P1, N=126, Completed, PharmaMar | Recruiting --> Completed

Caprin-1 silencing enhances cisplatin sensitivity in CC by suppressing the YY1/HSP90α axis, accelerating IDH1 degradation, and activating ferroptosis.

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.

P1/2, N=195, Recruiting, Grupo Espanol de Investigacion en Sarcomas | Active, not recruiting --> Recruiting

This review summarizes the anti-inflammatory effects of cordycepin on oxidative stress. These findings indicate that cordycepin exerts favorable anti-inflammatory effects during inflammatory responses.

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.

Importantly, CME caused no systemic toxicity, and its approximate lethal dose was over 5000 mg/kg. Together, these findings suggest CME as a potent ferroptosis-inducing agent against lung cancer and establish C. militaris as a promising candidate for redox-targeted cancer therapy.

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.

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.

P1/2, N=195, Active, not recruiting, Grupo Espanol de Investigacion en Sarcomas | Recruiting --> Active, not recruiting