GRIN2D (Glutamate Ionotropic Receptor NMDA Type Subunit 2D)

Esketamine, a GRIN2D inhibitor, and LY294002, a PI3K inhibitor, either alone or in combination, could suppress the tumor growth induced by high GRIN2D levels both in vitro and in vivo. This study is the first to identify the involvement of GRIN2D in lung cancer and to clarify the underlying mechanism of its effect; the findings further suggest that ketamine in cancer treatment may extend beyond relieving pain and depression.

P3, N=40, Recruiting, Meyer Children's Hospital IRCCS

Rutin mitigates THP-induced cardiotoxicity and enhances chemotherapeutic efficacy via the novel miR-129-1-3p/GRIN2D pathway. Our data show miR-129-1-3p to be an essential mediator, and suggest that the rutin-miR-129-1-3p-GRIN2D axis is a favorable target for improving the safety and effectiveness of breast cancer chemotherapy.

Innovative strategies that integrate stromal-targeting agents, complement modulators, anti-CLDN18.2 antibodies, and novel GRIN2D-targeted therapies, along with precision molecular profiling, offer potential for enhancing patient outcomes. Tailored approaches that incorporate early detection and dynamic biomarker monitoring may ultimately transform GSRCC management toward personalized, evidence-based therapies and prevention.

Moreover, interference with the glutamate-GRIN2D signaling at these neuron-cancer pseudo-synapses markedly improved survival in vivo. This discovery of peripheral cancer-neuron pseudo-synapses may provide an opportunity for cancer-neuroscience-instructed oncological therapies.

These findings support the incorporation of pharmacogenomic testing into clinical practice for HCC therapy, paving the way for customized treatment methods that may improve therapeutic efficacy and patient outcomes. Future research is needed to replicate these genetic connections.

ADAMTSL2 stands out as an independent predictor for the prognosis of GC and may play a crucial pathological role in the development of GC.

Overexpression of GRIN2D promoted calcium efflux, phosphorylation of p38 MARK protein, and proliferation of GES1 cells. Altogether, the findings derived from this study suggest that BHLHE40 knockdown suppresses the growth, mobility, and glycolysis of GC cells by inhibiting GRIN2D transcription and disrupting the BHLHE40/GRIN2D axis may be an attractive therapeutic strategy for GC.

Our findings uncover critical molecular dynamics within bladder cancer cells, offering a deeper understanding of its pathophysiology. Furthermore, the insights gained from this study underscore the potential of targeting the m6A-YTHDF1-GRIN2D pathway for the development of innovative therapeutic strategies in the treatment of bladder cancer.

Our findings collectively illustrate that the CircBIRC6-miR-488-GRIN2D axis fosters CAV1 expression in GC cells, thereby reducing autophagy levels. Both circBIRC6 and GRIN2D emerge as potential targets for treatment and independent prognostic factors for GC patients.

These findings indicated that upregulated Grin2d expression played an important role in esophageal carcinogenesis via the PI3K/Akt/mTOR pathway and might be a biological marker for aggressive tumor behavior and poor prognosis. Its silencing might represent a targeted therapy approach against esophageal cancer.