Figure 4 from Claudin-4 Modulates Autophagy via SLC1A5/LAT1 as a Mechanism to Regulate Micronuclei

Correlation of amino acids transport with the clinical significance of claudin-4 in ovarian cancer. Reported proteins interacting with claudin-4 in HGSOC cells were employed to construct PPN, aiming to identify key elements and cellular functions associated with the clinical significance of claudin-4 in HGSOC tumors. This analysis utilized publicly available data from HGSOC tumors, sourced from cBioPortal and Kaplan–Meier plotter. A, PPN (based on BioID) of claudin-4-interacting proteins (experimentally determined using STRING) and highly mutated proteins (cBioPortal) in HGSOC tumors shows clusters of proteins and distinctive associated cellular functions. B, Significantly different metabolites in OVCAR3 cells associated to claudin-4 downregulation (from global metabolomics using cell pellets and supernatants; claudin-4 KD/WT, where values close to 1 are similar results between KD and WT). It also indicates the corresponding mean fold change in the (top) of circles, (red and green; red indicates decreased while greed indicates increase of metabolites). C, Same as (B) but in OVCA429 cells. D, The median survival of HGSOC patients (criteria: p53 mutated; serous histology) was correlated with each identified cluster (based on claudin-4; continue lines) and without claudin-4 (dotted lines; significance, P < 0.05; P values and false discovery rate is indicated in Supplementary Tables S3 and S4).