CLAUDIN-2 PROMOTES INVASION, IMMUNE EVASION, AND PHENOTYPIC PLASTICITY IN COLORECTAL CANCER. kguzinska74@gmail.com

 

CLAUDIN-2 PROMOTES INVASION, IMMUNE EVASION, AND PHENOTYPIC PLASTICITY IN COLORECTAL CANCER.

5

Poland

Poster Exhibition only

Claudin-2 (CLDN2), a tight junction protein, plays a role in colorectal cancer (CRC) biology, but its clinical and molecular functions remain incompletely understood.

To evaluate associations between CLDN2 expression and histopathological, molecular, and immunological features of CRC, with a focus on its relationship with E-cadherin (E-CDH), tumor budding (TB), lymphoid follicles (LFs), and microsatellite instability (MSI). We analyzed CLDN2 and E-CDH immunoexpression in tumor samples from 54 CRC patients. Correlations were assessed with TB, TNM stage, lymph node metastasis, LF presence, and MSI status (determined via mismatch repair protein immunohistochemistry).

High CLDN2 expression correlated with reduced E-CDH levels, increased tumor budding, advanced TNM stage, and lymph node involvement. In contrast, CLDN2 expression was inversely associated with the presence of LFs. Interestingly, MSI tumors—typically considered less aggressive—exhibited higher CLDN2 levels and were the only group with distant metastases, indicating potential biological heterogeneity within this subgroup.CLDN2 is linked to key markers of CRC aggressiveness, including EMT features, immune evasion, and metastatic potential. Its inverse association with LFs suggests a role in suppressing antitumor immune responses.

These findings support CLDN2 as a candidate prognostic biomarker and therapeutic target, particularly in MSI tumors with unexpected aggressive traits. Validation in larger cohorts is warranted.