A fundamental discovery by University of Missouri scientists could help solve one of the most frustrating challenges in treating lung cancer: Why do some patients initially respond to drug treatment, only for it to stop working 18 months later?

The team, led by Dhananjay Suresh, Anandhi Upendran and Raghuraman Kannan at Mizzou’s School of Medicine, identified a hidden molecular “seesaw” involving two proteins inside cancer cells — AXL and FN14. When investigators try to block one protein to stop the cancer, the other one takes over, helping the tumor survive. To fix this, the team developed a new solution: a gelatin-based nanoparticle that can shut down both proteins at the same time.

In a study published in Science Bulletin, researchers from Tongji University led by Professors Yixuan Wang and Shaorong Gao constructed a novel in vitro model simulating the human preimplantation epiblast (EPI), primitive endoderm (PrE), and trophectoderm (TE) lineages. Through single-cell transcriptomic analysis and intercellular communication inference using CellChat toolkit, the team delineated the cell-cell communication landscape among tri-lineages.  Notably, they highlighted the critical role of secreted NRG signaling from EPI to TE, mediated by NRG1-ERBB3 axis, in regulating trophectoderm specification through the intracellular effector TFAP2C—a signaling axis validated in both trophectoderm induction system and human blastocyst development.