Dermoid cysts in the cavernous sinus (CSDCs) are scarce, and their key features are largely unknown. A systematic review was conducted following PRISMA guidelines up to March 2025, using PubMed and Google Scholar databases. Actual CSDCs with sufficient available information were selected. An additional case from the authors' series was included. Data collected included age, gender, CSDC size, symptoms, duration from symptom onset, physical findings, radiological features, treatment, and outcomes. Thirty-eight cases were analyzed (37 from databases plus the author's case). Headache and diplopia were the most common presenting symptoms. The most frequent signs were trigeminal, oculomotor, and abducens palsies. The average CSDC size was 42.6 mm (SD 20.3). Cyst shapes included oval (n = 21/37, 56.7%), circular (n = 6/37, 16.2%), and dumbbell (n = 10/37, 27%). Extracavernous growth was observed in 12 of 37 cases (32.4%), mainly among dumbbell-shaped cysts (p < 0.001). CSDC rupture was seen in 13 of 38 cases (34.2%), with associations to hydrocephalus (p < 0.001), larger cyst size, epilepsy, and aseptic meningitis (p < 0.05). Hydrocephalus (n = 5/38; 13%) correlated with cyst rupture and larger size (p < 0.001). Most CSDCs (30/38, 79%) were in the cavernous sinus lateral-interdural compartment, while 8 cysts (21%) were within the venous intracavernous space. Medial ICA displacement was only seen in interdural CSDCs (p < 0.001). CSDC removal was attempted in 33 of 38 cases (86.8%). Complete removal was achieved in 21 of 29 cases (72.4%), near-total in 6 (20.7%), and partial in 2 (6.9%). All clinical outcomes were satisfactory (median mRS 0, IQR 0-1). Transient postoperative abducens palsy was associated with endoscopic-endonasal approaches (p < 0.05). CSDCs are rare lesions that usually present with headache and cranial nerve palsies. They are mostly interdural, located at the CS lateral wall. Surgery remains the primary treatment for CSDCs and should be tailored to the cyst's location (interdural versus purely intracavernous).

Colon cancer (CC) stands as one of the most prevalent malignant neoplasms worldwide. Despite extensive investigations on the function of T cells in antitumor immunity and dynamics of tumor microenvironment (TME), their precise molecular contributions to the CC progression remain incompletely characterized. Differential gene expression analysis was implemented leveraging TCGA-COAD transcriptomic data, followed by the identification of T cell signature genes using single-cell RNA sequencing (scRNA-seq) dataset. Through intersectional analysis and subsequent prognosis-related gene screening using least absolute shrinkage and selection operator (LASSO) regression and multivariate Cox proportional hazards models, a prognostic model was established. Moreover, its performance was evaluated via receiver operating characteristic (ROC) curves. Participants were split into high-risk and low-risk cohorts based on risk scores, to explore potential immunological differences between groups. A prognostic model was developed based on seven genes, encompassing UBE2N, TUBA1C, FXR1, CBLB, YTHDC1, GPRIN3, and AGPAT2. The area under the ROC curve (AUC) for the training cohort at 3, 5, and 7 years reached 0.676, 0.715, and 0.721, respectively. External validation using three GEO datasets demonstrated consistent predictive performance of the model. The AUC values at 3, 5, and 7 years were 0.632, 0.617, and 0.582 in GSE39582, 0.689, 0.755, and 0.951 in GSE17537, and 0.667, 0.653, and 0.649 in GSE161158. The identified T cell signature genes may function as potential therapeutic targets, while the developed prognostic model and nomogram may facilitate clinical decision-making for CC management.

