Esophageal Squamous Cell Carcinoma

Mechanistically, ATG4B inhibition by compound a25 disrupted autophagic homeostasis, leading to impaired autophagy flux and enhanced cell death. Our study identifies compound a25 as a novel ATG4B inhibitor with compelling preclinical efficacy against ESCC, providing a strategic foundation for targeting pro-tumor autophagy in gastrointestinal cancers.

Eg5 represents not only an independent prognostic marker but also a promising drug target for ESCC, yet the findings still need to be validated in large-scale prospective studies. Inhibiting this kinesin protein with K858 may represent a novel therapeutic strategy to sensitize ESCC to radiotherapy.

In summary, metformin may inhibit the migration and invasion of ESCC cells through downregulation of GLUL and SP1, which play important roles in the mechanism of metformin's anti-tumor effects. These findings provide new insights into the therapeutic potential of metformin in the treatment of ESCC.

P2, N=50, Not yet recruiting, Tang-Du Hospital

In addition, HOXC9-OTUD1-FABP5 signaling was closely linked to the clinicopathological grade of ESCC patients. Our study comprehensively reveals the mechanism by which HOXC9 accelerates ESCC progression, and identifies potential biomarkers and therapeutic targets for the pathogenesis and clinical treatment of ESCC.

Interestingly, patients exhibiting co-high expression of stromal cell-derived CD39 rather than tumor cell-derived CD39 rather than tumor cell-derived CD39 with PD-L1 demonstrated optimal therapeutic outcomes. These findings suggest that CD39 and PD-L1 play critical roles in modulating the response to NIT and may serve as candidate biomarkers for guiding individualized treatment strategies in ESCC in the future.

The attenuation of arecoline-driven metastatic behavior in ESCC cells by EGCG is associated with alterations in EGFR-AKT-P38 signaling, supporting its potential role as a dietary or adjunctive agent in areca-associated esophageal cancer.

We developed an exploratory Rho GTPase-based prognostic model for ESCC and identified CTTN as a candidate adverse prognostic marker and functional contributor to ESCC cell migration and invasion. The model, immune-infiltration findings, nomogram, and CTTN-related mechanistic interpretations require further validation in larger prospective cohorts and additional experimental systems.

As a key oncogenic driver for ESCA, IGFBP1 may participate in the oncogenesis of ESCA, possibly influencing clinical outcomes via IGF signaling and the tumor microenvironment. Its dual functions in tumor and immune systems suggest it might be a candidate for ESCA immunotherapy research.

Notably, HNRNPA2B1 mediates the exosomal packaging of m6A-modified circTNRC6B to counteract TNRC6B driven pro-tumorigenic effects. This study highlights the TNRC6B/circTNRC6B axis as a key determinant for LVI, providing potential diagnostic biomarkers and therapeutic targets for upper gastrointestinal tumors.

This study establishes SPP1 as both a key driver of immunotherapy resistance in heterogeneous ESCC tumors and a promising therapeutic target for overcoming treatment failure.

Our findings identify the Nrf2-Gpx2 axis as a master regulator of immunogenicity in ESCC. Targeting this axis represents a promising strategy to convert "cold" tumors into "hot" environments, thereby improving the efficacy of radiotherapy and immunotherapy.