
@article {145426,
	title = {UBR7 in concert with EZH2 inhibits the TGF-β signaling leading to extracellular matrix remodeling.},
	journal = {Cell Rep},
	volume = {43},
	year = {2024},
	month = {2024 Jun 25},
	pages = {114394},
	abstract = {<p>The intricate interplay between resident cells and the extracellular matrix (ECM) profoundly influences cancer progression. In triple-negative breast cancer (TNBC), ECM architecture evolves due to the enrichment of lysyl oxidase, fibronectin, and collagen, promoting distant metastasis. Here we uncover a pivotal transcription regulatory mechanism involving the epigenetic regulator UBR7 and histone methyltransferase EZH2 in regulating transforming growth factor (TGF)-β/Smad signaling, affecting the expression of ECM genes. UBR7 loss leads to a dramatic reduction in facultative heterochromatin mark H3K27me3, activating ECM genes. UBR7 plays a crucial role in matrix deposition in adherent cancer cells and spheroids, altering collagen content and lysyl oxidase activity, directly affecting matrix stiffness and invasiveness. These findings are further validated in\&nbsp;vivo in mice models and TNBC patients, where reduced UBR7 levels are accompanied by increased ECM component expression and activity, leading to fibrosis-mediated matrix stiffness. Thus, UBR7 is a master regulator of matrix stiffening, influencing the metastatic potential of TNBC.</p>
},
	issn = {2211-1247},
	doi = {10.1016/j.celrep.2024.114394},
	author = {Adhikari, Swagata and Singh, Vipin and Nandi, Sandhik and Ghosal, Manorama and Raj, Nidharshan Sundar and Khanna, Jayati and Bhattacharya, Apoorva and Kabiraj, Aindrila and Mondal, Atanu and Vasudevan, Madavan and Senapati, Dulal and Roy, Himansu and Sengupta, Kundan and Notani, Dimple and Das, Chandrima}
}
@article {32474,
	title = {Rudhira/BCAS3 is essential for mouse development and cardiovascular patterning.},
	journal = {Sci Rep},
	volume = {8},
	year = {2018},
	month = {2018 Apr 04},
	pages = {5632},
	abstract = {<p>Rudhira/Breast Carcinoma Amplified Sequence 3 (BCAS3) is a cytoskeletal protein that promotes directional cell migration and angiogenesis in vitro and is implicated in human carcinomas and coronary artery disease. To study the role of Rudhira during development in vivo, we generated the first knockout mouse for rudhira and show that Rudhira is essential for mouse development. Rudhira null embryos die at embryonic day (E) 9.5 accompanied by severe vascular patterning defects in embryonic and extra-embryonic tissues. To identify the molecular processes downstream of rudhira, we analyzed the transcriptome of intact knockout yolk sacs. Genome-wide transcriptome analysis showed that Rudhira functions in angiogenesis and its related processes such as cell adhesion, extracellular matrix organization, peptidase activity and TGFβ signaling. Since Rudhira is also expressed in endothelial cells\&nbsp;(ECs), we further generated Tie2Cre-mediated endothelial knockout (CKO) of rudhira. CKO embryos survive to E11.5 and similar to the global knockout, display gross vascular patterning defects, showing that endothelial Rudhira is vital for development. Further, Rudhira knockdown ECs in culture fail to sprout in a spheroid-sprouting assay, strongly supporting its role in vascular patterning. Our study identifies an essential role for Rudhira in blood vessel remodeling and provides a mouse model for cardiovascular development.</p>
},
	issn = {2045-2322},
	doi = {10.1038/s41598-018-24014-w},
	author = {Shetty, Ronak and Joshi, Divyesh and Jain, Mamta and Vasudevan, Madavan and Paul, Jasper Chrysolite and Bhat, Ganesh and Banerjee, Poulomi and Abe, Takaya and Kiyonari, Hiroshi and VijayRaghavan, K and Inamdar, Maneesha S}
}
