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Article

Oncogenic KRAS mutations enhance amino acid uptake by colorectal cancer cells via the hippo signaling effector YAP1.

Molecular oncology - 1 Oct 2021

Kandasamy Palanivel, Zlobec Inti, Nydegger Damian T, Pujol-Giménez Jonai, Bhardwaj Rajesh, Shirasawa Senji, Tsunoda Toshiyuki, Hediger Matthias A

Abstract excerpt

Oncogenic KRAS mutations develop unique metabolic dependencies on nutrients to support tumor metabolism and cell proliferation. In particular, KRAS mutant cancer cells exploit amino acids (AAs) such as glutamine and leucine, to accelerate energy metabolism, redox balance through glutathione synthesis and macromolecule biosynthesis. However, the identities of the amino acid transporters (AATs) that are prominently...

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Topics

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Share to Amino Acids
Share to Cell Line, Tumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Colorectal Neoplasms

Share to Fibroblasts

Share to Hippo Signaling Pathway

Share to Minor Histocompatibility Antigens

Share to Proto-Oncogene Proteins p21(ras)

Share to YAP-Signaling Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 34003553
DOI: 10.1002/1878-0261.12999
PMCID: PMC8486573

Genes

KRAS
YAP1
SLC1A5
SLC38A2
SLC7A5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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