Feb 15, 2021 · Recently, EZH2 inact has been linked to RAS-signaling as Ezh2 deletion aggravated the development of Nras mut-driven MN in mice.

Nov 11, 2024 · In this new study, the research team found that mutant RAS is directly involved in the process of releasing a nuclear protein called EZH2 from a complex transported from the nucleus to the cytoplasm. Once released, EZH2 facilitates the breakdown of a tumor suppressor protein called DLC1.

Dec 2, 2024 · In this study, we show that combined EZH2 and RAS pathway inhibitors potently kill colorectal cancer cells and promote dramatic tumor regression in multiple models in vivo.

EZH2 inactivation in RAS-driven myeloid neoplasms hyperactivates RAS-signaling and increases MEK inhibitor sensitivity Leukemia . 2021 May;35(5):1521-1526. doi: 10.1038/s41375-021-01161-0.

Jan 20, 2012 · To evaluate the significance of Ezh2 upregulation in pancreatic carcinoma induced by activated RAS, we knocked Ezh2 down using the specific siRNA in a rat pancreatic carcinoma cell line, NOD634 exogenously expressing oncogenic human HRAS G12V.

By studying almost 450 primary patient specimens with chronic myelomono-cytic leukemia (CMML) and acute myeloid leukemia (AML), we show that inact and mut co-exist in MN, EZH2 RAS and that this...

May 4, 2023 · In the present study, we found that the pancreas tumor microenvironment suppresses NK cell and T cell surveillance after therapy-induced senescence through enhancer of zeste homolog 2...

Nov 12, 2024 · CCR researchers showed that RAS can colocalize with RAN-GAP (red dots) at the edge of the cell nucleus (bright blue), where it helps trigger nuclear transport machinery to release cargo proteins such as EZH2 into the cytoplasm.

By studying almost 450 primary patient specimens with chronic myelomonocytic leukemia (CMML) and acute myeloid leukemia (AML), we show that EZH2inact and RASmut co-exist in MN, and that this co-occurrence is associated with a poor prognosis in affected patients.

Jun 1, 2024 · EZH2 is a significant regulator in breast cancer resistance, covering key pathways. Targeting EZH2 may enhance breast cancer treatment efficacy. Targets:enzyme inhibition, PRC2 destabilization, EZH2 degradation, ncRNA blockage. Strategies: molecular inhibitors and possible combination therapy.