ArticleMolecular and cellular biochemistry2026
GALNT6-glycosylated LRG1 mediates the interaction between M2 macrophages and pancreatic cancer cells by activating CCR1/PI3K/AKT axis.
Article in Molecular and cellular biochemistry, 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
4 authors.
Funding
Abstract
Pancreatic cancer (PC) is a malignant tumor that often presents no obvious symptoms in its early stages, leading to late diagnosis and poor prognosis. Therefore, developing molecular markers for PC is essential for improving early diagnosis, optimizing treatment strategies, and enhancing patient outcomes. In this study, PC tissue and matched adjacent non-cancerous tissue were collected from patients. For in vitro analysis, the PC cell lines BxPC-3 and SW1990 were used. M2 macrophages were induced in THP-1 cells. Gene expression at both mRNA and protein levels was measured using real-time quantitative PCR and Western blotting. Cell counting kit-8 assay was used to evaluate cell activity. Flow cytometry was used to assess the cell apoptosis rate and M2 macrophage biomarkers. Transwell and wound-healing assays were used to determine cell migration and invasiveness. Co-immunoprecipitation assay was used to evaluate the binding relationship between leucine-rich α-2 glycoprotein 1 (LRG1), chemokine receptor 1 (CCR1), and GALNT6. LRG1 expression was upregulated in PC tissues compared to that in normal tissues. Co-culture with M2 macrophages enhanced gemcitabine (GEM) resistance, cell migration, and PC cell invasion. LRG1 overexpression in PC cells enhanced the effect of M2 macrophage cells to exacerbate GEM resistance, cell migration, and invasion, while LRG1 knockdown exhibited an opposite effect. LRG1 interacted with CCR1 to enhance PI3K/AKT signaling, thereby affecting GEM resistance, migration, and PC cell invasion. Moreover, GALNT6 was confirmed as an upstream regulator of LRG1, which glycosylated LRG1 and increased its stability. Rescue experiments demonstrated that GALNT6 promoted GEM resistance, movement, and invasion abilities of PC cells by regulating LRG1. The role of LRG1 in the interaction between PC cells and M2 macrophages was also verified in the xenograft model. These findings demonstrate that GALNT6-glycosylated LRG1 mediates the interaction between M2 macrophages and PC cells by activating CCR1. This study may provide promising therapeutic targets for PC treatment.
Indexed as
Identifiers
42570206What 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.