In breast cancer, dysregulated Hippo signaling results in activation of the YAP/TAZ-TEAD transcriptional complex, which induces a broad oncogenic transcriptional program. This gene expression network promotes tumor cell proliferation, survival, invasion and metastatic dissemination, while also contributing to resistance to anticancer therapies. Researchers from Harbin Medical University reported the preclinical characterization of M-511-0965, a YAP-TEAD4 inhibitor, in models of triple-negative breast cancer (TNBC).
Researchers at Theramir Ltd. presented preclinical proof-of-concept data for a new extracellular vesicle (EV) platform engineered to deliver miR-885-5p (EVmiR885-5p), targeting leukocyte-specific protein-1 (LCP-1)-mediated cytoskeletal remodeling in triple-negative breast cancer (TNBC) models.
Kolon Life Science Inc. is developing KLS-3021, a next-generation oncolytic vaccinia virus designed to express the PH20, IL-12 and PD-1-Fc transgenes to mediate receptor-independent tumor cell killing and enhance antitumor immune responses.
Previous work showed that RNase H2 activity helps triple-negative breast cancer (TNBC) cells manage high levels of replication stress, offering new therapeutic insights. Researchers from The University of Texas MD Anderson Cancer Center and Cleveland Clinic now show that cells escaping senescence depend on overexpression of RNase H2, which removes misincorporated ribonucleotides from genomic DNA. They confirmed that TNBCs rely on RNase H2 to tolerate high replication stress.
Researchers at the School of Pharmacy and Biomolecular Sciences from the Royal College of Surgeons in Ireland and collaborating institutions have detailed the design, synthesis and biological evaluation of a new series of triazine-based multitarget inhibitors aimed at dual inhibition of PI3K and HDAC for breast cancer therapy.
Transforming acidic coiled-coil-containing protein 3 (TACC3) is a core member of multiprotein complexes that regulate microtubule- and centrosome-related processes. Its aberrant expression is found in several cancer types with poor prognosis, thus highlighting it as a candidate therapeutic target. Researchers from Beijing Konruns Pharmaceutical Co. Ltd. have presented data for KC-1101, a TACC3 inhibitor for treating aggressive cancers with centrosome amplification.
BMAL1 expression is tied to important cellular processes, including cell proliferation, migration, cell cycle and DNA damage repairing. There is increasing evidence that it regulates the expression of various oncogenes and tumor-suppressor genes in cancer cells. Researchers hypothesized that modulating BMAL1 expression could be a new therapeutic approach for treating cancer, such as triple-negative breast cancer (TNBC).
Telomir Pharmaceuticals Inc. has submitted an IND application to the U.S. FDA for its lead candidate, Telomir-1 (Telomir-Zn), for the treatment of advanced and metastatic triple-negative breast cancer (TNBC). Telomir-1 is a first-in-class metal-modulating epigenetic agent designed to restore transcriptional control in tumor cells by targeting intracellular iron-zinc homeostasis.
HORMA domain-containing protein 1 (HORMAD1) is a protein that promotes meiotic recombination and its expression is usually restricted to germ-line cells, although it has been shown to be actively expressed out of context in about 60% of triple-negative breast cancers (TNBCs). A team at The Institute of Cancer Research has found that this aberrant expression in tumor cells perturbs mitotic arrest and generates aneuploidy, leading to a weakening of the spindle assembly checkpoint and in kinetochore-microtubule error correction.
CSN5, a key COP9 signalosome subunit, regulates protein stability in the cell cycle, apoptosis and DNA repair. Its overexpression in cancer promotes tumor growth, metastasis and therapy resistance, making it a potential therapeutic target.
