Yueyan Huang

Biomolecules play pivotal roles in cellular signaling, metabolic regulation and the maintenance of physiological homeostasis in the human body, and their dysregulation is closely associated with the onset and progression of various human diseases. Consequently, the development of highly sensitive, selective, and stable detection platforms for these molecules is of significant value for drug discovery, pharmaceutical quality control, pharmacodynamic studies, and personalized medicine. In recent years, electrochemical biosensors, particularly those integrated with functional nanomaterials and biorecognition elements, have emerged as powerful analytical platforms in pharmaceutics and biomedical analysis, owing to their high sensitivity, exquisite selectivity, rapid response, simple operation, low cost and suitability for real-time or in situ monitoring in complex biological systems. This review summarizes recent progress in the electrochemical detection of representative biomolecules, including dopamine, glucose, uric acid, hydrogen peroxide, lactate, glutathione and cholesterol. By systematically summarizing and analyzing existing sensing strategies and nanomaterial-based sensor designs, this review aims to provide new insights for the interdisciplinary integration of pharmaceutics, nanomedicine, and electrochemical biosensing, and to promote the translational application of these sensing technologies in drug analysis, quality assessment, and clinical diagnostics.

Exosomes, spherical lipid-bilayered particles secreted by cells, have recently emerged as a novel and highly promising drug delivery system, attracting extensive attention in the field of biomedical research. Dendritic-cell-derived exosomes (DC-Exos) possess surface protein and ligands characteristic of DC cells, such as functional MHC-I and MHC-II, CD80, CD86. These components play a crucial role in immune responses, facilitating antigen uptake, presentation, and the activation of antigen-specific CD4 and CD8 T cells. These properties make them striking and excellent drug delivery vehicles for use in various immune diseases and cancer therapy. This review summarizes and discusses the characteristics, current methods and types of drug loading of DC-Exos. Its surface modifications and application in disease treatment were also discussed, aiming to motivate the development of exosome-based theranostic nanoplatforms and nanotechnology for improved healthcare treatments.

Nanoparticle-based drug delivery systems hold promise for cancer treatment by enhancing the solubility and stability of anti-tumor drugs. Nonetheless, the challenges of inadequate targeting and limited biocompatibility persist. In recent years, cell membrane nano-biomimetic drug delivery systems have emerged as a focal point of research and development, due to their exceptional traits, including precise targeting, low toxicity, and good biocompatibility. This review outlines the categorization and advantages of cell membrane bionic nano-delivery systems, provides an introduction to preparation methods, and assesses their applications in cancer treatment, including chemotherapy, gene therapy, immunotherapy, photodynamic therapy, photothermal therapy, and combination therapy. Notably, the review delves into the challenges in the application of various cell membrane bionic nano-delivery systems and identifies opportunities for future advancement. Embracing cell membrane-coated biomimetic nanoparticles presents a novel and unparalleled avenue for personalized tumor therapy.

Background: Cases of both of small- (SCLC) and large-cell neuroendocrine lung carcinoma (LCNEC) were rarely reported. Although typical cases are morphologically distinct, the distinction between LCNEC and SCLC is still controversial, with some LCNECs showing close morphologies with SCLC. Here, we reported on a patient who had tumor with a mix of SCLC and LCNEC and uncovered these components’ histological and genomic features.Case Presentation: A 59-year-old man was diagnosed with lung cancer and had resection surgery in our hospital. The H&E and immunohistochemistry staining revealed that the tumor had 30%–35% LCNEC and 65%–70% SCLC cells. The whole-exome sequencing (WES) identified no potentially actionable alteration in the tumor sample but found five alterations all with allele frequency over 90%, including TP53 p.R273H, MYH8 p.Q1814K, SLC17A6 p.W505L, PTPN5 p.M40I, and RB1 p.L267X. The genomic results supported that these two different components shared a similar dominant clonal origin. Furthermore, fluorescence in situ hybridization analysis revealed that the LCNECs have a higher copy number of MET than the SCLC component while without notable difference in the copy number of HER2 and TP53. Chemotherapy with pemetrexed and carboplatin was administrated for two cycles after the surgery. Although the chest CT showed remission in the lung, he was diagnosed with bone metastasis in 1 year later. Then, he received chemotherapy with etoposide and carboplatin but had severe side effect, leading to the discontinuation of the regime. Unfortunately, he returned to the local hospital with supportive care and died shortly after.Conclusion: Based on these observations, we proposed that LCNEC and SCLC components in this patient may have a common clonal origin with dual mutations in TP53 and RB1, while the chromosome instability may cause multiple independent conversion that leads to LCNEC or SCLC morphologies.

Esophageal adenocarcinoma (EAC) is an aggressive and challenging disease to treat, with an overall five‑year survival rate of <20%. Early malignant cell dissemination contributes to this poor prognosis. Epithelial‑mesenchymal transition (EMT) induces the invasion and metastasis of carcinoma cells. Empty spiracles homeobox 2 (EMX2) is a homeodomain‑containing transcription factor, which is associated with numerous cancer types, and has been demonstrated to regulate EMT. In the present study, 48 pairs of EAC and adjacent normal tissues were analyzed. The results revealed that EMX2 was downregulated in EAC tissues, and its expression was negatively correlated with the DNA hypermethylation of its promoter. Additionally, the OE19 and OE33 EAC cell lines were treated with the DNA methyltransferase inhibitor 5‑aza‑2'‑deoxycytidine, and the results indicated that EMX2 expression was increased. Overexpressing EMX2 in EAC cell lines enhanced the expression of apoptotic markers, inhibited cell migration and invasion, led to the upregulation of E‑cadherin and the downregulation of mesenchymal markers, and suppressed AKT, mTOR and S6K phosphorylation. Furthermore, EMX2 overexpression sensitized EAC cells to cisplatin. These results demonstrated that EMX2 inhibited the AKT/mTOR/S6K signaling pathway and decreased EMT. However, the downregulation of EMX2 was revealed to be associated with EMT in EAC, indicating that EMX2 may be a potential target for the management of EAC.