ADAMTS6: Emerging roles in cardiovascular, musculoskeletal and cancer biology

Abstract

ADAMTS family members control mammalian development and disease, primarily through their function as proteases, by regulation of extracellular matrix composition. Until recently, ADAMTS6 was known as one of the orphan proteinases of the nineteen-member family with a relatively unknown expression pattern and function. Emerging focus on this enzyme has started to uncover these unknowns and revealed a vast importance and requirement of ADAMTS6 in cardiovascular and musculoskeletal development. In addition, ADAMTS6 has been linked to numerous disease settings including several types of cancer. This review summarizes the necessity of ADAMTS6 during development, its role in disease and requirement for essential prospective studies to fully realize its biological implications and potential for therapeutic intervention.

Transcriptomic Profiles of Normal Pituitary Cells and Pituitary Neuroendocrine Tumor Cells

“…In addition, they exhibit upregulation of metalloproteinase (i.e., ADAMTS6). The role of ADAMTS6 in tumor development is unclear, as it seems to act as either a tumor suppressor or pro-tumoral agent, depending on the cancer type [104]. While molecularly defining the invasiveness of prolactinoma remains challenging, future multiomics studies at a single-cell level are encouraged to capture further subtle but substantial transcriptomic variations that drive the heterogeneous lactotroph tumor behavior in well-characterized patients.…”

Multi-gradient Permutation Survival Analysis Identifies Mitosis and Immune Signatures Steadily Associated with Cancer Patient Prognosis

“…We also identified the most significant GEARs in individual cancer types, such as TLL1 (BLCA), PGK1 (BRCA), RFXANK (CESC), DPP7 (COAD), VWA8 (KIRC), SCMH1 (LGG), HILPDA (LIHC), TLE1 (LUAD), CD151 (LUSC), ANKRD13A (OV), SOCS2 (PAAD), DRG2 (PRAD), ADAMTS6 (STAD), PSMB8 (THCA), ASS1 (UCEC) (Table 3). Many of these genes were previously reported to associate with tumorigenesis 18,[29][30][31][32][33][34][35][36][37][38][39][40] . For example, TLE1 is known as a transcriptional repressor that promotes cell proliferation, migration, and inhibits apoptosis in LUAD 41,42 .…”