MaTAR25 lncRNA regulates the Tensin1 gene to impact breast cancer progression

Kung-Chi Chang, Sarah D. Diermeier, Allen T. Yu, Lily D. Brine, Suzanne Russo, Sonam Bhatia, Habeeb Alsudani, Karen Kostroff, Tawfiqul Bhuiya, Edi Brogi, Darryl J. Pappin, C. Frank Bennett, Frank Rigo and David L. Spector ()
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Kung-Chi Chang: Cold Spring Harbor
Sarah D. Diermeier: Cold Spring Harbor
Allen T. Yu: Cold Spring Harbor
Lily D. Brine: Cold Spring Harbor
Suzanne Russo: Cold Spring Harbor
Sonam Bhatia: Cold Spring Harbor
Habeeb Alsudani: Cold Spring Harbor
Karen Kostroff: Northwell Health
Tawfiqul Bhuiya: Northwell Health
Edi Brogi: Memorial Sloan Kettering Cancer Center
Darryl J. Pappin: Cold Spring Harbor
C. Frank Bennett: Ionis Pharmaceuticals
Frank Rigo: Ionis Pharmaceuticals
David L. Spector: Cold Spring Harbor

Nature Communications, 2020, vol. 11, issue 1, 1-19

Abstract: Abstract Misregulation of long non-coding RNA (lncRNA) genes has been linked to a wide variety of cancer types. Here we report on Mammary Tumor Associated RNA 25 (MaTAR25), a nuclear enriched and chromatin associated lncRNA that plays a role in mammary tumor cell proliferation, migration, and invasion, both in vitro and in vivo. MaTAR25 functions by interacting with purine rich element binding protein B (PURB), and associating with a major downstream target gene Tensin1 (Tns1) to regulate its expression in trans. The Tns1 protein product is a critical component of focal adhesions linking signaling between the extracellular matrix and the actin cytoskeleton. Knockout of MaTAR25 results in down-regulation of Tns1 leading to a reorganization of the actin cytoskeleton, and a reduction of focal adhesions and microvilli. We identify LINC01271 as the human ortholog of MaTAR25, and importantly, increased expression of LINC01271 is associated with poor patient prognosis and metastasis. Our findings demonstrate that LINC01271 represents a potential therapeutic target to alter breast cancer progression.

Date: 2020
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DOI: 10.1038/s41467-020-20207-y

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