ArticleScientific reports2025
LINC02159 modulated the glycolysis and proliferation of TNBC cell via targeting miR-1285-3p/G6PI axis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Glucose metabolic reprogramming: a novel strategy to enhance radiotherapy response to triple-negative breast cancer.Frontiers in public health · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
As a leading cause of cancer-related fatalities among women, triple negative breast cancer (TNBC) still remains a clinical challenge. Increasing evidence points to long non-coding RNAs (lncRNAs) as significant regulators in its progression. The aim of this study is to investigate the function and working mechanism of LINC02159 in TNBC. The expression of LINC02159 in TNBC tissues and cells was detected by RT-qPCR analysis. Regulation of LINC02159 on TNBC is determined by the in vitro proliferation and migration assay. Binding of LINC02159 with the targets was tested by the luciferase reporter assay. The function of LINC02159 in the glycolysis of TNBC cells was evaluated via detecting the glucose uptake and lactate production. Our study identified that LINC02159 is overexpressed in TNBC tissues and correlates with decreased overall survival in patients. Functionally, silencing LINC02159 reduced TNBC cell proliferation and migration in vitro and suppressed the tumor growth in vivo. By acting as a competing endogenous RNA (ceRNA), LINC02159 directly engaged with miR-1285-3p to increase the expression of Glucose-6-phosphate isomerase (G6PI). In line with G6PI's role in glycolysis, reducing LINC02159 expression decreased glucose uptake and lactate production in TNBC cells. Restoring G6PI greatly reversed the impact of LINC02159 silencing on the proliferation and glycolysis of TNBC cells. These results demonstrated that LINC02159 drives the aerobic glycolysis and TNBC progression via modulating the miR-1285-3p/G6PI axis, and it might act as a potential target for TNBC anti-tumor therapy.
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.