion of kidney with high recurrence rate and high mortality. MYB proto-oncogene-like 2 (MYBL2) is significantly expressed in cancer cells and closely linked to cancer development and poor prognosis. This study aimed to investigate the role and possible mechanisms of MYBL2 in renal cancer.

The early and accurate diagnosis of prostate cancer (PCa) bone metastases is of great importance for formulating the best treatment plan and improving the prognosis of patients. This work aimed to compare and analyse the application value of 18F-fludeoxyglucose (FDG) and 18F-prostate-specific membrane antigen-1007 (18F-PSMA-1007) positron emission tomography/computed tomography (PET/CT) in the diagnosis of PCa bone metastases.

Neuroendocrine (NE) prostate cancer (NEPC) is an aggressive and lethal subtype of prostate cancer. It is typically characterized by the expression of NE markers and the loss of androgen receptor expression. De novo NEPC is rare, accounting for <2% of all prostate cancer cases at diagnosis. More commonly, NEPC arises from prostate adenocarcinoma following androgen deprivation therapy, with 20‑25% of metastatic castration‑resistant prostate cancers undergoing NE differentiation due to lineage plasticity. During this transition, pathways associated with epithelial‑mesenchymal transition (EMT) and stemness are broadly activated, which is considered to be a key driver of NEPC's high metastatic potential, resistance to chemotherapy and radiotherapy and poor prognosis. EMT facilitates metastasis by enhancing cellular motility and invasiveness, while stemness properties contribute to post‑metastatic colonization, immune evasion, therapy resistance and cellular dormancy. As manifestations of cellular plasticity, these processes share overlapping molecular mechanisms. Targeting key regulators within these pathways may offer promising therapeutic strategies for NEPC.

The aim of the present study was to investigate the direct effects of BMS‑202 on melanoma cells. The small molecule programmed cell death ligand 1 (PD‑L1) inhibitor BMS‑202 was used to treat A375 melanoma cells. The cell distribution of BMS‑202 was examined using low‑power and high‑resolution confocal microscopy, focusing on its localization in mitochondria. The impact of BMS‑202 on mitochondrial gene expression levels, the activity of respiratory chain complexes, and the levels of reactive oxygen species and apoptosis‑related genes, including Bax, Bcl‑2, PARP and caspase‑3, were assessed by quantitative PCR and western blotting. Additionally, tumor cell viability, proliferation, migration and invasion were evaluated in vitro, with in vivo experiments conducted through the construction of tumor‑bearing mouse models and Ki‑67 immunohistochemical staining to validate tumor proliferation. The function of mitochondria was inhibited using a pyruvate carrier inhibitor to examine how this affected the action of BMS‑202. The results revealed that BMS‑202 can inhibit tumor cell function and promote apoptosis. Furthermore, BMS‑202 was shown to enter the mitochondria where it may bind to PD‑L1 and improve mitochondrial function. By inhibiting mitochondrial function, the antitumor effects of BMS‑202 can be enhanced. Overall, the present study provides information on the potential antitumor mechanisms of BMS‑202 as well as a theoretical basis for its application in melanoma therapy.

Histone deacetylase 6 (HDAC6), a distinctive member of the histone deacetylase family, plays a crucial role in regulating the cellular response to oxidative stress. Unlike other HDACs, HDAC6 primarily deacetylates non‑histone proteins, influencing various cellular functions critical to the pathogenesis of numerous oxidative stress‑related diseases. This review summarizes the latest research on how HDAC6 affects oxidative stress pathways and its impact on diseases such as neurodegeneration, cancer and cardiovascular disorders. Additionally, the therapeutic potential of targeting HDAC6, as evidenced by preclinical trials, was discussed, suggesting that HDAC6 inhibitors can ameliorate symptoms and alter disease progression in numerous disease models. By elucidating the multifaceted roles of HDAC6 in oxidative stress and disease, the review aims to underscore its potential as a therapeutic target. This review enhances the understanding of HDAC6 and presents new opportunities for innovative treatment approaches that can address oxidative stress‑related illnesses.

