SMYD3 (SET And MYND Domain Containing 3)

Consequently, inhibiting the SMYD3-SMAD3 interaction may represent a promising therapeutic strategy for addressing CRC metastasis. In conclusion, targeting the SMYD3-RACK1-SMAD3 transcriptional complex presents a viable approach for the treatment of CRC metastasis.

Furthermore, both PHD and CC-MYND domains interact with the nucleic acid repair protein ALKBH6, revealing a previously uncharacterized epigenetic mechanism. Overall, these novel characteristics enable ZMYND11 as a global tumor suppressor to accommodate many substrates, thereby providing the structural basis for its broad recognition mechanisms.

Our findings position the RNF113A-ASCC axis as a central modulator of chemoresistance, regulated through a post-translational methylation switch representing an innovative therapeutic vulnerability that could be exploited to enhance the efficacy of alkylating agents. Targeting this pathway may provide new opportunities to overcome chemoresistance, with KDM7B levels serving as a predictive biomarker to guide treatment in SCLC.

An apoptosis-related gene prognostic model (AS model) with high predictive performance was constructed and had close associations with the tumor immune microenvironment and intercellular communication. The HSPB1 had a good predictive effect on GBM prognosis.

A review of published ZMYND11::MBTD1 leukemias (n = 5) found immunophenotypes highly consistent with MNKPL, suggesting prior misclassification. These findings support ZMYND11::MBTD1 as a recurrent lesion in MNKPL and a practical aid to diagnosis and treatment selection.

Functional enrichment and protein-protein interaction analyses revealed that CTSC regulates the ECM-integrin-PI3K-Akt signaling pathway, contributing to tumor cell proliferation and survival. The findings establish a multi-omics-based biomarker panel with strong diagnostic utility and mechanistic relevance, suggesting a potential framework for future translational validation in clinical cohorts.

By inducing synergistic cell death and immune activation, this strategy provides a foundation for clinical translation and identifies novel molecular targets for future investigation. Our findings underscore the feasibility of engineered oral OV formulations to improve treatment outcomes in intestinal malignancies.

As a result, NG/ASOs decreased the translation of Smyd3 proteins from mRNA and thus inhibited the proliferation of HepG2 cells. This study underscores the potential of glycogen as an efficient nanovector for ASO delivery and cancer gene therapy.

To gain insights into PI3K/mTOR pathway dysregulation in this context, we perform a human genome-wide CRISPR/Cas9 screen for hits that synergistically blocked EBVaGC proliferation together with the PI3K antagonist alpelisib...Rather than perturbing mTORC1 lysosomal recruitment, ZMYND19 and MKLN1 block the interaction between mTORC1 and Rheb and also with mTORC1 substrates S6 and 4E-BP1. Thus, CTLH enables cells to rapidly tune mTORC1 activity at the lysosomal membrane via the ubiquitin/proteasome pathway.

The SMYD3-CDCP1 axis drives CRC progression by epigenetically promoting CDCP1 transcription and remodeling the tumor microenvironment. Targeting this pathway may provide a promising therapeutic strategy to restrain metastasis and enhance chemotherapy efficacy in CRC.

Using a degron-tagged ZMYND11 mouse model to enable the rapid degradation of ZMYND11 in primary cortical neurons, we show that gene expression changes induced by ZMYND11 loss are attenuated by treatment with the KMT2A inhibitor revumenib, a drug which has recently been approved for the treatment of KMT2A-rearranged leukemia. Our findings shed light on the convergence of chromatin mechanisms regulating neuronal gene expression and raise the possibility that modulation of KMT2A activity may be a useful therapeutic avenue for ZRSID.

It also examines how the metal ions in liver cancer impact HCC growth and the efficacy of anticancer immunotherapy. Furthermore, we discuss the vital role of SLCs as key transporters for the hepatic uptake of anionic anticancer drugs, highlighting novel therapeutic opportunities.