RAD21 (RAD21 Cohesin Complex Component)

Furthermore, in vitro experiments demonstrated that knockdown of MIF-AS1 expression significantly reduced cellular proliferation and invasion, and increased the sensitivity of NSCLC cells to the chemotherapeutic drug cisplatin...MIF-AS1 could be a novel biomarker for predicting the response of NSCLC to chemo- and radio-therapy. This model, which uses both CT radiomics and MIF-AS1 levels, increases the accuracy of predicting therapeutic response in NSCLC patients.

P1, N=13, Active, not recruiting, Dana-Farber Cancer Institute | Recruiting --> Active, not recruiting | Trial completion date: Dec 2025 --> Jan 2027 | Trial primary completion date: Dec 2025 --> Apr 2025

We show that one non-coding TOP2B-bound element at the non-coding RNA gene RMRP drives tumor initiation and growth in vivo. Our study highlights TOP2B as a safeguard of genome integrity and a marker of mutational processes and hotspots in cancer, underscoring implications for cancer genomics research.

NC exerts anti-CRC effects by downregulating BUB1, disrupting the RAD21-BUB1 axis, and alleviating BUB1-mediated immune suppression.

Notably, residual disease after primary surgery had limited prognostic effect in g BRCA pv-carriers compared to non-carriers. Our findings indicate that tumor HR proficiency in the context of therapy response and survival is not a binary property, and highlight genomic and immune modifiers of outcomes in BRCA -deficient HGSC.

METTL14 inhibits tumorigenesis in TC mice in vivo by mediating m6A modification of RAD21 and decreasing RAD21 mRNA stability.

Furthermore, we observed differential effects of Rad21 and Smc3 deletion on leukemia development and secondary engraftment despite only minor differences in gene expression. These results demonstrate that cohesin mutations are not only tolerated in Cbfb::MYH11-expressing cells, they likely do not confer a strong selective advantage and are therefore not preferentially selected for during clonal evolution of this leukemia.

A RAD21-PON1 risk signature robustly stratified survival. Our findings highlight the RAD21-PON1 axis as a central regulator connecting metabolism and immunity in HCC, providing prognostic and therapeutic insights.

Notably, residual disease after primary surgery had limited prognostic effect in g BRCA pv-carriers compared to non-carriers. Our findings indicate that tumor HR proficiency in the context of therapy response and survival is not a binary property, and highlight genomic and immune modifiers of outcomes in BRCA -deficient HGSC.

Our findings establish RAD21-mediated epigenetic regulation as a novel mechanism driving LUAD progression. The efficacy of ulixertinib in suppressing cancer metastasis in preclinical models highlights its translational potential for LUAD therapy.

We further validate the RNA-associating abilities of chromatin-conformation regulators SMC1A, SMC3 and RAD21, as well as the metabolic enzyme PHGDH. PRIM-seq enables systematic discovery and prioritization of RNA-binding proteins and their targets without gene- or protein-specific reagents.