Hsa_circ_0088036 promotes nonsmall cell lung cancer progression by regulating miR-1343-3p/Bcl-3 axis through TGFß/Smad3/EMT signaling.

Nonsmall cell lung cancer (NSCLC) is the leading cause of cancer-related mortality worldwide. Circular RNAs (circRNAs) have been the focus of numerous studies, and some circRNAs have been linked to the development of multiple malignant tumors, including NSCLC. Nevertheless, the functional role and mechanisms of circRNAs in NSCLC remain largely unknown. The primary objective of this study was to screen the associated circRNA in NSCLC and investigate its mechanism. CircRNA microarray was used to identify circRNAs that were abnormally expressed in NSCLC tissue samples. Expression of hsa_circRNA_0088036 was validated in NSCLC tissues and cell lines after the correlation between hsa_circRNA_0088036 and prognosis was determined. We then used a series of function gain-and-loss assays to determine the role of hsa_circ_0088036 in NSCLC progression. RNA-binding protein immunoprecipitation (RIP), RNA pull-down, and RNA interference assays were used to assess the interaction between hsa_circ_0088036 and miR-1343-3p/Bcl-3 axis. Moreover, mechanistic assays were applied to investigate the involved signaling pathway regulated by the hsa_circ_0088036/miR-1343-3p/Bcl-3 axis. Microarray analysis and reverse transcription polymerase chain reaction confirmed the presence of a circRNA termed hsa_circ 0088036 that was upregulated in NSCLC tissue samples and cell lines and indicated a positive association with patient prognosis. Functionally, hsa_circ_0088036 silencing inhibited proliferative, invasive, and migrative potential of NSCLC cells as well as epithelial-mesenchymal transition (EMT)-related proteins by sponging miR-1343-3p to inhibit Bcl-3. Furthermore, mechanistic experiments demonstrated that hsa_circ_0088036 promoted NSCLC progression by activating the TGFß/Smad3/EMT signaling pathway via miR-1343-3p/Bcl-3 axis. In conclusion, hsa_circ_0088036 functions as an oncogene by targeting the miR-1343-3p/Bcl-3 axis via TGFß/Smad3/EMT signaling pathway.

Long noncoding RNA DNAH17-AS1 promotes tumorigenesis and metastasis of non-small cell lung cancer via regulating miR-877-5p/CCNA2 pathway.

A growing number of studies have revealed that long noncoding RNAs (lncRNAs) can function as important oncogenes or tumor suppressors. This study aimed to investigate the regulatory role of lncRNA DNAH17 antisense RNA 1 (DNAH17-AS1) on non-small cell lung cancer (NSCLC) and the underlying molecular mechanisms. We observed that the expression of DNAH17-AS1 and CCNA2 mRNA was distinctly upregulated in NSCLC specimens and cell lines, while miR-877-5p expression was significantly decreased. DNAH17-AS1 could be used to distinguish NSCLC specimens from adjacent non-tumor tissues. Clinical assays revealed that high DNAH17-AS1 was associated with TNM stage, distant metastasis and shorter overall survival and disease-free survival. Functional assays indicated that knockdown of DNAH17-AS1 suppressed the proliferation, migration and invasion of H1299 and 95D cells, and promoted apoptosis. Mechanically, DNAH17-AS1 served as competing endogenous RNA (ceRNA) for miR-877-5p to positively recover CCNA2. Overall, we identified a novel NSCLC-related lncRNA, DNAH17-AS1 which may exert an oncogenic function via serving as a sponge for miR-877-5p to upregulate CCNA2. Our study presents novel insights into NSCLC progression and provided a prospective therapeutic target for NSCLC.

miR-762 activation confers acquired resistance to gefitinib in non-small cell lung cancer.

