The Wnt/β-catenin signaling pathway is a highly conserved pathway that is involved in cell development, proliferation, differentiation, apoptosis and autophagy. Among these processes, apoptosis and autophagy occur physiologically during host defense and the maintenance of intracellular homeostasis. Mounting evidence suggests that the crosstalk between Wnt/β-catenin-regulated apoptosis and autophagy has broad functional significance in various diseases. Herein, we summarize the recent studies in understanding the role of the Wnt/β-catenin signaling pathway in apoptosis and autophagy, and draw the following conclusions: a) For apoptosis, the regulation of Wnt/β-catenin is generally positive. However, a small amount of evidence indicates the presence of a negatively regulated relationship between Wnt/β-catenin and apoptosis; b) Wnt/β-catenin influences the occurrence and development of autophagy by regulating autophagy-related factors, and these factors in turn affect Wnt/β-catenin pathway; c) Wnt/β-catenin always balances the molecular damage caused by the crosstalk between autophagy and apoptosis in a compensatory manner. Understanding the specific role of the Wnt/β-catenin signaling pathway during different stages of autophagy and apoptosis may provide new insights into the progression of related diseases regulated by the Wnt/β-catenin signaling pathway.

Homoharringtonine (HHT), a natural alkaloid derived from the cephalotaxus, exhibited its anti-cancer effects in hematological malignancies clinically. However, its pesticide effects and mechanisms in treating solid tumors remain unclear. In this study, we found that HHT was capable of inhibiting tumor growth after 5-days treatment of breast cancer cells, MCF-7, in vivo. Furthemore, HHT also significantly inhibited the cancer cell growth and induced cell apoptosis in vitro. miRNA sequencing proved miR-18a-3p was noticeably downregulated in the cells after HHT treatment. Moreover, downregulating miR-18a-3p increased HHT-induced cell apoptosis; our data supported that HHT suppressed miR-18a-3p expression and inhibited tumorigenesis might via AKT-mTOR signaling pathway. In conclusion: our study proved that HHT suppressed breast cancer cell growth and promoted apoptosis mediated by regulating of the miR-18a-3p-AKT-mTOR signaling pathway, HHT may be a promising antitumor agent in breast cancer treatment.

Objective: To investigate the correlation between the expression of lipopolysaccharide-binding protein (LBP) in peripheral blood of spinal tuberculosis and clinical diagnosis and to evaluate its value as a diagnostic marker of spinal tuberculosis. Methods: In the experimental group, clinical history data and peripheral blood were collected from 100 patients with spinal tuberculosis who were admitted to the Department of Spine Surgery, General Hospital of Ningxia Medical University from May 2017 to May 2020, and peripheral blood was collected from 30 healthy volunteers in the control group. Screening of differential LBP expression by proteomics and ELISA to verify its expression in peripheral blood of spinal tuberculosis patients. t-test, Spearman analysis, linear regression and ROC curve were used to evaluate the diagnostic value of LBP in peripheral blood for spinal tuberculosis. Results: The expression of LBP protein in peripheral blood is significantly higher in patients with spinal tuberculosis than in the normal population; LBP assay values were significantly and positively correlated with CRP and ESR values (P < 0.01); the AUC of LBP in the diagnosis of spinal tuberculosis for pathological examination, bacteriological culture, T-cell spot test for tuberculosis infection (T-SPOT), imaging diagnosis, and acid fast bacillus were, respectively, 0.677 (P < 0.01), 0.707 (P < 0.01), 0.751 (P < 0.01), 0.714 (P < 0.01), and 0.656 (P < 0.05), and there was a correlation between LBP and the diagnostic evaluation of spinal tuberculosis. Conclusion: LBP could be a new candidate biomarker for the diagnosis of spinal tuberculosis.

Oral drug delivery systems designed for antitumor drug administration in colorectal cancer treatment encounter substantial challenges regarding effective delivery, controlled release, and intestinal microbiota homeostasis. In this study, dual-stimulation (pH + magnetic) responsive chitosan nanoparticles (Fe₃O₄/chitosan (CS)/TPP) loaded with hops β-acids were synthesized for colorectal cancer treatment. In vitro experiments revealed that the fabricated nanoparticles demonstrated sizes ranging from 233 to 381 nm, with zeta potential values exceeding 10 mV. Release studies indicated that β-acids release was pH-dependent. Notably, the β-acids-loaded nanoparticles proved antimicrobial activity through membrane protein interactions. Cell proliferation assays confirmed that these nanoparticles effectively eliminated HCT116 cells while showing minimal toxicity toward NCM460 cells. Following oral administration to mice with in situ colorectal cancer, histopathological evaluation demonstrated that the nanoparticles induced apoptosis at the tumor site, leading to reduced tumor growth. Additionally, the drug-loaded nanoparticles showed enhanced antitumor efficacy compared to free 5-FU. The findings suggest that these nanoparticles significantly increase beneficial bacterial populations while decreasing levels of harmful bacteria. These dual-function nanoparticles, which exhibit both chemotherapeutic and antimicrobial properties, present a promising novel strategy for treating colorectal cancer.