Relationship between early lung adenocarcinoma and multiple driving genes based on artificial intelligence medical images of pulmonary nodules.

Lung adenocarcinoma is one of the most common cancers in the world, and accurate diagnosis of lung nodules is an important factor in reducing its mortality. In the diagnosis of pulmonary nodules, artificial intelligence (AI) assisted diagnosis technology has been rapidly developed, so testing its effectiveness is conducive to promoting its important role in clinical practice. This paper introduces the background of early lung adenocarcinoma and lung nodule AI medical imaging, and then makes academic research on early lung adenocarcinoma and AI medical imaging, and finally summarizes the biological information. In the experimental part, the relationship analysis of 4 driver genes in group X and group Y showed that there were more abnormal invasive lung adenocarcinoma genes, and the maximum uptake value and uptake function of metabolic value were also higher. However, there was no significant correlation between mutations in the four driver genes and metabolic values, and the average accuracy of AI-based medical images was 3.88% higher than that of traditional images.

[Retracted] MicroRNA­629 inhibition suppresses the viability and invasion of non­small cell lung cancer cells by directly targeting RUNX3.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the data shown for the cell invasion assays in Figs. 4D and 5D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 19: 3933­3940, 2019; DOI: 10.3892/mmr.2019.9990].

circBIRC6 contributes to the development of non-small cell lung cancer via regulating microRNA-217/amyloid beta precursor protein binding protein 2 axis.

BACKGROUND: Circular RNAs (circRNAs) are considered to be important regulators in cancer biology. In this study, we focused on the effect of circRNA baculoviral inhibitor of apoptosis protein (IAP) repeat containing 6 (circBIRC6) on non-small cell lung cancer (NSCLC) progression. METHODS: The NSCLC and adjacent non-tumor tissues were collected at Shanghai Ninth People's Hospital. Quantitative real-time polymerase chain reaction was conducted for assessing the levels of circBIRC6, amyloid beta precursor protein binding protein 2 (APPBP2) messenger RNA (mRNA), baculoviral IAP repeat containing 6 mRNA (BIRC6), and microRNA-217 (miR-217). Western blot assay was adopted for measuring the protein levels of APPBP2, E-cadherin, N-cadherin, and vimentin. Colony formation assay, transwell assay, and flow cytometry analysis were utilized for evaluating cell colony formation, metastasis, and apoptosis. Dualluciferase reporter assay and RNA immunoprecipitation assay were carried out to determine the interaction between miR-217 and circBIRC6 and APPBP2 in NSCLC tissues. The murine xenograft model assay was used to investigate the function of circBIRC6 in tumor formation in vivo. Differences were analyzed via Student's t test or one-way analysis of variance. Pearson's correlation coefficient analysis was used to analyze linear correlation. RESULTS: CircBIRC6 was overexpressed in NSCLC tissues and cells. Knockdown of circBIRC6 repressed the colony formation and metastasis and facilitated apoptosis of NSCLC cells in vitro and restrained tumorigenesis in vivo. Mechanically, circBIRC6 functioned as miR-217 sponge to promote APPBP2 expression in NSCLC cells. MiR-217 inhibition rescued circBIRC6 knockdown-mediated effects on NSCLC cell colony formation, metastasis, and apoptosis. Overexpression of miR-217 inhibited the malignant phenotypes of NSCLC cells, while the effects were abrogated by elevating APPBP2. CONCLUSIONS: CircBIRC6 aggravated NSCLC cell progression by elevating APPBP2 via sponging miR-217, which might provide a fresh perspective on NSCLC therapy.

MicroRNA­92a promotes non­small cell lung cancer cell growth by targeting tumor suppressor gene FBXW7.

