Actinomycin D treatment combined with RT-qPCR was used to assess ILF3 mRNA stability...In vivo, DDX3X inhibitor, RK-33, markedly inhibited NB tumor growth and metastasis and enhanced M1 macrophage polarization, which was partially reversed by ILF3 overexpression. DDX3X promotes NB progression by stabilizing ILF3 mRNA, thereby facilitating M2 macrophage polarization.

Additionally, mRNA stability was evaluated using actinomycin D assay...NAT10 catalyzed ac4C acetylation on CEBPA mRNA, enhancing its stability and increasing CEBPA protein expression, thereby promoting the malignant progression of NSCLC. The identification of this feedback loop provides a preclinical rationale for developing NSCLC therapeutic strategies targeting NAT10 or CEBPA.

CSTF2 promotes gastric cancer progression by post-transcriptionally stabilizing TGM2 mRNA, and its overexpression is closely related to poor prognosis. The elucidated CSTF2-TGM2 regulatory axis may offer a promising and innovative therapeutic target for gastric carcinoma treatment.

WTAP stabilizes ICAM1 mRNA via m6A modification, thereby increasing ICAM1 expression and enhancing TF activity in LPS-stimulated HUVECs. Knocking down WTAP in rats improves sepsis-induced DIC.

The expression and in vitro functionality of circPSMA4 in T24 bladder cancer cell lines were analyzed using RNase R treatment, actinomycin D stability assay, nucleocytoplasmic separation, real-time quantitative PCR, Western blot, dual-luciferase reporter assay, cellular energy metabolism analysis, scratch assay, Transwell migration and invasion assay, CCK-8 proliferation assay, lactate and glucose uptake detection, and ATP production measurement...CircPSMA4 functions as a miR-767-3p sponge, regulating miR-767-3p to influence the expression of HIF1A, thereby promoting the proliferation, migration, invasion, and metabolic activities of bladder cancer cells, as well as tumor formation. CircPSMA4 facilitates the proliferation, migration, invasion, and metabolism of bladder cancer cells through the miR-767-3p/HIF1A pathway.

P=N/A, N=142, Active, not recruiting, Brigham and Women's Hospital | Trial completion date: Jan 2024 --> Dec 2026

METTL14 inhibits tumorigenesis in TC mice in vivo by mediating m6A modification of RAD21 and decreasing RAD21 mRNA stability.

The circular nature, subcellular localization, and stability of circCGNL1 were validated through RNase R digestion, actinomycin D treatment, and FISH assay...This study identifies circCGNL1 as a tumor-suppressive circRNA that inhibits NPC progression by binding to IGF2BP3 and suppressing the AKT/mTOR signaling. These findings reveal a novel regulatory mechanism in NPC and highlight circCGNL1 as a promising biomarker and therapeutic target.

P=N/A, N=20, Recruiting, Duke University | Trial primary completion date: Oct 2025 --> Apr 2026

Its circular nature and stability were confirmed via actinomycin D treatment and RNase R digestion...hsa_circ_0001776 suppresses AML progression via the miR-1269b/PTEN axis. These findings suggest that hsa_circ_0001776 may serve as a potential diagnostic biomarker and therapeutic target for AML.

METTL14 stabilizes SIRT5 mRNA via m6A modification, upregulating SIRT5 expression and inducing ferroptosis, thereby inhibiting GC progression.

Treatment with chemotherapy consisted of vincristine, dactinomycin, and cyclophosphamide, and received 8 cycles of photon beam radiation. Radiological surveillance up to 12 months showed no signs of recurrence or metastatic lesions. Patients with CS are at a high risk of developing rhabdomyosarcoma and clinicians should be vigilant in the context of any clinical orbital signs of disease.