Pleural thickness and the size of the biopsy needle were significantly correlated with the diagnostic yield.

The occurrence of distant tumor metastases is a major barrier in non-small cell lung cancer (NSCLC) therapy, and seriously affects clinical treatment and patient prognosis. Recently, long non-coding RNAs (lncRNAs) have been demonstrated to be crucial regulators of metastasis in lung cancer. The aim of this study was to reveal the underlying mechanisms of a novel lncRNA LNC CRYBG3 in regulating NSCLC metastasis. Experimental results showed that LNC CRYBG3 was upregulated in NSCLC cells compared with normal tissue cells, and its level was involved in these cells’ metastatic ability. Exogenously overexpressed LNC CRYBG3 increased the metastatic ability and the protein expression level of the metastasis-associated proteins Snail and Vimentin in low metastatic lung cancer HCC827 cell line. In addition, LNC CRYBG3 contributed to HCC827 cell metastasis in vivo. Mechanistically, LNC CRYBG3 could directly combine with eEF1A1 and promote it to move into the nucleus to enhance the transcription of MDM2. Overexpressed MDM2 combined with MDM2 binding protein (MTBP) to reduce the binding of MTBP with ACTN4 and consequently increased cell migration mediated by ACTN4. In conclusion, the LNC CRYBG3/eEF1A1/MDM2/MTBP axis is a novel signaling pathway regulating tumor metastasis and may be a potential therapeutic target for NSCLC treatment.

Long noncoding RNAs (lncRNAs) in eukaryotic transcripts have long been believed to regulate various aspects of cellular processes, including carcinogenesis. Herein, it is found that lncRNA AFAP1‐AS1 encodes a conserved 90‐amino acid peptide located on mitochondria, named lncRNA AFAP1‐AS1 translated mitochondrial‐localized peptide (ATMLP), and it is not the lncRNA but the peptide that promotes the malignancy of nonsmall cell lung cancer (NSCLC). As the tumor progresses, the serum level of ATMLP increases. NSCLC patients with high levels of ATMLP display poorer prognosis. Translation of ATMLP is controlled by m6A methylation at the 1313 adenine locus of AFAP1‐AS1. Mechanistically, ATMLP binds to the 4‐nitrophenylphosphatase domain and non‐neuronal SNAP25‐like protein homolog 1 (NIPSNAP1) and inhibits its transport from the inner to the outer mitochondrial membrane, which antagonizes the NIPSNAP1‐mediated regulation of cell autolysosome formation. The findings uncover a complex regulatory mechanism of NSCLC malignancy orchestrated by a peptide encoded by a lncRNA. A comprehensive judgment of the application prospects of ATMLP as an early diagnostic biomarker for NSCLC is also made.

Background: Hemoptysis is the most frequently reported complication of ultrasound-guided transthoracic needle lung biopsy (US-TTLB). However, factors influencing the occurrence of hemoptysis as a result of US-TTLB remain uncertain. Therefore, the aim of this study was to evaluate the incidence of hemoptysis as a complication of US-TTLB and to identify the related risk factors. Methods:We retrospectively analyzed all data of patients who underwent US-TTLB from February 2013 through December 2016. The incidence, severity, and treatment of hemoptysis in each case were carefully recorded. Study variables were classified into patient-related factors (age, sex, smoking history, pulse oxygen saturation, laboratory tests and emphysema), biopsy-related factors (use of contrast agent, number of punctures and operators), and lesion-related factors (lesion location, size, pathology, length of puncture path and the grade of air bronchial sign). Univariate and multivariate logistic regression analyses were performed to analyze the risk factors of hemoptysis. We investigated whether incidence of hemoptysis increased according to increased grade of air bronchial sign by Mantel-Haenszel test.Results: A total of 209 patients were evaluated. Hemoptysis occurred in 20 of the 209 patients (9.6%). In univariate analysis, the lesion pathology (P=0.037) and grade of air bronchial sign (P<0.001) were statistically significant factors between the hemoptysis group and the non-hemoptysis group. In multivariate analysis, the presence of multi-air bronchogram in sonographic image (odds ratio =8.946; 95% confidence interval: 2.873-27.863; P<0.001) was a statistically significant predictive risk factor for hemoptysis complicating US-TTLB. There was a significant tendency for incidence of hemoptysis with the grade of air bronchial sign (P<0.001). Conclusions:We found that the rate of hemoptysis complicating US-TTLB was 9.6% and the severity of hemoptysis was not serious. Target lesion without air bronchogram is a safety sign, minor bronchogram means relatively low-risk, while multiple bronchogram is a highly dangerous ultrasound sign of hemoptysis.

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with high recurrence and metastasis rates, and more than half of the patients diagnosed with NSCLC receive local radiotherapy. However, the intrinsic radio-resistance of cancer cells is a major barrier to effective radiotherapy for NSCLC. CRYBG3 is a long noncoding RNA (lncRNA) that was originally identified to be upregulated in NSCLC and enhanced metastasis of NSCLC cells by interacting with eEF1A1 to promote murine double minute 2 (MDM2) expression. The aims of this study were to reveal the contribution of CRYBG3 to the radioresistance of NSCLC and determine whether that is associated with MDM2-p53 pathway. Therefore, CRYBG3 was stably downregulated in A549 (wild-type p53) and H1299 (deficient p53) cells by infecting short hairpin RNA (shRNA) lentiviral particles. The results showed that downregulation of CRYBG3 increased DNA damage, enhanced apoptosis and pro-apoptotic protein expression in A549 or p53-overexpressed H1299 cells but not in H1299 or p53-silenced A549 cells after X-ray irradiation. However, the contribution of CRYBG3 to radioresistance was abolished by eEF1A1 or MDM2 knockdown in A549 cells. Thus, we concluded that downregulation of CRYBG3 enhanced radiosensitivity by reducing MDM2 expression then leading to decreased MDM2-mediated degradation of p53 in wild-type p53 expressing NSCLC cells. These findings suggested that CRYBG3 can be a potential target for therapeutic intervention of certain lung cancer subtypes.