Results indicate the expression of HOTAIR enhanced the aggressive behavior of non-small cell lung cancer (NSCLC) cells.

The levels of plasma lncRNAs, H19, HOX antisense intergenic RNA (HOTAIR), and metastasis associated lung adenocarcinoma transcript-1 (MALAT1), were analyzed in patients with gastric cancer (GC) and healthy controls.

The long non-coding RNA HOTAIR indicates a poor prognosis and promotes metastasis in non-small cell lung cancer.

upregulation of HOTAIR contributes to the cisplatin resistance of lung adenocarcinoma cells, at least in part, through the regulation of p21 expression.

HOTAIR is overexpressed in metastatic lung cancer tissue, which is prospectively associated with the ability of HOTAIR to promote lung cancer cell motility and invasion

The ratio of FoxA1 to FoxA2 in lung adenocarcinoma is regulated by LncRNA HOTAIR and chromatin remodeling factor LSH

CAV-1 coordinate the lung cancer through HOTAIR.

our study indicated that downregulation of HOTAIR suppressed tumorigenesis and metastasis of non-small cell lung cancer via upregulating the expression of miR-613.

HOTAIR was overexpressed in Non-Small Cell lung cancer cell lines. Silencing of HOTAIR decreased drug resistance of Non-Small Cell lung cancer cells to Crizotinib through inhibition of autophagy via suppressing phosphorylation of ULK1.

The two HOTAIR polymorphisms (rs12826786/rs1899663) has any significant association with the increased risk of lung cancer.The research indicated that carriers of Trs12826786/Crs1899663 had an increased risk of lung cancer susceptibility.

study showed that HOTAIR is an indicator of cell cycle dysregulation and could promote NSCLC cell line proliferation, metastasis and invasion through restraining the cell cycle from G1 to S phase, and then affect epithelial-mesenchymal transition and the beta-catenin pathway in lung cancer

persuasive evidence that SNP rs920778 is closely correlated with susceptibility to primary lung cancer

HOTAIR was up-regulated and miR-217 was down-regulated in non-small cell lung cancer (NSCLC) cell lines. Silencing of HOTAIR significantly repressed cell proliferation and inhibited cell migration and invasion in H1299 and A549 cells by facilitating miR-217 expression. Bioinformatics analysis and Luciferase reporter assay confirmed that DACH1 was a target of miR-217.

Effects of miR-221 on the apoptosis of non-small cell lung cancer cells by lncRNA HOTAIR.

Roles of HOTAIR in lung cancer susceptibility and prognosis.