PDIA4 (Protein Disulfide Isomerase Family A Member 4)

These findings suggest that PDIA4 may potentially serve as both a prognostic biomarker and a therapeutic target for OSCC patients.

PDIA4 is a key regulator of the unfolded protein response and MM cell survival. Targeting PDIA4 may enhance the efficacy of proteasome inhibitors and offers a potential strategy to overcome therapeutic resistance in multiple myeloma.

PDIA4 emerges as a novel molecular biomarker for prognostic prediction in glioma patients. Its elevated expression is associated with unfavorable outcomes, highlighting its potential as both a therapeutic target and a prognostic indicator in glioma management.

PDIA4 appears to function as a tumor suppressor in lung adenocarcinoma, suggesting that PDIA4 may act as a double-agent gene, with roles both on tumor suppression and promotion depending on the context.

The circPDIA4/miR-9-5p/SP1 feedback loop was shown to aggravate CRC progression. This finding suggests that the ceRNA axis may be a promising biomarker for CRC patient treatment.

The results of this study indicate that PDIA4 is an oncoprotein that promotes TNBC progression, and targeted therapy may represent a new and effective anti-tumor strategy, especially for patients with radiotherapy resistance.

In addition, the high-risk group exhibited higher half maximal inhibitory concentration (IC50) values for temozolomide, carmustine, and vincristine. PDIA4 knockdown reduced efferocytosis in vitro. In summary, the proposed prognostic model for GBM based on efferocytosis-related genes exhibited a robust performance.

Downregulation of PDIA4 expression counteracts the suppressive effect of lncRNA FAM225B overexpression in ovarian cancer cells. This research study supports the fact that lncRNA FAM225B in ovarian cancer can upregulate PDIA4 by directly binding to DDX17, inhibiting the activities of ovarian cancer cells.

Our findings revealed the pro-angiogenesis role of PDIA4 in GBM progression and its potential impact on GBM survival under a harsh microenvironment. Targeting PDIA4 might help to improve the efficacy of antiangiogenic therapy in patients with GBM.

Salinomycin (Sal) exhibits the potential of antitumor, while the underlying mechanism is not completely clear...Together, our findings reveal that PDIA4 promotes ferroptosis resistance in RCCs. Treatment of Sal sensitizes RCC to ferroptosis via suppressing PDIA4, suggesting the potential therapeutical application in RCCs.