Osteosarcoma is the most common primary bone cancer, primarily affecting children and young adults. Cancer stem cells (CSCs), a subpopulation presenting stemness, critically influence prognosis and promote recurrence and metastasis. Due to the crucial role of glycogen synthase kinase‑3 beta (GSK‑3β) in maintaining stemness, it is considered as an important target for drug development. The aim of the present study was to evaluate the inhibitory effect of AZD1080, a GSK‑3β inhibitor, on osteosarcoma CSCs. AZD1080 treatment clearly inhibited sphere formation in U2OS and 143B cells and dissociated spheres in CSCs derived from U2OS and 143B; in both processes, stemness markers OCT4 and SOX2 were markedly decreased, without affecting cell proliferation or apoptosis. AZD1080 treatment inhibited phosphorylation of GSK‑3β and its downstream regulated genes, including HEY1, HES1, CyclinD1 and β‑catenin. It was also observed that GSK‑3β activity was critical for the inhibitory effects of AZD1080 treatment on sphere formation and stemness. Moreover, GSK‑3β knockdown inhibited sphere formation and invasion capacity, indicating that AZD1080 exerts inhibitory roles in a GSK‑3β‑dependent manner. Taken together, the results showed AZD1080 as a specific inhibitor of CSC stemness, without cytotoxicity, and indicated it was a promising therapeutic agent that targeted GSK‑3β signaling in osteosarcoma.

MicroRNAs (miRs) are non‑coding RNAs that prevent the translation of mRNAs. miRs participate in cellular processes such as cell proliferation, migration and invasion, acting as oncogenes or tumor suppressors. In epithelial ovarian cancer (EOC), a decrease in tumor suppressor miRs, such as miR‑145 and miR‑23b, regulates the mRNAs of oncogenic proteins. The present study aimed to determine whether the co‑transfection of two oncosuppressor miRs (miR‑145‑5p and miR‑23b‑3p) decreased the proliferation, migration, invasion, and protein levels of c‑MYC, zinc finger E‑box binding homeobox 1 (ZEB1) and ATP binding cassette subfamily B1 (ABCB1) in EOC cell lines (A2780, SKOV‑3 and OV‑90). Reverse transcription‑quantitative PCR was employed to determine miR expression after co‑transfection. Cell proliferation was evaluated by Ki‑67 immunofluorescence staining and Ki‑67 positive cell counting. Transwell inserts, both with and without Matrigel, were used to assess invasion and migration, respectively. c‑MYC, ZEB1 and ABCB1 protein expression was determined by western blot analysis. The co‑transfection of miR‑145 and miR‑23b resulted in decreased proliferation, migration and invasion, along with reduced protein expression levels of c‑MYC, ZEB1 and ABCB1 in EOC cells. The combination of miR‑23b and miR‑145 transfection in EOC cells exhibited good antitumor effects, thus supporting the design of future complementary therapies for EOC.

Despite considerable advances in cancer treatment, gastric cancer (GC) remains a formidable challenge for oncologists worldwide, especially due to the poor survival rates associated with advanced‑stage cases. Circular RNAs (circRNAs) stand out as potential targets for more effective therapeutic strategies. The present review synthesizes insights into the roles of circRNAs in GC, highlighting their multifaceted influence on cancer progression and behaviors. circRNAs can regulate gene expression at multiple levels through modulating transcription, affecting alternative splicing, acting as molecular sponges for microRNAs, serving as RNA‑protein complexes and even encoding functional proteins. The marked stability of circRNAs in bodily fluids has also positioned them as promising diagnostic biomarkers, with some circRNA‑based tests demonstrating high accuracy. Furthermore, emerging evidence indicates that circRNAs carry out a key role in therapy resistance, affecting the therapeutic responses of patients to chemotherapy, targeted therapy and immunotherapy. Collectively, circRNA‑based therapeutic strategies, even with existing challenges in delivery methods, hold considerable promise, particularly when integrated with conventional treatment modalities, offering new avenues for improving GC management.

