ABSTRACT
The wavelength-dependent dynamics of the O(1D2) channel, formed by photoexcitation of CO2 to the 1Δu state at 143.53-153.03 nm, is investigated by using the time-sliced velocity-mapped ion imaging method. The measured ionic peaks of the O(1D2) images are analyzed to determine the total kinetic energy release (TKER) spectra and image anisotropy parameters. The structures observed in the TKER spectra can be directly assigned to the ro-vibrational state distributions of the counter CO photofragments. Compared to those observed at 157 and 155 nm, the highly rotationally excited CO photofragments still obviously appear in v = 0 and 1, but the fraction of rotational excitations is significantly reduced. Conversely, the CO photofragments exhibit substantially higher vibrational excitations, implying that the nearly linear 21A' state also contributes to dissociation in addition to the bend configuration. The image anisotropy parameters display an extremely slow decreasing trend with an increase of the CO ro-vibrational state besides those for the highest ro-vibrationally excited CO photofragments. Nevertheless, the nonaxial recoil effect, suggested in previous photodissociation studies of CO2 and other triatomic molecular systems, is still appropriate to explain the observations of internal energy dependences of image anisotropy parameters.
ABSTRACT
[This corrects the article DOI: 10.3389/fcell.2021.765772.].
ABSTRACT
Mastering nuclear fusion, which is an abundant, safe, and environmentally competitive energy, is a great challenge for humanity. Tokamak represents one of the most promising paths toward controlled fusion. Obtaining a high-performance, steady-state, and long-pulse plasma regime remains a critical issue. Recently, a big breakthrough in steady-state operation was made on the Experimental Advanced Superconducting Tokamak (EAST). A steady-state plasma with a world-record pulse length of 1056 s was obtained, where the density and the divertor peak heat flux were well controlled, with no core impurity accumulation, and a new high-confinement and self-organizing regime (Super I-mode = I-mode + e-ITB) was discovered and demonstrated. These achievements contribute to the integration of fusion plasma technology and physics, which is essential to operate next-step devices.
ABSTRACT
[This corrects the article DOI: 10.3389/fcell.2021.765772.].
ABSTRACT
Growing evidence has demonstrated that UBE2C plays a critical role in cancer progression, but there is no study focusing on the prognosis, upstream regulation mechanism, and immunological roles of UBE2C across diverse tumor types. In this study, we found that UBE2C was elevated in this human pan-cancer analysis, and high expression of UBE2C was correlated with poor prognosis. In addition, UBE2C expression was markedly associated with tumor mutation burden (TMB), microsatellite instability (MSI), immune cell infiltration, and diverse drug sensitivities. Finally, we showed that the METTL3/SNHG1/miRNA-140-3p axis could potentially regulate UBE2C expression. N(6)-Methyladenosine (m6A) modifications improved the stability of methylated SNHG1 transcripts by decreasing the rate of RNA degradation, which lead to upregulation of SNHG1 in non-small cell lung cancer (NSCLC). In vitro functional experiments showed that SNHG1, as a competing endogenous RNA, sponges miR-140-3p to increase UBE2C expression in NSCLC cell lines. Our study elucidates the clinical importance and regulatory mechanism of the METTL3/SNHG1/miRNA-140-3p/UBE2C axis in NSCLC and provides a prognostic indicator, as well as a promising therapeutic target for patients with NSCLC.
ABSTRACT
Lung cancer is the most common tumor with severe morbidity and high mortality. Increasing evidence has demonstrated that SNX20 plays crucial roles in the progression of human cancer. However, the functions and mechanism of SNX20 in LUAD are still barely known. Here, we employ the TCGA, GEO and CCLE databases to examine the expression of SNX20 in human varies cancer, the results shown that SNX20 is down-regulated in lung Adenocarcinoma, SNX20 level was significantly positive correlated with poor prognosis and lung cancer immune cell infiltration. We found that over-expression of SNX20 significantly restrain NSCLC cell proliferation and migration. Subsequently, we discover a network regulating SNX20 in LUAD, further study found that the decreased of the SNX20 likely caused by DNA hypermethylation. Furthermore, we identified that SNX20AR/miRNA-301a-3p mediated decreased of SNX20 correlated with lung cancer progression and cancer immune infiltration in LUAD. Our findings suggested that ncRNAs play a crucial role in the regulatory network of SNX20. Collectively, our findings demonstrate the suppressor roles of the SNX20AR/miRNA-301a-3p/SNX20 axis in Lung Adenocarcinoma, represent that SNX20 have the potential of as an effective therapeutic target in future.
ABSTRACT
In the tumor progression, transforming growth factor ß1 (TGFß1) plays a critical role in tumorigenesis as well as metastasis. It is known that high plasma level of TGFß1 in patients with advanced non-small cell lung cancer (NSCLC) is correlated with poor prognostics. In addition, the generation of cancer stem-like cells is associated with metastasis, drug resistance, and tumor recurrence, which also lead to poor outcomes in NSCLC patients. However, it remains unclear how TGFß1 promotes NSCLC cells to acquire stem-like properties and accelerate tumor metastasis. In our study, we found that short term TGFß1 treatment resulted in a significant epithelial-mesenchymal transition (EMT) morphological change in TGFß1-sensitive NSCLC cells but not in insensitive cells. Western blotting confirmed increased Vimentin and reduced E-Cadherin protein expression after TGFß1 treatment in A549, NCI-H1993, and NCI-H358 cells. TGFß1 incubation dramatically decreased in vitro cell proliferation and increased cell invasion in TGFß1-sensitive NSCLC cells but not in NCI-H1975, NCI-H1650, and HCC827 cells. Moreover, TGFß1 was able to enhance the mRNA expression of Oct4, Nanog and Sox2 and drastically increased anchorage-independent colony formation in TGFß1-sensitive NSCLC cells, suggesting the acquisition of cancer stem-like properties. Interestingly, we found that vascular endothelial growth factor receptor 3 (VEGFR3) mRNA expression was significantly elevated in TGFß1-sensitive NSCLC cells compared to insensitive cells. And TGFß1 was capable of inducing VEGF-C gene expression. Pharmacological blocking TGFß type I receptor kinase (ALK5) significantly inhibited TGFß1-induced VEGF-C expression. Silencing of ALK5 by siRNA also dramatically reduced TGFß1-induced VEGF-C expression in TGFß1-sensitive NSCLC cells. Therefore, TGFß1 contributes for NSCLC metastasis through promoting EMT, generation of high invasive cancer cells with stem-like properties, and increasing VEGF-C expression. Blocking TGFß pathway is a potential therapeutic target in human non-small cell lung cancer.
