Cancer medicine (Malden, MA), 2020-06, Vol.9 (11), p.3829-3839
2020
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- Autor(en) / Beteiligte
- Titel
- LIMD1‐AS1 suppressed non‐small cell lung cancer progression through stabilizing LIMD1 mRNA via hnRNP U
- Ist Teil von
- Cancer medicine (Malden, MA), 2020-06, Vol.9 (11), p.3829-3839
- Ort / Verlag
- United States: John Wiley & Sons, Inc
- Erscheinungsjahr
- 2020
- Quelle
- Wiley
- Beschreibungen/Notizen
- Background Non‐small cell lung cancer (NSCLC) occupies the majority of lung cancer cases and is notorious for the awful prognosis. LIM domains‐containing 1 (LIMD1) is suggested as a tumor suppressor in lung cancer, but its mechanism in NSCLC remains elusive. Present study aimed to uncover the mechanism of LIMD1 in NSCLC. Methods qRT‐PCR was performed to analyze the level of LIMD1. The functions of LIMD1 in NSCLC cells were evaluated by CCK‐8, EdU, and caspase‐3 activity assays. RIP and pull‐down assays were applied to determine the interaction of LIMD1 with heterogeneous nuclear ribonucleoprotein U (hnRNP U) and LIMD1‐AS1. Results LIMD1 was downregulated in NSCLC samples and cells. Functionally, LIMD1 hindered proliferation and drove apoptosis in NSCLC cells. Moreover, long noncoding RNA (lncRNA) LIMD1 antisense RNA 1 (LIMD1‐AS1) was downregulated in NSCLC samples and cell lines. LIMD1‐AS1 knockdown abrogated NSCLC cell growth in vitro and in vivo. Mechanistically, LIMD1‐AS1 stabilized LIMD1 mRNA through interacting with hnRNP U. Rescue experiments suggested that LIMD1‐AS1 repressed NSCLC progression through LIMD1. Conclusions LIMD1‐AS1 suppressed NSCLC progression through stabilizing LIMD1 mRNA via hnRNP U, providing new thoughts for the improvement of molecular‐targeted therapy for NSCLC. LIMD1 was downregulated in NSCLC, inhibited proliferation, and facilitated apoptosis of NSCLC cells. LIMD1‐AS1 was downregulated in NSCLC and positively regulated LIMD1 expression. LIMD1‐AS1 stabilized LIMD1 mRNA through interacting with hnRNP U.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 2045-7634eISSN: 2045-7634DOI: 10.1002/cam4.2898Titel-ID: cdi_doaj_primary_oai_doaj_org_article_b5e418c53aa8401d8eb3a7b22474f7d2
- Format
- –
- Schlagworte
- Animals, Antibiotics, Antisense RNA, Apoptosis, Biomarkers, Tumor - genetics, Biomarkers, Tumor - metabolism, Cancer Biology, Carcinoma, Non-Small-Cell Lung - genetics, Carcinoma, Non-Small-Cell Lung - metabolism, Carcinoma, Non-Small-Cell Lung - pathology, Caspase, Cell culture, Cell cycle, Cell growth, Cell Proliferation, Cholecystokinin, Female, Flow cytometry, Gene expression, Gene Expression Regulation, Neoplastic, Heterogeneous-Nuclear Ribonucleoprotein U - genetics, Heterogeneous-Nuclear Ribonucleoprotein U - metabolism, hnRNP U, Humans, Intracellular Signaling Peptides and Proteins - genetics, Intracellular Signaling Peptides and Proteins - metabolism, Laboratory animals, LIM Domain Proteins - genetics, LIM Domain Proteins - metabolism, LIMD1, LIMD1‐AS1, Lung cancer, Lung Neoplasms - genetics, Lung Neoplasms - metabolism, Lung Neoplasms - pathology, Mice, Mice, Inbred BALB C, Mice, Nude, mRNA, Non-small cell lung carcinoma, NSCLC, Original Research, Prognosis, RNA Stability, RNA, Antisense - genetics, RNA, Long Noncoding - genetics, Small cell lung carcinoma, Tumor Cells, Cultured, Tumor suppressor genes, Xenograft Model Antitumor Assays