ArticleTranslational cancer research2026
OSBPL3 promotes colorectal cancer progression through modulation of TGF-β signaling and immune cell infiltration.
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Colorectal cancer (CRC) is the third most common cancer worldwide, with prognosis often limited by disease progression. The role of oxysterol-binding protein-like 3 (OSBPL3) in various cancers remains unclear. This study aimed to investigate the expression, biological function, and relationship of OSBPL3 with the tumor microenvironment (TME) in CRC, and to assess its potential as a therapeutic target. Methods: We employed bioinformatic analysis, immunohistochemistry (IHC), Cell Counting Kit-8 (CCK-8) assay, Western blot (WB), ethynyl deoxyuridine (EdU) incorporation assay, wound healing assay, transwell assay, and animal models to characterize the expression pattern of OSBPL3 in CRC. We assessed the effects of OSBPL3 on CRC cell proliferation, migration, invasion, and apoptosis. Additionally, we investigated the mechanisms by which OSBPL3 drives CRC progression through the TGF-β signaling pathway and immune cell infiltration. Results: OSBPL3 was highly expressed in CRC, and its elevated expression was positively correlated with lymphatic metastasis. High OSBPL3 expression was associated with activity of the TGF-β signaling pathway and with epithelial-mesenchymal transition (EMT). Cellular experiments and animal models demonstrated that OSBPL3 knockdown suppressed CRC cell proliferation, migration, and invasion and increased apoptosis, whereas OSBPL3 overexpression produced the opposite effects. Furthermore, OSBPL3 knockdown inhibited TGF-β signaling and EMT, while OSBPL3 overexpression showed the reverse pattern. Additionally, OSBPL3 expression was positively correlated with central memory T cells (Tcm) and Th2 cells but negatively correlated with regulatory T cells (Tregs). Conclusions: OSBPL3 expression is positively associated with increased proliferative and invasive capacities of CRC cells. Our analyses further indicate that OSBPL3 is closely linked to TGF-β/SMAD signaling activity, EMT-related molecular features, and the immune infiltration landscape within the TME. Collectively, these findings suggest that OSBPL3 may serve as a clinically relevant biomarker and a potential therapeutic target in CRC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.