GRHL2-HER3 and E-cadherin mediate EGFR-bypass drug resistance in lung cancer cells
Fumiya Ito, Wakiko Iwata, Yoshihiro Adachi, Hiromi Sesaki, Miho Iijima · 2025
Read GRHL2-HER3 and E-cadherin mediate EGFR-bypass drug resistance in lung cancer cells by Fumiya Ito, Wakiko Iwata, Yoshihiro Adachi, Hiromi Sesaki, Miho Iijima (2025) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-11782226.txt.
Description
Fumiya Ito and co-authors uncover two routes by which lung cancer cells dodge a targeted drug, in a study published in 2024. The drug erlotinib blocks EGFR, a growth driver in many cancers. Resistance to it is a major barrier in lung cancer care, so its escape routes matter.
The team bred resistant A549 lung cells by long exposure to the drug. The cells lost EGFR protein yet grew faster, proof of a bypass. Gene scans named a factor called GRHL2, which switches on a sister receptor, HER3; cutting either restored drug sensitivity. The cells also stuck to each other more through raised E-cadherin, a second, separate prop for resistance. The authors suggest hitting both routes at once.
Catalog record
| CREATOR | Fumiya Ito, Wakiko Iwata, Yoshihiro Adachi, Hiromi Sesaki, Miho Iijima |
|---|---|
| YEAR | 2025 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 50 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |