P4HA2 (Prolyl 4-Hydroxylase Subunit Alpha 2)

This study highlights the oncogenic role of P4HA2 in gliomas and its potential as a therapeutic target. P4HA2 promotes glioma cell proliferation by activating the EGFR/ERK pathway through its interaction with Hsp27. These findings establish P4HA2 as a promising prognostic marker and therapeutic target, offering new directions for individualized glioma treatment.

Elevated mRNA levels of EMP3, THBS2, and ITGA5 were significantly correlated with poorer overall survival. Fn and Pg can promote invasive phenotypes in CRC through distinct mechanisms, each modulating a unique subset of p-EMT and without instigating a complete, coordinated EMT gene signature.

BRU inhibites GC progression by targeting P4HA2, disrupting glycolysis-histone lactylation signaling, and downregulating TTK. This metabolic-epigenetic mechanism positions BRU as a promising natural therapeutic for GC.

Collectively, our results show the molecular mechanism of mitophagy-mediated 125I radioresistance, which provides a potential therapeutic target and combinatorial strategy. Schematic diagram of the role of P4HA2 in 125I brachytherapy for tumors.

Collectively, GABPA inhibits P4HA2 expression and Col formation through the DICER1-miR30e axis, thereby repressing ECM deposition/stiffness and blocking mechanotransduction signaling, which consequently restrains BC aggressiveness. These findings unravel a novel role for GABPA in BC pathogenesis and have biological and therapeutic implications.

Mechanistically, P4HA2 depletion down-regulated PFKP expression, while PFKP overexpression partially rescued the oncogenic phenotype. Our data indicated that P4HA2 promoted cell proliferation, cell cycle, migration, invasion, glycolysis and tumor growth, suggesting that it might be a valuable therapeutic target for thyroid cancer.

Furthermore, BAY 11-7082, an inhibitor of the NF-κB signalling pathway, reversed the promotion of PTC proliferation and metastasis by P4HA2 both in vivo and in vitro. In conclusion, P4HA2 activates the NF-κB signaling pathway by promoting proteasome-dependent degradation of IκBα, which in turn contributes to the proliferation and migration of PTC. Therefore, P4HA2 could be used as a potential therapeutic target for the treatment of PTC patients.

Our findings reveal P4HA2 promotes CRC progression and suppresses anti-tumor immunity via STAT1/PD-L1 axis regulation. This study uncovers a novel pathogenic mechanism, positioning P4HA2 as a potential therapeutic target in CRC.

Moreover, P4H inhibitors also displayed notable anti-tumor effects in PTC cells. These findings collectively elucidate a novel mechanism through which P4HA2 potentially contributes to PTC progression, providing a promising therapeutic target.

This investigation reveals that quercetin compels apoptosis in HCC cells by diminishing P4HA2 and restraining the PI3K/Akt/mTOR axis.

Through bioinformatics and experimental validation, we identified P4HA2 as a key potential thyroid cancer biomarker. This finding provides new molecular targets for diagnosis and treatment. P4HA2 has the potential to be a diagnostic or therapeutic target, which could have significant implications for improving clinical outcomes in thyroid cancer patients.

Our findings reveal that sleep deprivation impairs intracellular lipolysis by KynA, leading to lipid droplets accumulation in colon cancer cells. This process ultimately promotes colon cancer liver metastasis. This suggests a promising strategy for colon cancer treatment.