ArticleWorld journal of surgical oncology2026
Integrated transcriptomic and metabolomic analyses reveal targeting hexokinase 2 disrupts glycolysis and nucleotide metabolism to inhibit NSCLC growth.
Article in World journal of surgical oncology, 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
8 authors.
Funding
Abstract
backgroundDysregulation of glycolysis is a hallmark of non-small cell lung cancer (NSCLC), with hexokinases (HKs) playing a critical role in cancer metabolism. Among them, HK2 is particularly involved in tumor energy homeostasis and has emerged as a potential therapeutic target. This study explores the impact of HK2 targeting on NSCLC cell growth and metabolism through a comprehensive analysis of transcriptomic and metabolomic data.
methodsData from The Cancer Genome Atlas (TCGA) were used to examine the correlation between the expression of different HK isoforms (HK1, HK2, HK3) and patient prognosis in NSCLC. siRNA-mediated knockdown of HK2 was performed in NCI-H1975 cells, which exhibit relatively high HK2 expression based on CCLE datasets. The effects on cell proliferation, cell cycle progression, and apoptosis were evaluated using CCK-8 assays, EdU incorporation, and flow cytometry. Integrated transcriptomic and metabolomic analyses were conducted to identify key metabolic pathways influencing cell growth and progression.
resultsElevated expression of HK2 in NSCLC was associated with poor prognosis. Knockdown of HK2 led to a significant reduction in both HK1 and HK2 levels, resulting in decreased cell proliferation and a marked shift in the cell cycle to the G0/G1 phase. Integrated omics analyses revealed that HK2 depletion disrupted nucleotide metabolism, specifically impairing the pentose phosphate pathway (PPP), which is vital for ribonucleotide synthesis.
conclusionTargeting HK2 disrupts NSCLC cell growth and cell cycle progression by modulating nucleotide metabolism under conditions of inhibited glycolysis, highlighting its potential as a therapeutic target in cancer metabolism.
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.