{'fraction_non_alphanumeric': 0.02773497688751926, 'fraction_numerical': 0.01926040061633282, 'mean_word_length': 5.070093457943925, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Long non‑coding RNA DANCR promotes HMGA2‑mediated invasion in lung adenocarcinoma cells.

Long non‑coding RNAs (lncRNAs) have been reported to be key regulators in various types of cancer, including lung adenocarcinoma (LAD). The roles of the lncRNA differentiation antagonizing non‑protein coding RNA (DANCR) and high mobility group AT‑hook 2 (HMGA2) in LAD remain unclear. In the present study, it was revealed that the lncRNA DANCR was upregulated in LAD tissue and cell lines, compared with para‑tumor tissue and a normal lung cell line. Additionally, elevated DANCR expression was associated with poor prognosis in the patients with LAD. Functionally, the study revealed that knockdown of DANCR inhibited invasion and HMGA2 expression in the LAD cell lines, SPCA1 and A549. Furthermore, HMGA2 was overexpressed in LAD tissue and in SPCA1 and A549 cells, compared with para‑tumor tissue and a normal lung cell line. Inhibition of HMGA2 suppressed the invasive ability of SPCA1 and A549 cells, and DANCR promoted the invasive ability via regulation of HMGA2 in SPCA1 and A549 cells. The findings of the present study revealed that DANCR promoted the invasion of LAD cells by positively regulating HMGA2. Thus, a DANCR/HMGA2 axis may be a novel potential target in the molecular treatment of LAD.