MicroRNA (miRNA/miR)­92a has been identified as being significantly downregulated in non­small cell lung cancer (NSCLC) tissues using a miRNA array. However, its biological function and molecular mechanisms in NSCLC have not been fully elucidated. The aim of the present study was to determine the role of miR­92a in NSCLC and the mechanisms by which it affects NSCLC cells. The expression levels of miR­92a in NSCLC tissues and cell lines were analyzed using reverse transcription­quantitative PCR. Cell viability and cell apoptosis were determined using an MTT assay and flow cytometry, respectively. It was observed that miR­92a was significantly upregulated in NSCLC tissues and cell lines. Inhibition of miR­92a significantly suppressed viability of NSCLC cells, with concomitant downregulation of key proliferative genes, such as proliferating cell nuclear antigen and Ki­67. miR­92a downregulation induced apoptosis of NSCLC cells, as evidenced by flow cytometry and apoptosis­related protein detection. Luciferase assays confirmed that miR­92a could directly bind to the 3'­untranslated region of tumor suppressor F­box/WD repeat­containing protein 7 (FBXW7) and suppress its translation. Furthermore, small interfering RNA­mediated FBXW7 inhibition partially attenuated the tumor suppressive effect of an miR­92a inhibitor on NSCLC cells. Collectively, these findings demonstrated that miR­92a might function as an oncogene in NSCLC by regulating FBXW7. In conclusion, miR­92a could serve as a potential therapeutic target in NSCLC treatment.

MicroRNA­629 inhibition suppresses the viability and invasion of non­small cell lung cancer cells by directly targeting RUNX3.

Dysregulated microRNAs (miRNAs/miRs) directly modulate the biological functions of non­small cell lung cancer (NSCLC) cells and contribute to the initiation and progression of NSCLC; however, the specific roles and underlying mechanisms of the dysregulated miRNAs in NSCLC require further investigation. The present study reported that miRNA­629­5p (miR­629) was upregulated in NSCLC tissues and cell lines. High miR­629 expression levels were significantly associated with tumour size, clinical stage and lymph node metastasis in patients with NSCLC. Functional experiments indicated that miR­629 inhibition suppressed the viability and invasion NSCLC cells in vitro. Furthermore, bioinformatics prediction, luciferase reporter assay, reverse transcription­quantitative polymerase chain reaction and western blot analysis demonstrated that runt­related transcription factor 3 (RUNX3) was a direct target gene of miR­629 in NSCLC. Restoration of RUNX3 expression suppressed the effects of miR­629 inhibition in NSCLC cells. Rescue experiments revealed that RUNX3 knockdown partially abrogated the effects of miR­629 inhibition on NSCLC cells. In summary, miR­629 directly targeted RUNX3 to inhibit the progression of NSCLC, suggesting that this miRNA may be considered as a diagnostic and therapeutic target for patients with NSCLC.

Cisplatin and photodynamic therapy exert synergistic inhibitory effects on small-cell lung cancer cell viability and xenograft tumor growth.

Lung cancer is the leading cause of cancer death worldwide. Small-cell lung cancer (SCLC) is an aggressive type of lung cancer that shows an overall 5-year survival rate below 10%. Although chemotherapy using cisplatin has been proven effective in SCLC treatment, conventional dose of cisplatin causes adverse side effects. Photodynamic therapy, a form of non-ionizing radiation therapy, is increasingly used alone or in combination with other therapeutics in cancer treatment. Herein, we aimed to address whether low dose cisplatin combination with PDT can effectively induce SCLC cell death by using in vitro cultured human SCLC NCI-H446 cells and in vivo tumor xenograft model. We found that both cisplatin and PDT showed dose-dependent cytotoxic effects in NCI-H446 cells. Importantly, co-treatment with low dose cisplatin (1 µM) and PDT (1.25 J/cm2) synergistically inhibited cell viability and cell migration. We further showed that the combined therapy induced a higher level of intracellular ROS in cultured NCI-H446 cells. Moreover, the synergistic effect by cisplatin and PDT was recapitulated in tumor xenograft as revealed by a more robust increase in the staining of TUNEL (a marker of cell death) and decrease in tumor volume. Taken together, our findings suggest that low dose cisplatin combination with PDT can be an effective therapeutic modality in the treatment of SCLC patients.