ERO1L induces macrophage infiltration to potentiate KrasG12D and inflammation-induced pancreatic tumorigenesis via oxidative protein folding of CCL2
Junfeng Zhang, Chengyu Hu, Yannan Xu, Macheng Lu, Yahui Ma, Ting Yang, Jing Li, Shu-Heng Jiang, Chengkai Jiang, Pengcheng Chen, Li Yao, Rong Hua · 2026
Read ERO1L induces macrophage infiltration to potentiate KrasG12D and inflammation-induced pancreatic tumorigenesis via oxidative protein folding of CCL2 by Junfeng Zhang, Chengyu Hu, Yannan Xu, Macheng Lu, Yahui Ma, Ting Yang, Jing Li, Shu-Heng Jiang, Chengkai Jiang, Pengcheng Chen, Li Yao, Rong Hua (2026) 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/PMC13479891.txt.
Description
Junfeng Zhang and coauthors published a 2026 study of how inflammation teams up with the Kras mutation to start pancreatic cancer. Pancreatitis is a strong risk factor, and Kras mutations dominate this cancer, yet their interaction was murky. In Kras-mutant mice with pancreatitis, most cell-stress pathways quieted down, while one protein-folding enzyme, ERO1L, rose abnormally.
The chain runs through a disposal protein that Kras suppresses, letting a hypoxia factor accumulate and switch ERO1L on. ERO1L then folds the chemokine CCL2 more efficiently, and that signal draws macrophages into the tissue, building a tumor-friendly crowd. Blocking ERO1L or deleting it only in the pancreas slowed cancer development in the animals. The authors nominate the enzyme as an early intervention point.
Catalog record
| CREATOR | Junfeng Zhang, Chengyu Hu, Yannan Xu, Macheng Lu, Yahui Ma, Ting Yang, Jing Li, Shu-Heng Jiang, Chengkai Jiang, Pengcheng Chen, Li Yao, Rong Hua |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 46067 |
| LICENSE | https://creativecommons.org/licenses/by/4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |