dactinomycin

Initial chemotherapy with the VAC regimen (vincristine, actinomycin D, and cyclophosphamide) was administered, but the response was poor. To our knowledge, this is the first reported case of infantile fibrosarcoma with RBPMS-NTRK3 fusion in China. Treatment with larotrectinib resulted in marked tumor shrinkage.

USP19 overexpression promoted deubiquitination and stabilization of fused in sarcoma (FUS), as confirmed by Western blotting, actinomycin D treatment, and ubiquitination assays...These findings suggest that USP19 alleviates TN by enhancing FUS deubiquitination and preserving mitochondrial integrity in neurons. This study reveals a novel USP19/FUS signaling axis in the regulation of mitochondrial homeostasis and provides a promising therapeutic target for the treatment of TN.

5-Fluorouracil (5-Fu) is a cornerstone chemotherapeutic agent in the treatment of colorectal cancer (CRC)...The circular structure, stability, and subcellular localization of circ-0023919 were confirmed using a combination of approaches, including actinomycin D treatment, RNase R digestion, specific primer PCR amplification, Sanger sequencing and FISH...In this scientific study, circ-0023919 is shown to enhance the resistance of CRC cells to 5-Fu by promoting EMT. Thus, circ-0023919 is considered a potential therapeutic target for CRC treatment.

These findings show that DjYTHDF2.2 promotes neoblast self-renewal and regeneration by targeting Djast mRNA for degradation, which is a novel m6A-dependent regulatory axis that is essential for stem cell maintenance and tissue regeneration in planarians. This study highlights the conserved role of YTHDF2-mediated post-transcriptional control in stem cell biology and regenerative mechanisms.

An actinomycin D assay analyzed FBXL16 mRNA stability. RBM7 promotes TMZ resistance by suppressing mitochondrial dysfunction and ferroptosis through destabilization of FBXL16. Targeting the RBM7-FBXL16 axis may represent a novel strategy to overcome GBM chemoresistance.

Our findings establish that circ_0001741 drives ESCC progression by modulating the miR-194-5p/E2F3 axis, underscoring its therapeutic potential for ESCC treatment.

It exhibited strong binding affinities with VX-11e, irinotecan, and dactinomycin. Endothelial cells were identified as key cells; the occurrence of PTC reduced their quantity and affected the frequency/intensity of their interactions with mast cells. In conclusion, PTPN11 holds promise as a prognostic marker for PTC and is of great value for clinical management.

The characteristics of circCOL5A1 were verified by RNase R and actinomycin D experiments, and its subcellular localization was analyzed by PARIS kit...CircCOL5A1 promoted cell proliferation, migration, invasion, EMT and glycolysis by cytoplasmic adsorption of miR-3940-3p and up-regulation of KPNA2 in RCC. CircCOL5A1 is anticipated to be a promising molecular target for diagnosing and treating RCC.

Mechanistic interrogation combined NSUN2 knockout, CRISPR knock-in mutants at K692 (K692R/E), co-immunoprecipitation, RIP-seq, MeRIP-qPCR, and actinomycin-D chase to test mRNA binding, m5C modification, and stability of CDCP1/STC1... This study identifies lactate-driven NSUN2 K692 lactylation as a key driver of perineural invasion in PDAC. We define a lactate-NSUN2-m5C-CDCP1/STC1 axis that links metabolic stress-induced lysine lactylation to mRNA methylation-dependent stabilization of pro-invasive transcripts, highlighting actionable therapeutic targets to restrain neural invasion and improve patient outcomes.

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.