Xifeng Xiong

Crowned dens syndrome (CDS) is a rare crystal deposition disorder characterized by distinctive halo‑like or coronal calcification surrounding the odontoid process, primarily manifesting as neck pain and restricted mobility, occasionally accompanied by systemic inflammatory signs. The present report describes two cases of patients with this condition with the aim of elucidating the clinical spectrum and management of CDS. The first case involved a 72‑year‑old male patient who exhibited marked symptom relief following treatment with non‑steroidal anti‑inflammatory drugs and a brief corticosteroid regimen, with no recurrence noted over a 2‑year follow‑up period. The second case involved an 81‑year‑old male patient who developed severe cervical spinal cord compression due to a calcified pseudotumor posterior to the odontoid process, leading to debilitating neurological deficits. This patient underwent a posterior atlas arch resection with microscopy assistance, resulting in the marked alleviation of spinal cord compression symptoms and sustained improvement over 3 years of follow‑up. On the whole, the present report underscores the importance of recognizing CDS and highlights that isolated posterior arch resection may serve as an effective intervention for patients with associated high cervical myelopathy. Given the rarity of this condition, further investigations through additional case reports are warranted to confirm these findings.

Nuciferine (NF), an aporphine alkaloid extracted from the leaves of Nelumbo nucifera Gaertn., has attracted considerable attention due to its wide range of pharmacological properties. The present review elucidates the multifaceted biological activities of NF, which encompass immunomodulatory and antioxidative effects, neuroprotective, musculoskeletal‑protective, cardioprotective, metabolism‑regulating, antipsychotic and anticancer effects. Notably, the underlying mechanisms involve the modulation of key signaling pathways, such as AMP‑activated protein kinase, peroxisome proliferator‑activated receptor α, TGF‑β1, Toll‑like receptor 4/NF‑κB and PI3K/Akt, which contribute to its metabolic regulation and anticancer properties. Furthermore, the present review discusses the findings of molecular docking simulations using an in silico approach, which offer valuable insights into the interactions of NF with various biological targets. However, despite its therapeutic potential, several challenges remain in translating the use of NF into clinical applications. These include concerns regarding its toxicity or undesirable effects, as well as issues associated with its bioavailability and drug delivery profile. Future research should focus on addressing these challenges to fully realize the therapeutic potential of NF across a range of diseases.

Skin cutaneous melanoma (SKCM) is an aggressive and life-threatening skin cancer arising from the malignant transformation of melanocytes. The incidence has risen in recent decades, significantly impacting patients’ quality of life and straining healthcare systems. Existing prognostic biomarkers for SKCM are not accurate enough, emphasizing the urgent need for new biomarkers and therapeutic targets. This study comprehensively explored the role of Melan-A (MLANA) in SKCM through bioinformatics analysis and in-vitro experiments. Results showed that MLANA is overexpressed in SKCM tissues, significantly linked to Breslow depth, and associated with poor patient prognosis. Functional assays revealed that interfering with MLANA expression inhibits melanoma cell proliferation, migration, and invasion, while inducing apoptosis and G1/S phase arrest. Immune infiltration analysis revealed a negative correlation between high MLANA expression and the infiltration levels of various immune cells, indicating that MLANA may facilitate SKCM progression by altering the tumor microenvironment. The study highlights MLANA’s biological importance in SKCM, suggesting its potential as a prognostic biomarker and immunotherapy target, thereby providing new insights for SKCM diagnosis and treatment.

Phosphoglycerate mutase 1 (PGAM1) has been identified as a key player in the progression and metastasis of various human cancer types, including breast cancer (BC); however, its precise oncogenic mechanism remains unclear. The present study aimed to investigate the oncogenic mechanisms of PGAM1 and establish its potential as a therapeutic target. Comprehensive analyses from the Tumor Immune Estimation Resource 2.0 and The Cancer Genome Atlas databases revealed a significant upregulation of PGAM1 in BC, correlating with poor clinical outcomes. Additionally, elevated expression of PGAM1 was confirmed in clinical BC samples. Silencing PGAM1 with specific small hairpin RNA in BC cells resulted in a marked reduction in cell proliferation, invasiveness and migration, alongside increased apoptosis and cell cycle arrest. In vivo experiments using tumor-bearing nude mice demonstrated that PGAM1 knockdown significantly reduced tumor volume and weight, effectively inhibiting tumor growth. Mechanistic investigations suggested that PGAM1 promoted BC tumorigenesis through the activation of the Wnt/β-catenin signaling pathway, both in vitro and in vivo. Therefore, the upregulation of PGAM1 in BC enhances malignancy via the Wnt/β-catenin signaling pathway, highlighting PGAM1 as a promising therapeutic target for BC treatment.

Helicase POLQ‑like (HELQ or Hel308), is a highly conserved, 3'‑5' superfamily II DNA helicase that contributes to diverse DNA processes, including DNA repair, unwinding, and strand annealing. HELQ deficiency leads to subfertility, due to its critical role in germ cell stability. In addition, the abnormal expression of HELQ has been observed in multiple tumors and a number of molecular pathways, including the nucleotide excision repair, checkpoint kinase 1‑DNA repair protein RAD51 homolog 1 and ATM/ATR pathways, have been shown to be involved in HELQ. In the present review, the structure and characteristics of HELQ, as well as its major functions in DNA processing, were described. Molecular mechanisms involving HELQ in the context of tumorigenesis were also described. It was deduced that HELQ biology warrants investigation, and that its critical roles in the regulation of various DNA processes and participation in tumorigenesis are clinically relevant.