In this review, the role of microRNA‑21 (miRNA‑21) as an oncogene in lung cancer was investigated. Studies have shown that miRNA‑21 can promote the progression of lung cancer by targeting downstream target genes, and its expression can be modulated by transcription factors, DNA methylation or competitive endogenous RNA as an upstream regulator. This review highlights that miRNA‑21 can promote the progression of lung cancer through multiple signaling pathways, with a focus on the PI3K/AKT, MEK/ERK, TGF‑β/SMAD, Hippo, NF‑κB and STAT3 signaling pathways. Mechanistically, miRNA‑21 plays an important role in the progression of lung cancer by regulating multiple biological processes, such as proliferation, invasion, metastasis, apoptosis and angiogenesis in lung cancer cells. Higher expression of miRNA‑21 is associated with chemotherapy, radiotherapy and immune resistance in lung cancer. Targeting these molecular pathways may be a novel therapeutic strategy for treating lung cancer. Additionally, miRNA‑21 can serve as a biomarker for lung cancer diagnosis, prognosis and treatment response. This review also summarized the following: i) Current methods employed to inhibit the expression of miRNA‑21 in lung cancer, including CRISPR/Cas9 technology; ii) the application of natural anticancer agents, oligonucleotides, small molecules and miRNA sponges; and iii) the nano‑delivery systems developed for miRNA‑21 inhibitors. Finally, the advancements in research on miRNA mimics and inhibitors in clinical trials, which may promote the application of miRNA‑21 in clinical trials in lung cancer, were discussed. Given that lung cancer is a considerable public health challenge, these studies provide new ways of treating patients with lung cancer.

Lung adenocarcinoma (LUAD) is the most prevalent form of lung cancer and the predominant cause of cancer-associated mortality. Given the low survival rate of patients with LUAD, there is a need to identify new therapeutic targets. Glycoprotein M6B (GPM6B) is a tumor‑associated gene in numerous types of malignancies; however, its specific role in LUAD remains largely unexplored. Integrated bioinformatics analyses of The Cancer Genome Atlas and Gene Expression Omnibus datasets, along with immunohistochemistry assays demonstrated that GPM6B was downregulated in LUAD compared with adjacent normal tissue. Elevated expression of GPM6B was associated with prolonged survival in patients with LUAD, suggesting that GPM6B serves as a prognostic biomarker in LUAD. Cell Counting Kit‑8 (CCK‑8) and Transwell assays demonstrated that exogenously expressed GPM6B significantly inhibited the proliferation and migration of the LUAD cell lines A549 and PC9. Notably, tumorigenesis assays conducted in nude mice demonstrated that the overexpression of GPM6B also suppressed tumor growth in vivo. Mechanistically, GPM6B may have inhibited the malignant behavior of LUAD cells by promoting the expression of 15‑hydroxyprostaglandin dehydrogenase and activating the p53 signaling pathway, as evidenced by transcriptome data analysis, western blotting and phenotypic assays. Furthermore, the qPCR results from LUAD cells treated with DNA methylation and histone deacetylase inhibitors indicated that low expression of GPM6B was associated with DNA methylation and histone deacetylation. Overall, the present study demonstrated that GPM6B may serve as a novel tumor suppressor and elucidated its potential mechanism in regulating the progression of LUAD.

Muscle excess 3A (MEX3A), a dual‑function RNA‑binding protein with E3 ubiquitin ligase activity, is a pivotal regulator of tumorigenesis. By modulating mRNA stability, translation and targeted protein degradation, MEX3A orchestrates key oncogenic processes, including tumor stemness maintenance, proliferation, migration and immune evasion. MEX3A is aberrantly expressed in various malignancies, such as colorectal and breast cancer, hepatocellular carcinoma and glioblastoma, where it engages key signaling pathways, including the Wnt/β‑catenin, PI3K/AKT and NF‑κB pathways. Mechanistically, MEX3A directly regulates oncogenic and tumor suppressor transcripts, influencing the cell dynamics within the tumor microenvironment. Furthermore, MEX3A upregulation is associated with a poor prognosis and therapy resistance, highlighting its potential as a prognostic biomarker and therapeutic target. The present review aimed to summarize the molecular functions, tumor‑specific roles and translational relevance of MEX3A, bridging the gap between mechanistic insight and clinical applications. Future studies exploring MEX3A‑targeted interventions may reveal novel strategies for precision oncology.

