Identification of a New Potent Inhibitor Targeting KRAS in Non-small Cell Lung Cancer Cells
Open accessAbstract
KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) is an oncogenic driver with mutations in 30% of non-small cell lung cancer (NSCLC). However, there is no effective clinical drug even though it has been identified as an oncogene for 30 years. In this study, we identified a small molecule inhibitor compound 0375-0604 targeting KRAS by using molecular docking based virtual screening approach. Compound 0375-0604 had a good binding affinity to KRAS in vitro and exhibited cytotoxicity in oncogenic KRAS expressing NSCLC cell lines. Further mechanism study showed that compound 0375-0604 can block the formation of the complex of guanosine triphosphate (GTP) and KRAS in vitro. In addition, compound 0375-0604 inhibited KRAS downstream signaling pathway RAF/MEK/ERK and RAF/PI3K/AKT. Finally, we also found that this compound can inhibit the cell growth through G2/M cell cycle arrest and induce apoptosis on the NSCLC cell lines harboring KRAS mutation. Therefore, compound 0375-0604 may be considered as a potential KRAS inhibitor for treatment of NSCLC carrying KRAS oncogene.
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MRTX1133 treatment results in G2/M phase blockade in CRC cells.
“Furthermore, MRTX1133 treatment resulted in G2/M phase blockade in CRC cells (Fig. 1B), which is a typical consequence of KRAS mutant allele inhibition [17–19].”
From Feedback activation of EGFR/wild-type RAS signaling axis limits KRASG12D inhibitor efficacy in KRASG12D-mutated colorectal cancer (2023) · cites this paper as [19]
The Results section ('Compound 0375-0604 Induced Cell Cycle Arrest and Apoptosis in NSCLC') reports G2/M arrest after treatment with a KRAS-targeting compound, supporting the cited clause's connection between KRAS inhibition and G2/M blockade. It does not establish that this is a typical consequence across KRAS mutant allele inhibitors; it studies compound 0375-0604 in NSCLC cells, not MRTX1133 in CRC cells. The MRTX1133 result is presented as the citing paper's own Figure 1B finding, rather than as a finding from this source. (LLM, conf=0.84)
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- Authors
- Xie, C., Li, Y., Li, L.-L., Fan, X.-X., Wang, Y.-W., Wei, C.-L., Liu, L., Leung, E. L.-H., & Yao, X.-J.
- Affiliations
- Macau University of Science and Technology (MO)
- Corresponding author
- Liu, Liang
- Leung, Elaine Lai-Han
- Venue
- Frontiers in Pharmacology
- Publisher
- Frontiers Media SA
- Published
- 2017-11-14
- Volume
- 8
- Pages
- 823-823
- ISSN
- 1663-9812 (ISSN-L)
- PMC
- PMC5694459
- OpenAlex
- W2767236761
- Cited by
- 40
- References
- 40
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 9 · 2022: 5 · 2021: 5 · 2020: 6 · 2019: 8 · 2018: 1
- FWCI
- 1.68
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Pharmacology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Lanzhou University Institutional Repository (submittedVersion)
- Funders
- Fundo para o Desenvolvimento das Ciências e da Tecnologia (082/2013/A3, 086/2015/A3, 046/2016/A2, 005/2014/AMJ)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Physical Sciences › Computer Science › Computational Theory and Mathematics › Computational Drug Discovery Methods
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Keywords
- KRAS, non-small cell lung cancer, KRAS inhibitors, small molecule inhibitors, GTP binding, MAPK/ERK pathway, G2/M cell cycle arrest, apoptosis, KRAS mutation, virtual screening
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