MaTAR25 lncRNA regulates the Tensin1 gene to impact breast cancer progression.
Kung-Chi ChangSarah D DiermeierAllen T YuLily D BrineSuzanne RussoSonam BhatiaHabeeb AlsudaniKaren KostroffTawfiqul BhuiyaEdi BrogiDarryl J PappinC Frank BennettFrank RigoDavid L SpectorPublished in: Nature communications (2020)
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.
Keyphrases
- long non coding rna
- poor prognosis
- binding protein
- extracellular matrix
- genome wide
- cell proliferation
- genome wide identification
- endothelial cells
- copy number
- gene expression
- transcription factor
- papillary thyroid
- dna damage
- case report
- squamous cell carcinoma
- long noncoding rna
- genome wide analysis
- pluripotent stem cells
- childhood cancer
- amino acid
- young adults
- oxidative stress
- lymph node metastasis
- bioinformatics analysis