Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Curcumin functions as a MEK inhibitor to induce a synthetic lethal effect on KRAS mutant colorectal cancer cells receiving targeted drug regorafenib.

The Journal of nutritional biochemistry - 1 Dec 2019

Wu Chi-Shiuan, Wu Shan-Ying, Chen Hsin-Chih, Chu Chien-An, Tang Han-Hsuan, Liu Hsiao-Sheng, Hong Yi-Ren, Huang Chi-Ying F, Huang Guan-Cheng, Su Chun-Li

Abstract excerpt

Curcumin, a major yellow pigment and spice in turmeric and curry, has been demonstrated to have an anticancer effect in human clinical trials. Mutation of KRAS has been shown in 35%-45% of colorectal cancer, and regorafenib has been approved by the US FDA to treat patients with colorectal cancer. Synthetic lethality is a type of genetic interaction between two genes such that simultaneous perturbations of the two...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Butadienes
Share to Curcumin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to HCT116 Cells

Share to HT29 Cells

Share to MAP Kinase Kinase Kinases

Share to Nitriles

Share to Phenylurea Compounds

Share to Pyridines

Source

Identifiers

PMID: 31675556
DOI: 10.1016/j.jnutbio.2019.108227

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Curcumin functions as a MEK inhibitor to induce a synthetic lethal effect on KRAS mutant colorectal cancer cells receiving targeted drug regorafenib.PMID 31675556Read ↗

RAF suppression synergizes with MEK inhibition in KRAS mutant cancer cells.Semantic proximity Read ↗

Genome-wide CRISPR-cas9 knockout screening identifies GRB7 as a driver for MEK inhibitor resistance in KRAS mutant colon cancerSemantic proximity Read ↗

Aspirin Synergizes with Regorafenib to Reduce Growth of Colorectal CancerSemantic proximity Read ↗

Selective Eradication of Colon Cancer Cells Harboring PI3K and/or MAPK Pathway Mutations in 3D Culture by Combined PI3K/AKT/mTOR Pathway and MEK Inhibition.Semantic proximity Read ↗

Pathway-driven analysis of synthetic lethal interactions in cancer using perturbation screens.Semantic proximity Read ↗

Synthetic lethal interaction between oncogenic KRAS dependency and STK33 suppression in human cancer cells.Semantic proximity Read ↗

Efficacy of the combination of MEK and CDK4/6 inhibitors in vitro and in vivo in KRAS mutant colorectal cancer models.Semantic proximity Read ↗

Determination of synthetic lethal interactions in KRAS oncogene-dependent cancer cells reveals novel therapeutic targeting strategies.Semantic proximity Read ↗

Synthetic Lethality of a Novel Small Molecule Against Mutant KRAS-Expressing Cancer Cells Involves AKT-Dependent ROS ProductionSemantic proximity Read ↗

MEK162 Enhances Antitumor Activity of 5-Fluorouracil and Trifluridine in KRAS-mutated Human Colorectal Cancer Cell Lines.Semantic proximity Read ↗

Genotype-Tailored ERK/MAPK Pathway and HDAC Inhibition Rewires the Apoptotic Rheostat to Trigger Colorectal Cancer Cell DeathSemantic proximity Read ↗

Dual MAPK and HDAC inhibition rewires the apoptotic rheostat to trigger colorectal cancer cell deathSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.