PIP5K1A (Phosphatidylinositol-4-Phosphate 5-Kinase Type 1 Alpha)

Collectively, these findings establish DCLK1 functions as a context-specific amplifier, exacerbating aggressive tumor progression and chemotherapy resistance in pancreatic cancer. Targeting the calcium/DCLK1 signaling axis may therefore enhance the efficacy of adjuvant therapies in pancreatic cancer.

In summary, the present study identifies GPR176 as a novel prognostic biomarker in gastric cancer. Mechanistically, GPR176 promotes EMT and tumor progression, at least in part, through activation of the PI3K/AKT/mTOR signaling pathway.

In vivo and in vitro assays revealed that ecDNA-driven PIP5K1A amplification enhanced HCC proliferation, migration, and apoptosis resistance. Our study provides a genome-wide eccDNA profiling of HCC, implicating 1q21 ecDNA and PIP5K1A as prognostic markers and therapeutic targets, offering insights into HCC treatment strategies.

Furthermore, ISA-2011B, a PIP5K1A-specific inhibitor, effectively inhibits HCC growth and sensitized HCC cells to sorafenib. In conclusion, PIP5K1A is a promising therapeutic target for improving the efficacy of sorafenib and other ferroptosis inducers in HCC.

Furthermore, combining Mcl-1 inhibitors with IGF-1R inhibitors resulted in synergistic cell death by overcoming drug tolerance conferred by the activation of IGF signaling and suppressed tumor growth in MCL1-amplified OS xenograft models. These results suggest that genomic amplification of MCL1 in the 1q21.2-3 region, which occurred in approximately half of OS patients, may serve as a predictive biomarker for the combination therapy with an Mcl-1 inhibitor and an IGF1R inhibitor.

CSS also activates the SLC7A11/GPX4 pathway via TGFBR2, reducing lipid peroxidation and intracellular iron accumulation to suppress cisplatin-induced ferroptosis. This study discovers that the major component CSS in A. sessiliflorus leaves reverses CIO by regulating actin homeostasis via Dock1 and inhibiting ferroptosis through TGFBR2, providing a theoretical basis for expanding CIO treatment targets and related drug development.

with TILs in breast cancer patients. Collectively, we identified multiple gene targets for an increase in MHC-I expression in breast cancer in this study.

PIP5K1A is a potential drug target for treating CRC. Rupatadine, which targets PIP5K1A, could serve as a new option for treating CRC, its therapeutic mechanism being related to regulation of the Akt/GSK-3β signaling pathway.

These compounds were evaluated on their antiproliferative effects in a panel of prostate cancer cell lines. Compound 3r inhibited the proliferation of LNCaP, PC3 and DU145 cells at 20 µM, strongly, but also has strong cytotoxic effects on all tested cells.

ARHGAP1 serves as an oncogenic gene in liver cancer and the expression thereof is regulated by CircPIP5K1A through sponging miR-101-3p.

Besides that, circ-PIP5K1A was packaged into exosomes and exosomal circ-SKA3 could mediate intercellular communication between OC cells. These findings provided a promising therapeutic target for OC.