dactinomycin

Ovarian cancer is highly lethal, largely due to the rapid development of paclitaxel resistance...RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D mRNA decay assays were conducted to elucidate the molecular interactions between lncRNA-PRLB, the RNA-binding protein fused in sarcoma (FUS), and glutathione peroxidase 4 (GPX4) mRNA...This study identifies lncRNA-PRLB as a critical upstream regulator of ferroptosis resistance and chemoresistance in ovarian cancer. By scaffolding FUS to stabilize GPX4 mRNA, lncRNA-PRLB maintains GPX4 expression and enables tumor cells to evade ferroptotic cell death.

The Actinomycin D and dual-luciferase reporter assays confirmed that YTHDF1 can affect the stability of LRP5 mRNA. Further in vitro experiments indicated that YTHDF1 knockdown reduces the protein levels of key Wnt pathway components and inhibits the cell malignant phenotype, while LRP5 overexpression reverses the effects induced by YTHDF1 knockdown. In conclusion, YTHDF1-mediated RNA m1A modifications facilitate the malignant progression of HCC by modulating the LRP5/Wnt/β-catenin signaling pathway.

A double-J ureteral stent was placed, and systemic therapy with vincristine, actinomycin D, and cyclophosphamide (VAC) was initiated. This case highlights a brisk response of disseminated intratesticular rhabdomyosarcoma to VAC chemotherapy and supports comprehensive staging and response-adapted multidisciplinary management. The complete case-level extraction and full citations are provided in the Supplementary material.

P3, N=808, Active, not recruiting, Children's Oncology Group | Trial completion date: Sep 2025 --> Mar 2026

P3, N=118, Active, not recruiting, Children's Oncology Group | Trial completion date: Sep 2027 --> Jun 2026 | Trial primary completion date: Sep 2027 --> Jun 2026

RNase R digestion and actinomycin D assays were employed to assess its stability...Animal experiments confirmed that silencing circ_0017521 suppressed tumor growth and glycolysis. This study revealed that hypoxia-induced circ_0017521 activated the PI3K/AKT pathway through the miR-532-3p/PFKFB3 axis, synergistically driving EMT and glycolysis, thereby promoting NSCLC progression.

The relationship between SERPINF1 and FTO was determined through correlation analysis, methylated RNA immunoprecipitation, luciferase, RT-qPCR, Western blotting, RNA immunoprecipitation, and actinomycin D treatment assays...Rescue experiments demonstrated that SERPINF1 overexpression reversed FTO-induced oncogenic phenotypes. These findings suggest that FTO-mediated m6A demethylation suppressed SERPINF1 expression in MM, whereas SERPINF1 overexpression inhibited tumor progression via the Wnt/β-catenin pathway.

Functional validation using actinomycin D and cycloheximide treatments demonstrated that compound 2 suppresses RPL27A and RPLP0 expression at the translational level, thereby inhibiting tumor cell invasion and migration and exerting robust antitumor effects. Collectively, these findings provide novel insights into the anticancer mechanisms of EEF1A1-targeting agents and highlight EEF1A1 as a promising therapeutic target for the treatment of TNBC.

The WTAP/TP53BP1 axis impairs periodontal tissue regeneration by promoting P-PDLSC senescence and suppressing osteogenic differentiation in an m6A-dependent manner, revealing a new cellular-level target for treating periodontitis.

Cancer chemotherapy mainly vincristine, dactinomycin, and cyclophosphamide, surgery, radiotherapy, and brachytherapy were the common keywords of treatment. The more common keywords such as age, facial neoplasms, mouth neoplasms, orbital neoplasms, gingiva, mandible, DNA-binding proteins, gene silencing, and Rh30 cell line were reported by stomatologists. This study is the first comprehensive report of the scientometric characteristics of RMS publications by pediatricians and stomatologists, highlighting the need for increased awareness among clinicians to avoid diagnostic delays and ensure timely treatment.

He was treated with vincristine, dactinomycin, and cyclophosphamide, followed by cabozantinib and pembrolizumab, and finally pembrolizumab and concurrent radiation therapy to the targetable lesions. He had a continual, rapid progression of disease and expired 2 months following radiation. This case is notable because it presents a rare example of an aggressive, TFCP2::FUS gene fusion-positive RMS presenting with multiple cutaneous metastases, and highlights that this entity is highly resistant to multiple chemotherapies, immunotherapy, and radiation therapy.

NSUN2-mediated m5C modification of EPYC contributed to GC cell growth and metastasis, which provided a novel regulatory axis for understanding the pathogenesis of GC.