dactinomycin

Cell viability was quantified using a tetrazolium-based colorimetric assay and apoptosis was evaluated by the Muse® Annexin V & Dead Cell assay based on Annexin V and 7-amino-actinomycin D staining; the expression levels of JNK, p38, ERK, beclin-1, microtubule-associated protein 1 light chain 3B (LC3B), p62/sequestosome 1 (SQSTM1) and poly (ADP-ribose) polymerase (PARP) were assessed by western blotting. Pharmacological inhibition with SP600125 attenuated JNK phosphorylation, reduced apoptotic responses and diminished autophagy-associated marker accumulation, supporting the notion that JNK signaling contributes, at least in part, to these effects. These findings indicate that RTA-408 exerts nanomolar antiproliferative activity in both hormone receptor-positive and triple-negative BC cells through a JNK-dependent mechanism that simultaneously engages apoptosis and autophagy, supporting further in vivo and translational investigation.

Cell death and viability were assessed via flow cytometry, LDH release assays and CCK-8 assays; circPDSS1 stability was determined by agarose gel electrophoresis and actinomycin D treatment; ferroptosis was determined by measuring lipid ROS, MDA, and Fe2+ levels; and key molecular interactions were determined by performing dual-luciferase reporter assays and RIP and RNA pull-down experiments...Mechanistically, circPDSS1 sponged miR-142-3p to upregulate ACSL4 expression, promoting NK cell ferroptosis. Exosomal circPDSS1 derived from GC cells contributes to NK cell ferroptosis by sponging miR-142-3p to increase ACSL4 expression and exacerbate GC.

Drug sensitivity analysis revealed differential responses to 4 drugs between the risk groups, with the 3 ORGs (ACSS2, CLTCL1 and PLD3) showing positive correlations with 2 drugs (BI_2536, Dactinomycin). Additionally, functional experiments confirmed the role of ACSS2 in OS cell behavior. This novel ORG signature not only provides a valuable tool for patient stratification but also offers insights into the biological processes driving OS progression and potential therapeutic targets.

The stability of TBX1 mRNA was analyzed by actinomycin D assay...Collectively, these findings reveal an exosome-mediated piRNA regulatory mechanism that synergistically amplifies VEGFC/VEGFR3 signaling to drive LN metastasis in BC, highlighting piR-hsa-28212 as a potential therapeutic target. Trial Registration: KYLL-2022-338.

Mechanistic studies, including chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), luciferase reporter, and actinomycin D assay, were conducted to elucidate HIF1-mediated transcriptional regulation of TARDBP and TDP-43-dependent stabilization of thyroid receptor-interacting protein 6 (TRIP6) mRNA...In vivo, TARDBP depletion inhibited tumor growth and downregulated metastasis-related factors in xenograft models. In conclusion, the HIF1-TARDBP-TRIP6 axis promotes CRC malignancy under hypoxia by integrating transcriptional activation and post-transcriptional mRNA stabilization, offering potential therapeutic targets for advanced CRC.

P1/2, N=36, Not yet recruiting, Assistance Publique Hopitaux De Paris

She was managed according to the Chinese Children Cancer Group (CCCG)-WT-2019 protocol, receiving neoadjuvant VAD (vincristine, actinomycin D, and doxorubicin) chemotherapy, followed by staged bilateral nephron-sparing surgery. This highlights the limitations of current histology- and stage-based approaches for specific molecular subtypes. Current evidence supports more aggressive surgical intervention for high-risk cases, but it is essential to balance the need for renal function preservation with the goal of achieving oncological control.

Our study demonstrates that ALKBH5 promotes cisplatin resistance in OSCC through m6A-dependent demethylation of FOXA1 transcripts, highlighting the ALKBH5-FOXA1 axis as a promising therapeutic target for overcoming this resistance.

The present study aimed to investigate the functional role and molecular mechanisms of long intergenic non‑protein coding RNA 1117 (LINC01117) in lung adenocarcinoma (LUAD)...Actinomycin D was used to inhibit RNA transcription...In conclusion, LINC01117 may serve as a notable prognostic biomarker that promotes cell proliferation in LUAD. HOXD8 may function as a downstream target of LINC01117, with LINC01117 exerting its pro‑proliferative effects by increasing HOXD8 mRNA stability.

METTL3 may drive DE-DLBCL cell cycle progression and RTX resistance by activating MYC and BCL2 transcription via YTHDF2-mediated m6A modification of β-catenin, revealing a novel mechanism of indirect transcriptional regulation in lymphoma and a potential therapeutic target.

TRIM71 may function as a tumor suppressor in CC by regulating Nectin4 expression and influencing Wnt/β-catenin signaling, EMT, tumor progression, and angiogenesis.

The m5C modification level and stability of Snail mRNA were determined by MeRIP and actinomycin D assays...In vivo, AGR2 overexpression promoted tumor growth and EMT through neutrophil-dependent activation of the ALYREF-Snail axis. TAN-secreted AGR2 enhances ALYREF stability, thereby promoting m5C-dependent Snail mRNA stabilization and sustaining EMT and CRC progression.