In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-β2.

Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a

Hippo signaling pathway；MAPK signaling pathway；Cytokine-cytokine receptor interaction；Cell cycle；Endocytosis；Renal cell carcinoma；Dilated cardiomyopathy； Colorectal cancer；Rheumatoid arthritis；TGF-beta signaling pathway；Tuberculosis；Proteoglycans in cancer；Osteoclast differentiation；Amoebiasis；Chronic myeloid leukemia；Leishmaniasis；Chagas disease (American trypanosomiasis)；Malaria；HTLV-I infection；Pancreatic cancer；Hypertrophic cardiomyopathy (HCM)；Hepatitis B；Pathways in cancer；Toxoplasmosis

Moreover, TGF-β actives lnc-ATB and TGF-β2 directly binds mir-141-3p

Lnc-ATB contributes to gastric cancer growth through a MiR-141-3p/TGFβ2 feedback loop

Transcriptional misregulation in cancer

Collectively, silica-stimulated macrophages secreted TGF-β1 to induce lncRNA-ATB in epithelia cells, promoting EMT by binding with miR-200c and releasing ZEB1

Long non-coding RNA-ATB promotes EMT during silica-induced pulmonary fibrosis by competitively binding miR-200c.

Using immunohistochemistry and quantitative RT-PCR analysis, we showed that lncRNA-ATB and ZNF217, a transcriptional activator of TGF-β, were overexpressed and miR-200c, which targets ZNF217, was under-expressed in keloid tissue and keloid fibroblasts.

Knockdown of lncRNA-ATB suppresses autocrine secretion of TGF-β2 by targeting ZNF217 via miR-200c in keloid fibroblasts