Curcumin, a polyphenolic compound derived from Curcuma longa, has gained significant attention as a potential anticancer agent due to its anti-inflammatory, antioxidant, and antitumor properties. Despite its therapeutic potential, the clinical application of curcumin is limited by its poor aqueous solubility, rapid metabolism, and limited bioavailability. To address these limitations, various nanomaterial-based encapsulation strategies have been developed, including polymeric nanoparticles, liposomes, solid lipid nanoparticles, micelles, dendrimers, and hybrid nanomaterials. These formulations aim to improve curcumin's solubility, stability, cellular uptake, and controlled release, thereby enhancing its targeted delivery to tumor sites. Such approaches not only reduce systemic toxicity but also improve therapeutic efficacy. Recent studies demonstrate that curcumin-loaded nanocarriers exhibit enhanced antitumor effects, selective cytotoxicity toward cancer cells, and minimized side effects. However, challenges such as achieving tissue specificity, evaluating potential toxicity, and the need for thorough clinical validation persist. Future research should prioritize the development of tissue-specific delivery systems, assess safety profiles, and ensure biocompatibility to optimize curcumin's clinical efficacy. This review provides an overview of the latest advancements in curcumin nanocapsules, critically comparing their advantages and limitations in cancer therapy.

The aim of the present study was to explore the effect of chaperon‑mediated autophagy (CMA) through pyruvate kinase isoform M2 (PKM2) on the development of renal carcinoma (RCC) and its possible mechanisms. Lysosome‑associated membrane protein 2A (LAMP‑2A) and PKM2 expression levels were detected by collecting tissue samples from RCC patients. RNA interference was used to silence the LAMP‑2A and PKM2 expression levels in renal cell line A498 to detect the proliferation, apoptosis and invasion of cells. The levels of mRNA and protein of related genes were also examined. Co‑immunoprecipitation was used to detect the interaction between PKM2 and heat shock cognate 70 (HSC70). The results revealed that LAMP‑2A and PKM2 expression levels were significantly increased in RCC tissues and cell lines (P<0.01). LAMP‑2A silencing increased the expression level of PKM2 in A498 and 786‑O cells. LAMP‑2A and PKM2 silencing suppressed the proliferation and invasion and induced the apoptosis of A498 cells, and also affected the expression levels of related genes. Co‑immunoprecipitation revealed the interaction between PKM2 and HSC70. In conclusion, CMA could affect the proliferation, invasion and apoptosis of RCC cells through PKM2, and our findings provided new biomarkers and targets for molecular targeted therapy of RCC.

This review summarizes the recent progress in the design and application of highly sensitive fluorescent probes for liver fibrosis.

The diagnostic criteria for cM0 (i+) stage proposed by American Joint Committee on Cancer (AJCC) in renal cell carcinoma (RCC) still remains unclear. The present study aimed to establish and validate the criteria of cM0 (i+) stage based on postoperative circulating tumor cells (CTCs) monitoring in patients with localized renal cell carcinoma (LRCC). This study enrolled 204 patients with LRCC who received partial or radical nephrectomy from January 2015 to November 2021. Cases were randomly divided into test set and validation set. The correlation between clinicopathological features and CTCs counts were analyzed and prognostic variables were determined by Lasso regression. Receiver operating characteristic curve of the prognosis-related CTCs terms were plotted to determine their optimal cut-off value to establish the criteria of cM0 (i+) stage. Its clinical prognostic significance was explored by Kaplan-Meier analysis and Log-rank test. The above analysis was conducted by SPSS26.0 software and R Studio software. P < 0.05 was considered to be statistically significant. A total of 204 patients were analyzed in this study.There were no significant differences in variables between the validation and test sets (P>0.05). Total CTCs, mesenchymal CTCs (MCTCs), and CTCs showing a progressive trend were selected as the diagnostic basis for the cM0 (i+) stage through correlation analysis and Lasso regression. The cM0 (i+) stage identified patients meeting the following criteria simultaneously: (1) total CTCs ≥ 6; (2) MCTCs ≥ 1; and (3) a demonstrated trend of progression in either total CTCs or MCTCs. In the validation group, Kaplan-Meier analysis showed that patients with cM0 (i+) stage had significantly shorter progression-free survival than the control group(P<0.05). The results of multivariate Cox regression analysis also showed cM0 (i+) was an independent risk factor for postoperative progression of LRCC patients [12.448 (1.874-82.666) P < 0.05]. Its 1-3 years' prediction discrimination is better than that of UISS score and SSIGN score, which was also verified in the validation set. The study proposed a diagnostic criterion for M0 (i+) stage in LRCC based on postoperative CTCs monitoring. It was identified as an independent risk factor for postoperative progression and demonstrated potential advantages over the UISS and SSIGN scores in internal validation.

Background: Although the mucin glycoprotein MUC16 is well established as an oncogenic biomarker in ovarian cancer, its mechanistic contribution to lung adenocarcinoma (LUAD) remains poorly defined. This study integrates multi-omics profiling and functional validation to uncover MUC16 as a novel determinant of detachment-induced survival in LUAD.