To identify cuproptosis-related genes as potential diagnostic, therapeutic, and prognostic biomarkers for glioblastoma (GBM). The GBM GSE16011 dataset was downloaded from the GEO database, and the dataset was subjected to differential gene analysis via Perseus software. Cuproptosis-related genes were obtained from the PubMed database. Venn analysis was used to obtain the cuproptosis-related DEGs (CuDEGs) between the DEGs and the cuproptosis-related genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were conducted to explore the functions of the CuDEGs, and cluster analysis was performed to assess the similarity of the CuDEGs between the GBM group and the control group. Potential targets were screened through protein-protein interaction (PPI) analysis and the fold change values of differential expression. The expression of potential targets in GBM tissues was validated via the GEPIA database, and survival analysis was used to determine the prognostic value of potential targets. Potential targets and core targets were further verified through analysis of the GSE16011 dataset, Human Protein Atlas (HPA) database, and experimental validation in U87-MG and U251 GBM cells using immunofluorescence and western blot. A total of 39 CuDEGs were obtained from the intersection of 9,849 DEGs and 88 cuproptosis-related genes. GO and KEGG enrichment analyses revealed that the CuDEGs were closely associated with the occurrence and development of GBM. Among the 39 CuDEGs, 11 potential targets with a fold change greater than 1.2 were selected. The expression of 11 potential targets was subsequently validated. Compared with that in the control group, the expression of the 6 upregulated CuDEGs significantly increased in the GBM group. Among the 6 upregulated CuDEGs, VEGFA, LOX, and LOXL1 were significantly different in overall survival (P < 0.05), with high expression correlated with lower survival rates and shorter survival times. However, no significant differences in overall survival were observed for the 5 downregulated CuDEGs. Three upregulated VEGFA, LOX and LOXL1 were selected as potential core targets for GBM. Significant differences in overall survival were shown for these three potential core targets combined, with high expression still associated with lower survival rates and shorter survival times. The expression levels of the three potential core targets were positively correlated with glioma grade, and significant differences were detected in grade IV gliomas compared with other grades in the GEPIA database. Experimental validation confirmed significantly elevated expression of these three genes in GBM cells compared to normal controls. The cuproptosis-related genes VEGFA, LOX, and LOXL1 are highly expressed in GBM and closely associated with tumor progression and poor prognosis, suggesting their potential as core biomarkers for GBM diagnosis, therapy, and prognosis evaluation.

Cancer survivors experience a range of side effects during and after treatment. There is a need for a rigorous synthesis of the most recent and best available evidence on the role of nutritional supplements for supportive care in cancer, to inform shared decision-making. We searched 5 databases for umbrella reviews, meta-analyses and systematic reviews on nutritional supplements for supportive cancer care, excluding studies on pain, anxiety and depression, which are covered in recent guidelines. We found 52 reviews that reported on 250 RCTs on 18 supplements for 16 indications. Almost all reviews were of low/critically low quality (assessed using A MeaSurement Tool to Assess systematic Reviews version 2). There was moderate-certainty evidence for benefit from the following supplements: amino acids and oral proteolytic enzymes for severity of radiation-induced dermatitis, N-acetyl cysteine for prevention of chemotherapy-induced peripheral neuropathy (CIPN) in individuals with gastrointestinal cancers. There was low to very low certainty evidence that glutamine, zinc, probiotics and melatonin may be effective for oral mucositis; Vitamin E, omega-3 fatty acids, glutamine and other amino acids may be effective for preventing CIPN. Serious adverse events were reported for high-dose Vitamin A, and dose-related adverse events were reported with zinc and Vitamin E. However, the majority of nutritional supplements were associated with only minor adverse events. Due to the low to very low certainty of the majority of evidence, firm clinical recommendations cannot be made. Further research to conclusively evaluate benefit and harm, including potential impact on efficacy of standard treatments, should be conducted.

TROP2, a critical cell surface oncogenic signal transducer, is increasingly linked to refractory metastatic colorectal cancer (CRC) and other solid tumours. Robust lactate accumulation within metastatic niches correlates with pathological metastatic progression. Anti-TROP2 antibody-drug conjugates (ADCs) are clinically available but show limited efficacy in advanced metastatic CRC. Elucidating how TROP2 signalling orchestrates molecular and cellular programs enabling CRC metastatic progression would help improve metastasis therapies.

Tissue microarray, immunohistochemistry, and western blotting delineated TROP2's pathological role in CRC liver metastasis (CRLM). Metabolomics characterised TROP2-mediated metabolic effect. Western blot detected TROP2 responsive lactylation sites. Cell-derived xenograft (CDX), intra-splenic injection models, and patient-derived xenografts (PDX) validated TROP2 or TROP2-induced H3K18 lactylation (H3K18la) in CRLM pathogenesis and Acriflavine therapeutic response. Genome-wide H3K18la profiling was performed by ChIP-seq.

