EREG (Epiregulin)

To encapsulate our findings, we have determined eight MAPK pathway-associated CRC prognostic biomarkers and developed a prognostic model accordingly. This model has proven effective in stratifying the risk levels among CRC patients.

Furthermore, we identified a progenitor-like cell population with a minimal CNV burden, potentially serving as a reservoir for tumor persistence. These findings offer novel insights for developing targeted strategies to eliminate resistant cell pools and improve cervical cancer outcomes.

P4, N=280, Not yet recruiting, Gruppo Oncologico del Nord-Ovest | Initiation date: Nov 2025 --> Apr 2026

Bioinformatic analysis showed that Cavin-3 can inhibit LUSC tumor cells by regulating the expression of EREG and IL1A, thereby activating the MAPK pathway to promote the release of tumor necrosis factor (TNF) and other inflammatory factors. Moreover, in vitro experiments have shown that Cavin-3 may promote the expression of inflammatory factors by regulating the MAPK signaling pathway, thereby killing tumor cells and inhibiting tumor proliferation.

The tumor promoting effect of benzophenone-3 in mice fed adult high-fat diet plausibly results from reduced Tc activity and increased RANKL expression interacting with high-fat diet increased expression of mammary growth factors and M2 macrophage polarization. Dietary fat and benzophenone-3 have immunomodulatory consequences that may interact in affecting mammary tumorigenesis in either a protective or promotional fashion.

Functional experiments demonstrated that radioresistant ESCC cells (KYSE410R) exhibited elevated OXPHOS activity, which is reversed by targeting TCA cycle enzymes (CPI-613 (Devimistat), fumarate hydratase-IN-1 (FH-IN-1), etc.) or Oxidative phosphorylation (OXPHOS) inhibitors (IACS-010759, Rotenone, etc.). Clinically, high Amphiregulin/Epiregulin (AREG/EREG) levels correlated with nCRT resistance and poor prognosis. Collectively, the CEBPB/AREG/EREG axis drives radioresistance by reprogramming OXPHOS, suggesting inhibition of this pathway or OXPHOS itself as a promising strategy to enhance ESCC therapeutic responses.

This prognostic model constructed based on CCCR genes represents a valid tool for the prognosis of LUAD patients. Our findings provide valuable insights into the prognostic and immunological relevance of CCCR genes in LUAD, offering a robust foundation for personalized treatment strategies and future research.

PRKD2 integrates secretory stress, stem-like programmes and immune evasion, driving aggressive MM yet exposing a vulnerability to VEGFR/PDGFR blockade. Direct PRKD2 targeting or axitinib-based combinations-including proteasome inhibition-deserve clinical evaluation for high-risk MM.

It inhibits proliferation by destabilizing EREG mRNA in an m6A-dependent manner, thereby inactivating the PI3K/Akt signaling cascade. These results highlight FTO as a potential prognostic biomarker and a promising therapeutic target for glioma.

Furthermore, TRIM31 facilitates the entry of P65 into the nucleus, which in turn creates a positive feedback pathway that promotes inflammatory-carcinogenic transformation and tumorigenesis of colorectal. Our findings indicate that TRIM31 may be an important factor driving colorectal carcinogenesis, providing a potential target for intervention in CRC targeted therapy.