The study revealed that long non‑coding RNA LINC00673 was significantly upregulated in thyroid cancer tissues compared with paired adjacent non‑tumor tissues using RT-qPCR and that high expression of LINC00673 is was associated with larger tumor size and lymph node metastasis in the validated cohort.
We report that loss of LINC00673 is sufficient to trigger cellular senescence, a tumor suppressive mechanism associated with permanent cell cycle arrest, both in lung cancer and normal cells in a p53-dependent manner.
In our previous work, we reported a positive correlation of increased expression of linc00673 in NSCLC tissues with tumor size, lymph node metastasis, TNM stage, and increased proliferation of NSCLC cells, both, in vitro and in vivo.
In addition, the low expression of linc00312 was associated with the Tumor‑Node‑Metastasis stage of NSCLC (P<0.05), whereas the high expression of linc00673 was related with the histological types of NSCLC (P<0.05).
Here, by using genome-wide association analysis and functional characterization, we identify a long intergenic noncoding RNA (lincRNA), LINC00673, as a potential tumor suppressor whose germline variation is associated with pancreatic cancer risk.
Analysis of RNAseq data revealed linc00673 could modulate the transcription of a large amount of genes including oncogene and tumor suppressor gene, so we investigated the role and regulatory mechanism of linc00673 in NSCLC proliferation.