ArticleCells2021
Suppression of the HBP Function Increases Pancreatic Cancer Cell Sensitivity to a Pan-RAS Inhibitor.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Exploring the metabolic signaling network of GFPT in cancer.Cell death discovery · 2025Review
- The HBP Pathway Inhibitor FR054 Enhances Temozolomide Sensitivity in Glioblastoma Cells by Promoting Ferroptosis and Inhibiting O-GlcNAcylation.CNS neuroscience & therapeutics · 2025Article
- Breast cancer therapy: from the perspective of glucose metabolism and glycosylation.Molecular biology reports · 2024Review
- Current knowledge and potential intervention of hexosamine biosynthesis pathway in lung cancer.World journal of surgical oncology · 2023Review
- Review
- PGM3 inhibition shows cooperative effects with erastin inducing pancreatic cancer cell deathFrontiers in oncology · 2023Article
- O-GlcNAcylation promotes pancreatic tumor growth by regulating malate dehydrogenase 1.Nature chemical biology · 2022Article
- PGM3 regulates beta-catenin activity to promote colorectal cancer cell progression.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- opnMe.com: a digital initiative for sharing tools with the biomedical research community.Nature reviews. Drug discovery · 2022Article
- Article
- Unraveling and targeting RAS-driven metabolic signaling for therapeutic gain.Advances in cancer research · 2022Review
- Oncogenic KRAS blockade therapy: renewed enthusiasm and persistent challenges.Molecular cancer · 2021Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related death and the search for a resolutive therapy is still a challenge. Since KRAS is commonly mutated in PDAC and is one of the main drivers of PDAC progression, its inhibition should be a key strategy for treatment, especially considering the recent development of specific KRAS inhibitors. Nevertheless, the effects of KRAS inhibition can be increased through the co-inhibition of other nodes important for cancer development. One of them could be the hexosamine biosynthetic pathway (HBP), whose enhancement is considered fundamental for PDAC. Here, we demonstrate that PDAC cells expressing oncogenic KRAS, owing to an increase in the HBP flux, become strongly reliant on HBP for both proliferation and survival. In particular, upon treatment with two different compounds, 2-deoxyglucose and FR054, inhibiting both HBP and protein
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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.