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Background and purpose: Lung adenocarcinoma is a subtype of non-small cell lung cancer. Although much progress has been made in the diagnosis and treatment of lung adenocarcinoma, the clinical prognosis and overall survival of advanced lung adenocarcinoma are still poor. In recent years, a number of studies have shown that miRNA can play a role in a variety of cancers, and play an important role in cell proliferation, metastasis, inflammation and other biological processes. This study aimed to explore the effect of miR-625-5p on the proliferation and invasion ability of lung adenocarcinoma cells and its molecular mechanism, so as to provide a new idea for the diagnosis and treatment of lung cancer. Methods: GEO database was used to search for differentially expressed miRNA in lung adenocarcinoma. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the expression of miR-625-5p in various lung adenocarcinoma cell lines. The effects of miR-625-5p on the proliferation and invasion of lung adenocarcinoma cells were investigated by EdU cell proliferation assay and transwell invasion assay. Key genes of miR-625-5p targeted binding were predicted by bioinformatics. Western blot experiment validated the expression of protein kinase cAMP-activated catalytic subunit alpha (PRKACA) in lung adenocarcinoma cells. The targeted relationship between miR-625-5p and PRKACA was analyzed by double luciferase assay and Western blot. Western blot assay was used to detect the expression of PRKACA after co-transfection of si-PRKACA and si-miR-625-5p in each group. The effect of miR-625-5p on the proliferation and invasion ability of lung adenocarcinoma cells by targeting PRKACA was observed by EdU cell proliferation assay and transwell invasion assay. Results: The expression of miR-625-5p was up-regulated in lung adenocarcinoma tissues (P

Objective To investigate the molecular mechanism by which miR-93-5p promotes the invasion and migration of triple negative breast cancer (TNBC) cells. Methods The miR-93-5p and faciogenital dysplasia-5 (FGD5) were screened out by Gene Expression Omnibus (GEO). Bioinformatics software was used to predict the candidate target genes for miR-93-5p. The relative expression of miR-93-5p in cells was detected by real-time quantitative PCR. Western blot was used to detect the relative expression of FGD5. Transwell TM assay was performed to detect the effects of miR-93-5p on the invasion and migration of MDA-MB-231 cells. The expression of FGD5 and survival curve in breast cancer and the correlation between miR-93-5p and FGD5 were analyzed by bioinformatics database. Dual luciferase reporter gene experiment was employed to verify the targeting relationship between miR-93-5p and FGD5. Results The miR-93-5p was highly expressed in TNBC tissues and cell lines. The higher the expression of miR-93-5p was, the worse the prognosis of breast cancer patients were. Knockdown of miR-93-5p inhibited the invasion and migration ability of MDA-MB-231 cells. Bioinformatics analysis showed that there were complementary sequences between miR-93-5p and FGD5. FGD5 presented low expression in breast cancer tissues and lower FGD5 expression in breast cancer patients corresponded to poorer prognosis. The expression levels between miR-93-5p and FGD5 were negatively correlated. Transfection of miR-93-5p inhibitor plasmid up-regulated the expression of FGD5 in TNBC cells. Dual luciferase reporter gene experiments confirmed that miR-93-5p could down-regulate the luciferase activity of wild-type FGD5. Conclusion The miR-93-5p can promote the invasion and migration of TNBC cells by targeting FGD5.

Background: Derlin 3 (DERL3) is downregulated in colorectal cancer (CRC) samples. Its level is closely linked to lymphatic metastasis or distant metastasis rate in CRC patients. However, its biological behavior in lung adenocarcinoma were rarely reported. The aim of this study is to investigate the ectopic expression of DERL3 in lung adenocarcinoma tissues and its effect on the invasion and metastasis of lung adenocarcinoma A549 cell line to reveal the possible mechanism of invasion and metastasis of lung adenocarcinoma., Methods: Lung adenocarcinoma microarray gene chip data included 3 cases of lymph node metastasis and 3 cases of lung adenocarcinoma tissue without lymph node metastasis. The GEDS and Kaplan-Meier plot queries the survival curve and expression level of DERL3. Western blot was used to detect the expression of DERL3 in lung adenocarcinoma cells. The efficiency of knockdown DERL3 gene was detected by Western blot assay. Transwell detected the number of cells passing through the basement membrane of the transwell. EDU assay detected cell proliferation ability. Western blot detected the expression of epithelial-mesenchymal transition related proteins E-cadherin and Vimentin., Results: The microarray gene chip results showed that compared with lung adenocarcinoma tissues without lymph node metastasis, 1,314 mRNAs in lung adenocarcinoma tissues with lymph node metastasis were up-regulated, 400 mRNAs were down (P<0.05). The expression of DERL3 increased in lung adenocarcinoma (P<0.05). The results of survival curve showed that the lung cancer patients with high expression of DERL3 with poor prognosis (P<0.05). Western blot results indicated that plasmid transfection was successful. Knockdown of DERL3 suppressed the ability of proliferation, invasion and migration in A549 cells (P<0.05). After knockdown of DERL3, the expression level of Vimentin was decreased, while E-cadherin expression increased (P<0.05)., Conclusions: Knockdown of DERL3 inhibited the proliferation, invasion and metastasis of A549 cells.

