ArticleJournal of genetics2025
YY1 as a mediator to enhance the resistance of KRAS mutant colorectal cancer cells to cetuximab.
Article in Journal of genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Targeting Plasma Membrane CaCancers · 2026Review
- Koumine's Therapeutic Impact on Hepatocellular Carcinoma: A Combined Network Pharmacology and Experimental Study.Biomedicines · 2026Article
- Review
- Prognostic Power of Ensemble Learning in Colorectal Cancer with Peritoneal Metastasis: A Multi-Institutional Analysis.Bioengineering (Basel, Switzerland) · 2026Article
- Yin Yang 1 (YY1) as a Central Node in Drug Resistance Pathways: Potential for Combination Strategies in Cancer Therapy.Biomolecules · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cetuximab has been indicated as the mainstay of metastatic colorectal cancer (CRC) therapy, of which application was impeded by chemoresistance that was casually attributed to KRAS mutation. This study sought to determine whether YY1 mediated the resistance of CRC cells harbouring KRAS mutation (KRASmut) to cetuximab. The expression of YY1 between cetuximab response and resistance was investigated in cancerous tissues from CRC patients received cetuximab therapy comprising eight KRAS wild-type (KRASwt) and 12 KRASmut. The relationship between YY1 expression and cetuximab resistance was explored based on KRASmut and KRASwt CRC cell lines. To explore the role of YY1 in the cetuximab resistance of KRASmut CRC cells, the response to cetuximab was investigated in cetuximab-resistant cells (SW620-R) with YY1 silence and cetuximab sensitive cells (HCT116) with YY1 overexpression. EGFR/Akt/ERK signalling activation, as well as mRNA and active GTP-bound KRAS level were assessed after the treatment. In KRASmut CRC tissues, YY1 expression was correlated with the histological grade and the cetuximab resistance. Significantly markable differences in YY1 expression between cetuximab-resistant and the parental cell lines were found in KRASmut cells. Silencing YY1 resensitized SW620-R cells to cetuximab and led to an elevation of the active GTP-binding KRAS. Conversely, the capability against cetuximab and GTP-binding KRAS activation of HCT116 cells was enhanced by overexpressing YY1. The blockage of EGFR/Akt/ERK signalling by cetuximab was re-observed in SW620-R cells after silencing YY1 but impaired in HCT116 by overexpressing YY1. The YY1 mediates the resistance of KRASmut CRC cells to cetuximab.
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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.