The neural correlation of emotion recognition ability and depressive symptoms-evidence from the HCP database.

Introduction: Negative bias of emotional face is the core feature of depression, but its underlying neurobiological mechanism is still unclear. The neuroimaging findings of negative emotional recognition and depressive symptoms are inconsistent. Methods: The neural association between depressive symptoms and negative emotional bias were analyzed by measuring the associations between resting state functional connectivity (FC), brain structures, negative emotional bias, and depressive problems. Then, we performed a mediation analysis to assess the potential overlapping neuroimaging mechanisms. Results: We found a negative correlation between depressive symptoms and emotional recognition. Secondly, the structure and function of the inferior and lateral orbitofrontal gyrus are related to depressive symptoms and emotional recognition. Thirdly, the thickness of the inferior orbitofrontal cortex and the FC between the inferior orbitofrontal gyrus and fusiform gyrus, precuneate and cingulate gyrus mediated and even predicted the interaction between emotion recognition and depressive symptoms. Finally, in response to a negative stimulus, the activation of the frontal pole and precuneus lobe associated with the inferior orbitofrontal gyrus was higher in participants with depressive symptoms. Conclusion: The core brain regions centered on the inferior orbitofrontal cortex such as middle temporal gyrus, precuneus lobe, frontal pole, insula and cingulate gyrus are the potential neuroimaging basis for the interaction between depressive symptoms and emotional recognition.

C1q-like 1 is frequently up-regulated in lung adenocarcinoma and contributes to the proliferation and invasion of tumor cells.

This study aims to investigate the effects of C1q-like 1 (C1QL1) on the growth and migration of lung adenocarcinoma (LUAD) cells and the underlying mechanism. The expression of C1QL1 in LUAD tissues and its prognostic value were analyzed using the data from The Cancer Genome Atlas (TCGA) database. To investigate the function of C1QL1, loss-of-function and gain-of-function assays were conducted in Calu-3 cells and LTEP-a-2 cells, respectively. Cell growth was evaluated by CCK-8 and colony formation assays. Transwell assays were performed to assess cell invasive and migratory abilities. qRT-PCR and Western blotting were performed to detect RNA and protein expression, respectively. Firstly, we found that C1QL1 was highly expressed and predicted poor outcomes in LUAD patients from TCGA database. Moreover, the mRNA and protein expression levels of C1QL1 were higher in LUAD cells than that in normal lung cells. Results of functional experiments illustrated that depletion of C1QL1 restrained the growth, invasion and migration of Calu-3 cells, meanwhile over-expression of C1QL1 presented the opposite results in LTEP-a-2 cells. Furthermore, we discovered that down-regulation of C1QL1 elevated the protein level of E-cadherin and reduced the protein levels of N-cadherin, Vimentin and Snail in Calu-3 cells, whereas over-expression of C1QL1 led to the opposite outcomes in LTEP-a-2 cells. Our data indicated that C1QL1 functioned as a crucial driver in LUAD cell growth and motility, which might be achieved by modulating epithelial-mesenchymal transition (EMT). These consequences are of important relevance for the design of therapeutic strategies for LUAD.

Antitumor activity of fucoidan in anaplastic thyroid cancer via apoptosis and anti-angiogenesis.

The present study demonstrated the effect of fucoidan, isolated from Fucus vesiculosus, on cell growth and apoptosis in anaplastic thyroid cancer cells. The cell viability was analyzed using a Cell Counting Kit­8 cell proliferation kit. Diamidino-2-phenylindole and terminal deoxynucleotidyl transferase-mediated dUTP nick­end labeling assays were used to examine the apoptotic effect of fucoidan, which revealed the presence of apoptotic bodies and DNA fragmentation. Fucoidan inhibited the growth of FTC133 and TPC1 ATC cells in a dose­dependent manner. It also induced the apoptosis of FTC133 cells by promoting the expression levels of cleaved poly ADP­ribose polymerase and caspase­3. Significant decreases in the levels expression of hypoxia-inducible factor 1α and vascular endothelial growth factor were observed in the FTC133 cells following treatment of the cells with fucoidan. In addition, inhibition in tube formation and the migration of FTC133 cells were observed in the cells treated with fucoidan, compared with the cells in the control group. Therefore, fucoidan inhibited cell growth, induced apoptosis and suppressed angiogenesis in the thyroid cancer cells.