Objective: To investigate the effect of miR-204 on the invasion and metastasis of breast cancer by targeted regulation of HNRNPA2B1., Methods: The bioinformatics database was used to obtain data of the expressions of miR-204 in breast cancer patients and the survival rate of the patients. RT-qPCR was used to detect the expression of miR-204 in breast cancer cell lines. The expression vector GV369-miR-204 was used to overexpress miR-204 in MDA-MB-231 cells. Transwell assay was performed to detect the effect of miR-204 on the migration and invasion ability of the breast cancer cells. The key genes (hub genes) of miR-204 were determined by bioinformatics method. A dual luciferase assay was used to analyze the targeting relationship between miR-204 and HNRNPA2B1. The expression of HNRNPA2B1 in MDA-MB-231 cells after miR-204 overexpression was detected by Western blotting, and Transwell assay was used to examine the changes in the cell invasion ability., Results: The expression of miR-204 was decreased in both breast cancer tissues, and was significantly lower in breast cancer MDA-MB-231 cells than in MCF-10A cells ( P &lt; 0.05). The decreased expression of miR-204 was associated with poorer prognosis of breast cancer patients ( P &lt; 0.05). Upregulation of miR-204 in MDA-MB-231 cells significantly inhibited the invasion and migration of the cells ( P &lt; 0.05). Analysis of the data from the Starbase revealed that the expression of miR-204-5p was negatively correlated with the expression of HNRNPA2B1, and the expression of HNRNPA2B1 was increased in breast cancer patients ( P &lt; 0.05) in association with a poorer prognosis of the patients ( P &lt; 0.05). Dual luciferase assay demonstrated that miR-204 could bind to HNRNPA2B1 in a target-specific manner. Western blotting and Transwell assay showed that miR-204 significant inhibited the migration and invasion ability of breast cancer cells by targeting HNRNPA2B1 ( P &lt; 0.05)., Conclusions: miR-204 expression is decreased in breast cancer tissues and cells, and its overexpression can inhibit the invasion and metastasis of breast cancer cells by targeted regulation of HNRNPA2B1.

Objective: To evaluate the prognostic value of the difference between peripheral venous and arterial partial pressure of carbon dioxide in patients with septic shock following early resuscitation., Methods: This prospective study was conducted among the patients with septic shock treated in our department during the period from May, 2017 to May, 2018. Peripheral venous, peripheral arterial and central venous blood samples were collected simultaneously and analyzed immediately at bedside after 6-h bundle treatment. Arterial blood lactate concentration (Lac) and the arterial (PaCO 2 ), peripheral venous (PpvCO 2 ) and central venous partial pressure of carbon dioxide (PcvCO 2 ) were recorded. The differences between PpvCO 2 and PaCO 2 (Ppv-aCO 2 ) and between PcvCO 2 and PaCO 2 (Pcv-aCO 2 ) were calculated. Pearson correlation analysis was used to test the agreement between Pcv-aCO 2 and Ppv-aCO 2 . Multivariable logistic regression analysis was performed to analyze the possible risk factors for 28-day mortality, and the receiver-operating characteristic curve (ROC) was plotted to assess the prognostic values of these factors for 28-day mortality., Results: A total of 62 patients were enrolled in this study, among who 35 survived and 27 died during the 28-day period. Compared with the survivor group, the patients died within 28 days showed significantly higher Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score (24.2±6.0 vs 20.5±4.9, P =0.011), sequential organ failure assessment (SOFA) score (14.9±4.7 vs 12.2±4.5, P =0.027), PcvaCO 2 (5.5±1.6 vs 7.1±1.7, P &lt; 0.001), PpvaCO 2 (7.1±1.8 vs 10.0±2.7, P &lt; 0.001), and arterial lactate level (3.3±1.2 vs 4.2±1.3, P =0.003) after 6-h bundle treatment. Pearson correlation analysis showed that Ppv-aCO 2 was significantly correlated with Pcv-aCO 2 ( r =0.897, R 2 = 0.805, P &lt; 0.001). Multiple logistic regression analysis identified Ppv-aCO 2 (β=0.625, P =0.001, OR=1.869, 95% CI: 1.311-2.664) and lactate level (β=0.584, P =0.041, OR=1.794, 95%CI: 1.024-3.415) as the independent risk factors for 28-day mortality. The maximum area under the ROC (AUC) of Ppv-aCO 2 was 0.814 (95%CI: 0.696- 0.931, P &lt; 0.001), and at the best cut- off value of 9.05 mmHg, Ppv-aCO 2 had a sensitivity of 70.4% and a specificity of 88.6% for predicting 28-day mortality. The AUC of lactate level was 0.732 (95%CI: 0.607-0.858, P =0.002), and its sensitivity for predicting 28-day mortality was 70.4% and the specificity was 74.3% at the best cut-off value of 3.45 mmol/L; The AUC of Pcv-aCO 2 was 0.766 (95%CI: 0.642-0.891, P &lt; 0.001), and its sensitivity was 66.7% and the specificity was 80.0% at the best cut-off value of 7.05 mmHg., Conclusions: A high Ppv-aCO 2 after early resuscitation of septic shock is associated with poor outcomes. Ppv-aCO 2 is well correlated with Pcv-aCO 2 and can be used as an independent indicator for predicting 28-day mortality in patients with septic shock.

