dactinomycin

Mechanistically, MeRIP-qPCR, RIP-qPCR, dual-luciferase reporter assay, and actinomycin D treatment revealed that IGF2BP1 targeted the 3'UTR of the C-MYC transcript for m6A modification and enhanced its stability. Furthermore, IGF2BP1 induced epithelial-mesenchymal transition (EMT) through the overexpression of C-MYC. In conclusion, these findings suggest that IGF2BP1-mediated m6A modification of C-MYC promotes LSCC progression via the EMT pathway, providing potential biomarkers and therapeutic targets for LSCC.

RNA sequencing, Western blotting, Actinomycin-D assays, and RNA immunoprecipitation (RIP) and methylated RNA immunoprecipitation (MeRIP) assays were performed to investigate the regulatory mechanisms of IGF2BP2 on RELB expression...Our study demonstrates that IGF2BP2 plays a critical role in HCC progression by stabilizing RELB mRNA and activating the NF-κB signaling pathway. The results suggest that IGF2BP2 may be a potential therapeutic strategy for HCC.

In addition, actinomycin D (ActD) chase experiments indicated altered transcript dynamics of MEG3 and BCYRN1 under spike-related conditions. Collectively, these findings suggest that SARS-CoV-2 spike protein exerts antitumor activity in A549 cells and may contribute to the regulation of MEG3 and BCYRN1. Further studies, including formal rescue and biochemical interaction assay, will be required to establish causality and direct molecular mechanisms.

Luciferase reporter and actinomycin D assays were further applied to clarify the regulatory mechanism of GSDMC on OTUB1 and programmed cell death-ligand 1 (PD-L1) expression...This study identifies a novel regulatory axis of m⁶A-modified circFOXA1/GSDMC/OTUB1/PD-L1 in mediating TNBC immune escape, where GSDMC enhances PD-L1 protein stability via OTUB1-dependent deubiquitination. These findings reveal a new molecular mechanism underlying TNBC immune evasion and identify circFOXA1 as a potential therapeutic target to improve the efficacy of anti-PD-1/PD-L1 immunotherapy in TNBC.

The stability of BACH1 mRNA following actinomycin D (ActD) treatment was analyzed after YTHDC1 silencing...Collectively, YTHDC1 regulates BACH1 expression in an m6A-dependent mechanism, contributing to TNBC progression. Implications: Our findings provide a rationale for further investigation of the YTHDC1/BACH1 axis as a potential therapeutic target in TNBC.

P2, N=30, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Apr 2026 --> Apr 2027 | Trial primary completion date: Apr 2026 --> Apr 2027

LUCAT1/PTBP1/HIF-1α positive feedback loop drives excessive T cell differentiation and Th1/Th2-skewed immune imbalance in sepsis via glucose metabolic reprogramming, which may contribute to disease progression.

YTHDF3 is highly expressed in AAA tissues and Ang II-induced VSMCs. YTHDF3 hinders the proliferation of Ang II-induced VSMCs while promoting apoptosis and inflammation. YTHDF3 deficiency exerts protective effect by interfering with SIRT2/FOXO1 axis.

Our work uncovers a previously unrecognized PRKN-METTL3-CLDN2 signaling network that orchestrates colorectal tumorigenesis, providing a compelling rationale for developing METTL3-targeted therapies against CRC.

Our findings establish the ALKBH5/IGF2BP1-TRIM37-RBMX signaling axis as a pivotal driver of PDAC progression, highlighting the intersection of m6A modification, ubiquitin signaling, and metabolic reprogramming. These findings may provide potential therapeutic avenues for this intractable malignancy.

We have established the circ-ZBTB38/RALGAPB axis as a novel regulatory circuit in melanoma. Circ-ZBTB38 mediates RALGAPB post-translational degradation to hyperactivate Ral signaling. This work uncovers a new mechanism of circRNA-mediated regulation of enzyme activity (RalGAPs) in signaling crosstalk and highlights circ-ZBTB38 as a prognostic biomarker and therapeutic target for melanoma.

Here, we demonstrate that expression of DYRK1B - but not its closely related paralog DYRK1A - is upregulated by cytostatic drugs (Actinomycin D, Doxorubicin) in multiple cancer cell lines. In conclusion, our study identifies DYRK1B as an indirect p53 target that suppresses p53-mediated activation of RFX7. These findings suggest that pharmacological inhibition of DYRK1B may represent a therapeutic strategy to enhance RFX7 tumor suppressor function.