BACKGROUND: Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) (e.g. gefitinib) currently remain the first-line treatment for patients with advanced non-small-cell lung cancer (NSCLC) with activating EGFR mutation. However, acquired resistance to gefitinib, which occurs frequently through unidentified mechanisms, significantly attenuate therapeutic effectiveness. Previous miRNA microarray analysis reveals that expression levels of a conserved oncomiR miR-762 are significantly upregulated in gefitinib-resistant NSCLC cells. We therefore aim to elucidate the role and underlying mechanisms of miR-762 during the pathogenesis of gefitinib resistance. METHODS: miR-762 expression in gefitinib-resistant NSCLC tissues and cells was evaluated using RT-qPCR. The potential regulation of miR-762 expression by IL-6 was studied using pharmacological and biochemical approaches. Effects of miR-762 manipulation on sensitivity to gefitinib was assessed using MTT, apoptotic ELISA and xenograft model. Finally, the posttranscriptional regulation of active BCR related protein (ABR) by miR-762 was determined using luciferase assay and site-directed mutagenesis. RESULTS: miR-762 expression was upregulated in gefitinib-resistant NSCLC tissues and cells, and this upregulation predicted a poor post-chemotherapy prognosis in NSCLC patients. miR-762 upregulation, induced by IL-6 signaling, significantly enhanced cell survival and rendered NSCLC cells unresponsiveness to gefitinib-elicited cell death. We finally provided the evidence that the oncogenic effect of miR-762 was mediated mainly through posttranscriptional repression of ABR in gefitinib-resistant NSCLC cells. CONCLUSIONS: Our findings provide a rationale for future efforts testing miR-762 inhibition and ABR restoration co-treatment in patients with recurrent EGFR mutant NSCLC to therapeutically combat the heterogeneity of EGFR-TKIs resistance mechanisms.

Detection of organophosphorous pesticides in soil samples with multiwalled carbon nanotubes coating SPME fiber.

A headspace solid phase microextraction (HS-SPME) technique using stainless steel fiber coated with 20 µm multi-walled carbon nanotubes (MWCNTs) and gas chromatography with thermionic specific detector (GC-TSD) was developed to determine organophosphorous pesticides (OPPs) in soil. Parameters affecting the extraction efficiency such as extraction time and temperature, ionic strength, the volume of water added to the soil, sample solution volume to headspace volume ratio, desorption time, and desorption temperature were investigated and optimized. Compared to commercial polydimethylsiloxane (PDMS, 7 µm) fiber, the PDMS fiber was better to be corrected as phorate, whereas the MWCNTs fiber gave slightly better results for methyl parathion, chlorpyrifos and parathion. The optimized SPME method was applied to analyze OPPs in spiked soil samples. The limits of detection (LODs, S/N = 3) for the four pesticides were <0.216 ng g(-1), and their calibration curves were all linear (r (2) ≥ 0.9908) in the range from 1 to 200 ng g(-1). The precision (RSD, n = 6) for peak areas was 6.5 %-8.8 %. The recovery of the OPPs spiked real soil samples at 50 and 150 ng g(-1) ranged from 89.7 % to 102.9 % and 94.3 % to 118.1 %, respectively.

An optimized EEGNet decoder for decoding motor image of four class fingers flexion.

As a cutting-edge technology of connecting biological brain and external devices, brain-computer interface (BCI) exhibits promising applications on extensive fields such as medical and military. As for the disable individuals with four limbs losing the motor functions, it is a potential treatment way to drive mechanical equipments by the means of non-invasive BCI, which is badly depended on the accuracy of the decoded electroencephalogram (EEG) singles. In this study, an explanatory convolutional neural network namely EEGNet based on SimAM attention module was proposed to enhance the accuracy of decoding the EEG singles of index and thumb fingers for both left and right hand using sensory motor rhythm (SMR). An average classification accuracy of 72.91% the data of eight healthy subjects was obtained, which were captured from the one second before finger movement to two seconds after action. Furthermore, the character of event-related desynchronization (ERD) and event related synchronization (ERS) of index and thumb fingers was also studied in this study. These findings have significant importance for controlling external devices or other rehabilitation equipment using BCI in a fine way.

lncRNA FOXD2-AS1 confers cisplatin resistance of non-small-cell lung cancer via regulation of miR185-5p-SIX1 axis.

