The C terminal fusion partners of TAZ-CAMTA1, YAP-TFE3 and potentially other TAZ/YAP fusion proteins in cancer recruit epigenetic modifiers that modulate a baseline TEAD-based transcriptional program.
The endogenous 3′UTR does not regulate TP53 mRNA or protein level and the 3′UTR is repressive when used alone in reporters, but addition of the coding region has a dominant repressive effect.
Low-dose treatment targeting multiple pathways of a pro-metastatic signaling network reduces the metastatic output of heterogeneous tumors while minimizing compensatory network activation.
Genetic analyses reveal that the tropism towards specific Kras driver mutations during urethane carcinogenesis appears to arise from the selection of an oncogenic mutation in normal cells that imparts a narrow window of signaling conducive for tumorigenesis.
FOXM1 is co-expressed with its bidirectional gene partner RHNO1, and the two genes promote DNA repair, cell growth and survival, and chemotherapy resistance in ovarian cancer.
Genetically engineered murine models reveal novel mechanisms of cell identity regulation in lung cancer and provide insights into the complex interplay between lineage specifiers and oncogenic signaling pathways in this disease.
The expression of the major circadian component CLOCK is a key regulator of stemness in breast cancer cells, which can be a novel strategy for breast cancer treatment.
In the absence of ROCK1 activation by caspases, apoptotic cells don’t undergo typical morphological changes, leading to sterile inflammation in the liver that increases tissue damage and suppresses tumor formation.