Here, we identify a self-reinforcing positive feedback loop between H3K18la and TROP2 in CRC cells that drives CRC metastatic progression. We show that TROP2 is elevated during CRC metastatic process, with high TROP2 levels in liver metastases predicting increased post-therapy recurrence in two distinct cohorts. We find that H3K18la levels are upregulated in CRC cells in response to TROP2 expression level. TROP2 promotes robust lactate production via the YBX1-HIF-1α signal axis. Targeting glycolytic flux decreases H3K18 lactylation and curbs TROP2-driven CRLM colonisation and progression. Mechanistically, ChIP-seq detection reveals H3K18la deposition at a set of pro-metastatic gene promoters, promoting their expression. Crucially, TROP2-induced H3K18la is found in turn sustaining TROP2 expression, forming a positive feedback loop that further accelerated metastatic progression. Pharmacologic HIF-1α inhibition with acriflavine, an old FDA-approved agent, suppresses TROP2-high CRLM progression in multiple pre-clinical models.

Collectively, we establish H3K18la as a crucial epigenetic driver of TROP2-mediated CRLM progression and propose that disrupting the H3K18la-TROP2 feedback loop offers a novel therapeutic strategy against CRC metastasis.

H3K18la is specifically increased in CRC cells in response to TROP2 signalling and drives TROP2-mediated CRLM progression Genome-wide analysis shows H3K18la deposition at the promoters of metastasis-promoting genes drives their expression in TROP2-high CRC. Lactate sustains TROP2 expression in CRC cells via H3K18la Acriflavine suppresses TROP2-driven CRLM by targeting the H3K18la/TROP2 feedback loop.

Luffa cylindrica flower has been used to treat haemorrhoids and breast hyperplasia, but the mechanism is unclear.

In this study, the antiproliferation activity of L. cylindrica flower extract (LCFE) was tested in breast cancer cells.

Following LCFE treatment, the CCK-8 assay, Hoechst staining and wound healing assay were used to evaluate cell proliferation, apoptotic cell morphology, and cell migration, respectively. qRT-PCR and western blot were used to analyze the expression of genes and proteins involved in the apoptosis and autophagy pathways. LC-MS was performed to characterize chemical constituents of LCFE.

CCK-8 and wound healing assays revealed that LCFE suppressed the proliferation and migration of MCF-7 and MDA-MB-231 cells. In these two breast cancer cells, the extract treatment induced apoptotic morphological changes. LCFE treatment induced apoptosis by upregulating ZFP36 and BNIP3 expression, while downregulating Bcl-2 expression in MCF-7 cells. LCFE increases ZFP36 expression while decreasing BMP4 expression in MDA-MB-231 cells, promoting apoptosis. Meanwhile, LCFE treatment induced autophagy by increasing VMP1 expression and activating LC3 in MCF-7 cells. It also triggered autophagy by decreasing TBC1D14 expression, increasing ATG5 and VAMP8 expression, and activating LC3 in MDA-MB-231 cells.

LCFE exerts an anti-tumor effect by activating apoptosis and autophagy processes in breast cancer cells, while having low cytotoxicity for normal breast cells, highlighting the potential of LCFE as a natural agent for cancer treatment.

Paclitaxel is used in oral cancer treatment, but drug sensitivity remains a concern. CHFR has been implicated in tumor regulation, yet its role in modulating paclitaxel sensitivity in oral cancer requires further investigation.

This study aimed to evaluate the effect of CHFR on enhancing the drug sensitivity of paclitaxel in oral cancer cells.

A rat oral tumor model was established, followed by paclitaxel intervention. Observations included tongue tissue morphology, immune function, cell cycle, apoptosis, and the expression levels of NF-κB and CHFR proteins and mRNAs.

The modeling success rate was 100%, with visible tongue masses and ulceration. CHFR protein expression increased in the CHFR mimic group. The high-dose paclitaxel group showed the highest immune indices, increased G0/G1 phase cell proportion, and significantly decreased tumor cell viability. The CHFR mimic group exhibited the smallest tumor volume, marked tumor cell death, and active proliferation. CHFR downregulated NF-κB expression; CHFR mRNA was higher, and NF-κB mRNA lower, compared to the high-dose paclitaxel and CHFR mimic groups.

CHFR enhances paclitaxel sensitivity in oral cancer cells by downregulating NF-κB, effectively inhibiting tumor cell activity and suppressing tumor progression.