Objective: To investigate the value of the difference between peripheral arterial and venous blood gas analysis for the prognosis of patients with septic shock after resuscitation., Methods: Patients with septic shock aged 18 to 80 years admitted to intensive care unit (ICU) of Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine from May 2016 to December 2017 were enrolled. The peripheral arterial blood and peripheral venous blood gas analysis were measured simultaneously after the early 6 hours resuscitation, including pH, partial pressure of oxygen (PO 2 ), partial pressure of carbon dioxide (PCO 2 ), base excess (BE), bicarbonate (HCO 3 - ) and lactate (Lac) level, and the difference values between peripheral arterial and venous blood were calculated. According to the 28-day survival, the patients were divided into survival group and death group. Multiple Logistic regression analysis was used to analyze the risk factors of death, and the receiver operating characteristic curve (ROC) was used to analyze the prognostic value of blood gas analysis parameters for prognosis., Results: A total of 65 patients with septic shock resuscitation were enrolled in the study, 35 survived while 30 died during the 28-day period. (1) There was no significant difference in gender, age, and mean arterial pressure (MAP), central venous pressure (CVP), central venous oxygen saturation (ScvO 2 ) and norepinephrine (NE) dose between the two groups. (2) The arterial and venous Lac, the difference of Lac (ΔLac) and PCO 2 (ΔPCO 2 ) between arterial and venous blood in death group were significantly higher than those in survival group [arterial Lac (mmol/L): 7.40±3.10 vs. 4.82±2.91, venous Lac (mmol/L): 9.17±3.27 vs. 5.81±3.29, ΔLac (mmol/L): 1.77±0.54 vs. 0.99±0.60, ΔPCO 2 (mmHg, 1 mmHg = 0.133 kPa): 9.64±5.08 vs. 6.70±3.71, all P < 0.01], and there was no significant difference in the other arterial and venous blood gas analysis index and its corresponding differential difference between two groups. (3) Multiple Logistic regression analysis showed that ΔPCO 2 [β = 0.247, odd ratio (OR) = 1.280, 95% confidential interval (95%CI) = 1.057-1.550, P = 0.011], and ΔLac (β = 2.696, OR = 14.820, 95%CI = 2.916-75.324, P = 0.001) were the independent risk factors for the prognosis of septic shock. (4) It was shown by ROC curve analysis that arterial blood Lac, ΔLac and ΔPCO 2 had predictive value on prognosis of septic shock, the area under ROC curve (AUC) was 0.792, 0.857, 0.680, respectively (all P < 0.05). When the best cut-off value of arterial Lac was 4.00 mmol/L, the sensitivity was 100%, and the specificity was 62.86% for predictor of death in 28-day; when the best cut-off value of ΔLac was 1.25 mmol/L, the sensitivity was 93.33%, and the specificity was 68.57% for predictor of death in 28-day; when the best cut-off value of ΔPCO 2 was 4.35 mmHg, the sensitivity was 83.33%, and the specificity was 37.14% for predictor of death in 28-day., Conclusions: Compared to other parameters, the difference between peripheral arterial and venous blood gas analysis, ΔPCO 2 and ΔLac had the best correlation with the prognosis of septic shock. The ΔPCO 2 and ΔLac are the independent prognostic predictors for 28-day survival.