Lung adenocarcinoma (LUAD) is a predominant type of lung cancer in never-smoker patients. In this study, we identified a long noncoding RNA (lncRNA) LINC00857 that might regulate radio-sensitivity of LUAD cells. Expression of LINC00857 and baculoviral IAP repeat containing 5 (BIRC5) was determined to be upregulated in LUAD cells and tissues using qRT-PCR and western blot analysis. The correlation between LINC00857 and nuclear factor kappa B subunit 1 (NF-kB1) was verified using RNA immunoprecipitation and chromatin immunoprecipitation assays, while the binding relationship between NF-kB1 and BIRC5 was determined by dualluciferase reporter assay. It was suggested that LINC00857 could recruit NF-kB1 in BIRC5 promoter region. BIRC5 promoter activity was repressed in response to small interfering-LINC00857 (si-LINC00857) in LUAD cells. Silencing LINC00857 or BIRC5 reduced proliferation and colony formation but enhanced apoptosis and radio-sensitivity of LUAD cells. The experiment in vivo verified the function of silencing LINC00857 on enhancing radio-sensitivity of LUAD cells. Our results reveal a functional regulatory LINC00857-NF-kB1-BIRC5 triplet in LUAD cells, suggesting LINC00857 as a potential target for LUAD treatment.
BackgroundTo explore the diagnostic method in assessing the malignancy of pulmonary adenocarcinoma characterized by ground glass opacities (GGO) on computed tomography (CT).MethodsPreoperative CT data for preinvasive and invasive lung adenocarcinomas were analyzed retrospectively. GGO lesions that were detected on lung windows but absent using the mediastinal window were subject to adjustment of the window width, which was reduced with the fixed interval of 100 HU until the lesions were no longer evident, with a fixed mediastinal window level of 40 HU. The shape, smoking habits, size of the lesion on the lung window, and window width at which lesions disappeared were compared and receiver operating characteristic curves were used to determine the optimal cut‐off of the lesion size and window width to differentiate between these invasive and preinvasive lesions.ResultsOf the 209 lung adenocarcinomas, 102 were preinvasive (25 atypical adenomatous hyperplasia and 77 adenocarcinoma in situ), while 107 were invasive (78 minimally invasive adenocarcinoma and 29 invasive adenocarcinoma). The shape, lesion size, and window width at which lesions were no longer evident differed significantly between the two groups (P < 0.05). The size of 8.9 mm and a window width of 1250 HU were the optimal cut‐off to differentiate between preinvasive and invasive lesions.ConclusionThe shape, size of the lesion, and window width on high‐resolution CT may be useful in assessing the invasiveness of lung adenocarcinoma that manifests as GGO. Irregular lesions that disappear at window width <1250 HU, with a diameter of > 8.9 mm are more likely to be invasive.
Lung adenocarcinoma (LUAD), as the most common subtype of non‐small cell lung cancer, is responsible for more than 500 000 deaths worldwide annually. In this study, we identify a novel microRNA‐26b‐5p (miR‐26b‐5p) and elucidated its function on LUAD. The survival rate of parent LUAD cells and radiation‐resistant LUAD cells were determined using clonogenic survival assay. We overexpressed or inhibited miR‐26b‐5p in LUAD, and the correlation between activating transcription factor 2 (ATF2) and miR‐26b‐5p was determined using integrated bioinformatics analysis and dual‐luciferase reporter gene assay. Exosomes derived from A549 cell lines were then detected using Western blot assay, followed by co‐transfection with radiation‐resistant A549R cells. LUAD tissues and serum were collected, followed by miR‐26b‐5p relative expression quantification using RT‐qPCR. miR‐26b‐5p was identified as the most differentially expressed miRNA and was down‐regulated in LUAD. Radiation‐resistant cells were more resistant to X‐radiation compared with parent cells. miR‐26b‐5p overexpression and X‐irradiation led to enhanced radiosensitivity of LUAD cells. ATF2 was negatively targeted by miR‐26b‐5p. Exosomal miR‐26b‐5p derived from A549 cells could be transported to irradiation‐resistant LUAD cells and inhibit ATF2 expression to promote DNA damage, apoptosis and radiosensitivity of LUAD cells, which was verified using serum‐based miR‐26b‐5p. Our results show a regulatory network of miR‐26b‐5p on radiosensitivity of LUAD cells, which may serve as a non‐invasive biomarker for LUAD.
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