This study assessed the anticancer activity of boron-containing and structurally diverse small molecules in 4T1 breast cancer and Caco-2 colon adenocarcinoma cells. Initial screening showed that five boronic acids lacked significant cytotoxicity, underscoring the structural specificity required for boron-mediated bioactivity. Similarly, reference compounds, including fumaric acid, caffeic acid, ferulic acid, dimethyl malonate and N-(tert-butoxycarbonyl)-L-alanine, showed no cytotoxic effect under identical conditions. Among the tested agents, 1-acetyl-4-(4-hydroxyphenyl)piperazine (1A4HP) displayed the most potent cytotoxicity, with IC₅₀ values of 149.7 μM in 4T1 and 825 μM in Caco-2 cells. For comparison, the clinically investigated antimetastatic agent tasquinimod showed moderate activity in 4T1 cells (IC₅₀ = 180.7 μM), serving as a pharmacological benchmark. Mechanistic assays revealed that 1A4HP induced apoptosis and significantly impaired 4T1 cell migration, suggesting combined antiproliferative and antimetastatic effects. Computational analyses further supported 1A4HP's drug-like potential by predicting favourable physicochemical properties, including balanced lipophilicity and high solubility. Molecular docking studies indicated a strong binding affinity to oestrogen receptor alpha (ERα), surpassing that of tamoxifen. Notably, despite 4T1's ER-negative status, 1A4HP suppressed cell growth, suggesting possible ER-independent or off-target mechanisms, similar to tamoxifen's secondary effects. Collectively, these results identify 1A4HP as a promising lead compound for further exploration in breast cancers.

Tumor metastasis is a key factor in cancer progression, yet its molecular mechanisms are not fully understood. ERBB2-positive lung cancer exhibits aggressive behavior, and the role of miR-139 in its metastasis requires investigation.

This study aimed to explore the function of miR-139 in ERBB2-positive lung cancer and its underlying molecular mechanism involving the ERBB2/Rac1/NF-κB signaling axis.

The study utilized A549 lung cancer cells and tissue samples from 106 lung cancer patients. Methods included RT-PCR, bioinformatics analysis, dual-luciferase reporter assay, Western blot, cell migration/invasion assays, wound healing tests, Rac1 activity assays, and rescue experiments using Rac1-Q61L.

MiR-139 expression was significantly downregulated in lung cancer tissues, especially in lymph node metastases (P<0.01). MiR-139 directly targeted the 3'UTR of ERBB2 and inhibited its expression (P<0.01). Overexpression of miR-139 reduced Rac1 activity (P<0.01) without affecting RhoA or Cdc42, and decreased NF-κB signaling activity in ERBB2-positive tissues. MiR-139 overexpression significantly suppressed cell migration and invasion (P<0.01), an effect partially reversed by Rac1-Q61L.

MiR-139 inhibits lung cancer cell migration and invasion by targeting ERBB2, suppressing Rac1 activity, and downregulating NF-κB signaling. Its downregulation promotes metastasis through the ERBB2/Rac1/NF-κB axis.

Cutaneous squamous cell carcinoma (CSCC) is a malignant tumor originating from epidermal keratinocytes. In various types of tumors, ferroptosis is a vital iron-dependent form of regulated cell death. Recent studies suggest that heat shock protein 27 (HSP27), encoded by the heat shock protein family B member 1 (HSPB1) gene, is involved in the regulation of ferroptosis, but the specific mechanism remains unclear. In this study, CSCC cell lines were transfected with lentivirus-mediated HSPB1-shRNA or lentivirus carrying overexpressed HSPB1. CSCC cell lines, xenograft mouse models, and ferroptosis inhibitors or inducers were applied to verify the mechanism and function of HSP27. Downregulation of HSP27 inhibited the proliferation, migration, and invasion of CSCC cells, whereas upregulation of HSP27 showed the opposite results. Similarly, tumor volume and weight were reduced after HSP27 was downregulated in vivo. Further studies revealed that HSP27 promoted the growth of CSCC cells and tumors by inhibiting ferroptosis, and the downregulation of HSP27 enhanced ferroptosis induced by Erastin. Ferrostatin-1 or Erastin successfully reversed the phenotype triggered by HSP27 alterations. HSP27 can induce the growth of CSCC by inhibiting ferroptosis, and is expected to become a new target for the treatment of CSCC.