Hepatocellular carcinoma (HCC) is a major global health concern, accounting for a significant proportion of liver cancer cases and related deaths. Clonorchis sinensis (C. sinensis) infection, a recognized carcinogen, has been implicated in the progression of liver diseases, including HCC. However, the precise epigenetic mechanisms underlying C. sinensis-associated HCC remain to be elucidated.

Cervical cancer (CC) is one of the most prevalent malignancies in women, posing a significant challenge globally. However, the precise molecular mechanism regulating CC progression through methyltransferase-like protein 3 (METTL3) and UL16 Binding Protein 2 (ULBP2) remains largely unknown.

Phosphoglycerate dehydrogenase (PHGDH) is the rate-limiting enzyme in the de novo Serine synthesis pathway (SSP), a highly regulated pathway overexpressed in several tumors. Specifically, PHGDH expression is dynamically regulated during different stages of tumor progression, promoting cancer aggressiveness. Previously, we demonstrated that high Serine (Ser) availability, obtained by increased exogenous uptake or increased PHGDH expression, supports 5-Fluorouracil (5-FU) resistance in colorectal cancer (CRC). Beyond its metabolic role in sustaining Ser biosynthesis, different "non-enzymatic roles" for PHGDH have recently been identified. The present study aims to investigate non-enzymatic mechanisms through which PHGDH regulates 5-FU response in CRC.

Skin cutaneous melanoma (SKCM) is one of the highly malignant tumor. This study aimed to investigate the expression levels of MTHFD1L in cutaneous melanoma and to uncover its potential biological significance.

The role of post-translational modifications(PTMs) in PD-L1-mediated immune resistance and melanoma progression remains poorly understood.

Iron is an essential trace element in the human body, and its imbalance is closely linked to the initiation and progression of various malignancies. The solute carrier family 11 (SLC11) transporters, comprising SLC11A1 and SLC11A2, play pivotal roles in iron metabolism and cellular homeostasis, processes intricately linked to oncogenesis. SLC11A1, primarily expressed in macrophages, modulates immune responses and reshapes the tumor microenvironment, while SLC11A2, a ubiquitous iron transporter, regulates dietary iron absorption and ferroptosis, an iron-dependent form of programmed cell death. Dysregulation of these transporters is associated with tumor initiation, progression, metastasis, and therapy resistance. In this review, we provide an overview of the physiological functions of SLC11 transporters in iron metabolism and their pathological roles in cancer biology. Emerging evidence highlights their involvement in key oncogenic pathways, including p53, JAK/STAT, Wnt and HIF signaling. Pharmacological and genetic interventions targeting SLC11 transporters have shown the potential to disrupt tumor progression and enhance treatment efficacy. By exploring the intricate roles of SLC11A1 and SLC11A2 in cancer progression, this review offers insights into their potential as biomarkers and therapeutic targets, paving the way for innovative cancer treatment strategies.

Triple-negative breast cancer (TNBC) lacks targeted therapies, leading to a poor prognosis. Younger patients with TNBC often present with aggressive disease and exhibit distinct tumor microenvironments (TME). We performed spatial profiling to understand the influence of menopausal status on the immune environment, tumor progression, and therapy response.

Glioblastoma is the most aggressive type of brain tumor and is associated with a poor prognosis. First-line treatment is surgical resection followed by radiotherapy and temozolomide-based chemotherapy. However, the duration of treatment with temozolomide is limited due to both its toxicity and the development of drug resistance. The prognostic and predictive factor for response to temozolomide is the methylation status of the MGMT promoter. Indeed, loss of MGMT promoter methylation is a major cause of chemoresistance. However, the development of drug resistance is not only associated with changes in MGMT methylation. The entire epigenome changes and acquires specific properties necessary for tumor progression.