Background: Chemoresistance is a major obstacle for chemotherapy failure in non-small-cell lung cancer (NSCLC). lncRNAs are a class of pivotal regulators in various cancers, and the lncRNA FOXD2-AS1 is implicated in the progression of NSCLC. However, it is still unclear whether it regulates chemosensitivity. Methods: Expression levels of FOXD2-AS1, miR185-5p, and SIX1 mRNA were identified by reverse-transcription qPCR. CCK8 assay was performed to assess cell proliferation and chemosensitivity of cisplatin-resistant A549/DDP and H1299/DDP cells. Colony-forming assay was utilized to detect colony numbers. Cell migration and invasion ability were measured by transwell assay. The protein levels of LRP, Pgp, MRP1, and SIX1 were examined by Western blot assay. The correlation between FOXD2-AS1 and miR185-5p or miR185-5p and SIX1 were validated by bioinformatic, dual-luciferase, and RNA immunoprecipitation assays. Tumor xenografts were constructed to confirm the function and mechanism of FOXD2-AS1 in chemosensitivity of DDP-resistant NSCLC. Results: FOXD2-AS1 and SIX1 were upregulated and miR185-5p downregulated in DDP-resistant NSCLC. Absence of FOXD2-AS1 enhanced drug sensitivity of A549/DDP and H1299/DDP cells, reflected by the reduced colony formation, cell proliferation, migration, invasion, and drug resistance-associated protein expression. FOXD2-AS1 acted as a molecular sponge for miR185-5p and relieved the binding of miR185-5p and its target gene SIX1, leading to the derepression of SIX1 in A549/DDP and H1299/DDP cells. Rescue experiments validated the functional interaction among FOXD2-AS1, miR185-5p, and SIX1. Moreover, FOXD2-AS1 interference receded the growth of DDP-resistant NSCLC tumors in vivo. Conclusion: FOXD2-AS1/miR185-5p/SIX1 regulates the progression and chemosensitivity of DDP-resistant NSCLC, suggesting a potential therapeutic target for cisplatin-resistant NSCLC patients.

MicroRNA-29a functions as a potential tumor suppressor through directly targeting CDC42 in non-small cell lung cancer.

The expression and function of microRNA-29a (miR-29a) have been investigated in various types of cancer. In the present study, the expression, function and underlying molecular mechanism of miR-29a were investigated in non-small cell lung cancer (NSCLC). The expression level of miR-29a in NSCLC was determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, migration and invasion ability were determined using Cell Counting Kit-8, cell migration and invasion assays, respectively. Bioinformatics analysis and dual-luciferase reporter assays were performed to determine whether cell division cycle 42 (CDC42) is a direct target gene of miR-29a. To assess CDC42 mRNA and protein expression following transfection with miR-29a, RT-qPCR and western blotting were performed. Following knockdown of CDC42, functional assays were performed to investigate the roles of CDC42 in NSCLC. The results demonstrated that miR-29a was downregulated in NSCLC and the decreased expression level of miR-29a was significantly associated with advanced tumor-node-metastasis classification and metastasis. In addition, upregulation of miR-29a inhibited cell proliferation, migration and invasion in NSCLC, whereas downregulation of miR-29a had the opposite effects. Furthermore, CDC42 was identified as a direct target gene of miR-29a in vitro. miR-29a was demonstrated to function as a tumor suppressor in NSCLC by directly targeting CDC42 and may be investigated further as a target therapy for NSCLC.

[Determination of trace elements in pumpkin by FAAS].

Conditions for simultaneous determination of multi-trace elements in pumpkin by FAAS were studied. K, Ca, Mg, Na, Zn, Cu, Mn, Fe, Co and Cr in different parts and different growth periods of pumpkin were determined, the relative standard deviation of the method is between 0.1% and 2.6%, and the recovery is between 96.7% and 106.5%. Analytical results were satisfactory. The results showed that some elements essential to human such as K, Ca, Mg, Zn, Cr and Mn in pumpkin are abundant, implying that the nutritive value of pumpkin is high.

[Study on cadmium absorption in pumpkin by atomic absorption spectrophotometry].

A study was carried out on the characteristic of cadmium absorption in pumpkin by atomic absorption spectrophotometer. The results show that the cadmium absorption amount in pumpkin increased with the increase in cadmium concentration. Meanwhile the cadmium absorption amount in pumpkin increased with time. Eight hours after being cultured in the liquid, the cadmium absorption amount became saturated. The cadmium absorption rate reached the peak after 2 hours, then the absorption rate gradually reduced. The cadmium absorption amount in pumpkin is less in acid or alkali compared with neutral condition. And the absorption amount became minimum in pH 3, while maximum in pH 7.

[Spectrometric determination of trace elements in 'Jinguang' prunus mume var. bungo of different growth periods].

A study was carried out on the content of trace elements such as Ca, Fe, Zn, Mn and Cu of prunus mume var. bungo in different growth periods by WFX-110 atomic absorption spectrometry. The results indicated that the linear relationships of different elements within the limits of working curves are good and the range of the recovery is 98% -105%, hence showing that the results are satisfactory. The total content of these five trace elements increases as the fruit grows, but the concentration is related to the growth of fruit and fruit core, which provides us with valuable data. The contents of the trace elements essential to human body are relatively high, which shows that this fruit breed has a relatively high nutritive value.