Probiotics, living microorganisms with demonstrated health benefits when administered in sufficient quantities, have a rich history as dietary supplements to benefit human health. Recently, understanding of their mechanisms in the gastrointestinal tract has prompted exploration of probiotics in treating human diseases. However, the effective and precise delivery of probiotics remains a significant challenge in therapeutic applications. Here, we review the mechanisms of action of probiotics in human health and the most advanced strategies for efficient probiotic delivery. We also discuss the potential applications of engineered probiotics in disease treatment. This review contributes insights into the evolving landscape of probiotic research for therapeutic applications.

Acidithiobacillus ferridurans JAGS is a newly isolated acidophile from an acid mine drainage (AMD). The genome of isolate JAGS was sequenced and compared with eight other published genomes of Acidithiobacillus. The pairwise mutation distance (Mash) and average nucleotide identity (ANI) revealed that isolate JAGS had a close evolutionary relationship with A. ferridurans JCM18981, but whole-genome alignment showed that it had higher similarity in genomic structure with A. ferrooxidans species. Pan-genome analysis revealed that nine genomes were comprised of 4601 protein coding sequences, of which 43% were core genes (1982) and 23% were unique genes (1064). A. ferridurans species had more unique genes (205–246) than A. ferrooxidans species (21–234). Functional gene categorizations showed that A. ferridurans strains had a higher portion of genes involved in energy production and conversion while A. ferrooxidans had more for inorganic ion transport and metabolism. A high abundance of kdp, mer and ars genes, as well as mobile genetic elements, was found in isolate JAGS, which might contribute to its resistance to harsh environments. These findings expand our understanding of the evolutionary adaptation of Acidithiobacillus and indicate that A. ferridurans JAGS is a promising candidate for biomining and AMD biotreatment applications.

Lung adenocarcinoma (LUAD) accounts for ~40% of lung cancer cases, and the 5‐year relative survival rate is no more than 1%. Dysregulation of components of striatin‐interacting phosphatase and kinase (STRIPAK) complexes is associated with various diseases, including cancer. Striatin‐interacting protein 2 (STRIP2), also called Fam40b, has been reported to regulate tumor cell growth and migration. Here, we investigated the role of STRIP2 in LUAD growth, migration and the underlying mechanisms. Analysis of data from The Cancer Genome Atlas database revealed that STRIP2 is highly expressed and predicted poor outcomes in patients with LUAD. Moreover, quantitative RT‐PCR (qRT‐PCR) analysis revealed that the mRNA expression of STRIP2 is greater in all tested LUAD cells than in a normal lung cell line. To investigate the function of STRIP2, we overexpressed STRIP2 in SPC‐A1 cells and depleted STRIP2 in Calu‐3 cells. Cell proliferation was evaluated by Cell Counting Kit‐8 and colony‐forming assays, and Transwell assay was employed to test cell invasion and migration. Our results indicate that STRIP2 depletion suppressed cell proliferation, invasion and migration in Calu‐3 cells, and overexpression of STRIP2 had the opposite effects in SPC‐A1 cells. Moreover, we discovered that STRIP2 depletion reduced the protein levels of p‐Akt and phosphorylated‐mammalian target of rapamycin (p‐mTOR) in Calu‐3 cells, whereas STRIP2 overexpression increased levels of these proteins in SPC‐A1 cells. Furthermore, we found that silencing of STRIP2 clearly enhanced protein levels of E‐cadherin and reduced levels of N‐cadherin, Vimentin and matrix metalloproteinase‐9 in Calu‐3 cells, whereas overexpression of STRIP2 had the opposite effect in SPC‐A1 cells. Our data indicate that STRIP2 promotes the proliferation and motility of LUAD cells, and this may be mediated through the regulation of the Akt/mTOR pathway and epithelial–mesenchymal transition. These results may facilitate the development of therapeutic strategies to treat LUAD.