Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025212
Spatial biology aims to elucidate cellular organization, function, and interactions within native tissue contexts, offering key insights into both normal physiology and disease. Spatial proteomics complements this by enabling high-resolution mapping of protein localization and abundance, directly reflecting functional cellular states. Unlike transcriptomics, which infers potential activity, proteomics captures actual molecular functions, including post-translational modifications and dynamic interactions. However, in situ protein profiling poses significant challenges, as proteins cannot be directly sequenced or easily targeted via nucleic acid hybridization. Antibody-oligonucleotide conjugates (AOCs) address this limitation by converting protein recognition into a DNA-based readout, thereby enabling sensitive and scalable detection. In this review, we outline the core principles of AOC-based spatial proteomic technologies, including multiplexed protein analysis, in situ protein-protein interactions, and integration with other biomolecular data. We highlight their applications in decoding tissue complexity and disease pathology and examine key technical challenges that remain. Overall, AOCs offer distinct advantages, including DNA-mediated signal amplification, spatially resolved proteomic profiling, and compatibility with multi-omics approaches, positioning them as powerful platforms in the advancement of spatial biology.
Stem Cell Research & Therapy•2024•DOI: 10.1186/s13287-024-04031-5
The Editor-in-Chief has retracted this article. The authors of this article subsequently contacted the journal to request to replace components of Figs. 1B, 6E, 6H and 7A. Further investigation raised concerns regarding the provenance of the replacement figures and the rationale behind the need to replace these figures. The Editor-in-Chief therefore no longer has confidence in the reliability of the data reported in this article. Author Yong-lan Wang has stated that all authors disagree with this retraction.
Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-04919-4
Lung cancer remains the leading cause of cancer mortality worldwide, with non-small cell lung cancer (NSCLC) accounting for approximately 85% of diagnoses. Lung cancer stem-like cells (LCSCs) drive metastasis, recurrence, and therapeutic failure, yet effective targeting strategies remain elusive. Oxysterol-binding protein-like 2 (OSBPL2/ORP2) is a lipid transport protein that localizes to lipid droplets (LDs) and regulates cholesterol homeostasis, but its role in lung cancer stemness has not been defined. Here, we demonstrate that OSBPL2 reduces cellular cholesterol content, as quantified by HPLC-MS, and inhibits lipid droplet accumulation in lung cancer cells. OSBPL2-mediated lipid transportation significantly suppressed tumor sphere formation, stemness marker expression (ALDH1A1, CD133, Nanog), and in vivo tumorigenesis and metastasis. In peritoneal carcinomatosis models using BALB/c mice (n=10 per group) injected with L-Osbpl2 or L-Vector transduced LLC cells (5×10^6 cells/100µL), OSBPL2 overexpression reduced metastatic tumor burden. Clinical specimen analysis revealed that OSBPL2 represses LCSC marker expression and its level negatively correlates with tumor stage progression and lymph node metastasis. These findings establish OSBPL2 as a critical regulator of lung cancer stemness through lipid metabolic reprogramming, offering a potential therapeutic target for aggressive NSCLC.
Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-04919-4
Lung cancer is the first leading cause of cancer death worldwide. Oxysterol-binding protein-like 2 (OSBPL2) is a lipid transport protein regulating cholesterol homeostasis. Here, we clarified the previously unreported role of OSBPL2 in lung cancer stemness properties. We observed that OSBPL2 reduced cholesterol content by HPLC-MS. It inhibited the accumulation of lipid droplets (LDs) in lung cancer. OSBPL2-mediated lipid transportation significantly suppressed tumor sphere formation, stemness markers expression and in vivo tumorigenesis and tumor metastasis. In clinical specimens, we also demonstrated that OSBPL2 repressed the expression of Lung cancer stem-like cells (LCSCs) markers-ALDH1A1, CD133 and Nanog. The level of OSBPL2 was negatively correlated with malignant of lung cancer, such as tumor stage progression and lymph node metastasis. Taken together, these findings illustrated that OSBPL2-mediated lipid transportation inhibited the stemness and aggressiveness of lung cancer cells. OSBPL2 was a potential therapeutic target to develop novel cancer-preventive compound.