ArticleAmerican journal of translational research2025
LncRNA HCP5 promotes the progression of gastric cancer through the miR-526b/PBX3 axis.
Article in American journal of translational research, 2025. 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo investigate whether LncRNA HLA complex P5 (HCP5) promotes gastric cancer (GC) via the miR-526b/Pre-B Cell Leukemia Homeobox 3 (PBX3) pathway.
methodsThirteen paired GC and adjacent non-tumorous tissues, along with NCI-N87 GC cells, were analyzed. HCP5 expression levels were measured, and its impact on cell viability, proliferation, and migration were evaluated. Dual-luciferase reporter assays were performed to confirm the direct interactions among HCP5, miR-526b, and PBX3. The effects of HCP5 overexpression or silencing on miR-526b and PBX3 expression were analyzed. A miR-526b mimic was transfected for functional rescue.
resultsHCP5 was significantly upregulated, while miR-526b was downregulated in GC tissues. Dual-luciferase assays confirmed the direct binding of HCP5 to miR-526b and of miR-526b to PBX3. In NCI-N87 cells, HCP5 overexpression downregulated miR-526b and upregulated PBX3 expression, whereas silencing HCP5 showed the opposite effects. Moreover, HCP5 overexpression decreased Bax and increased Bcl-2 levels, which was reversed by miR-526b mimic transfection. Functionally, HCP5 enhanced GC cell viability and migration, both of which were suppressed by miR-526b. HCP5 promoted cell proliferation, as evidenced by a reduced proportion of cells in the G0/G1 phase, which was reversed by miR-526b.
conclusionsHCP5 acts as an oncogenic lncRNA in GC by promoting cell viability, migration, and proliferation via the miR-526b/PBX3 axis. Targeting the HCP5/miR-526b/PBX3 axis may represent a promising therapeutic strategy for GC.
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.