Attention control training and transfer effects on cognitive tasks.

Attention control is the common element underlying different executive functions. The backward Masking Majority Function Task (MFT-M) requires intensive attention control, and represents a diverse situation where attentional resources need to be allocated dynamically and flexibly to reduce uncertainty. Aiming to train attention control using MFT-M and examine the training transfer effects in various executive functions, we recruited healthy young adults (n = 84) and then equally randomized them into two groups trained with either MFT-M or a sham program for seven consecutive days. Cognitive evaluations were conducted before and after the training, and the electroencephalograph (EEG) signals were recorded for the revised Attention Network Test (ANT-R), N-back, and Task-switching (TS) tasks. Compared to the control group, the training group performed better on the congruent condition of Flanker and the double-congruency condition of Flanker and Location in the ANT-R task, and on the learning trials in the verbal memory test. The training group also showed a larger P2 amplitude decrease and P3 amplitude increase in the 2-back task and a larger P3 amplitude increase in the TS task's repeat condition than the control group, indicating improved neural efficiency in two tasks' attentional processes. Introversion moderated the transfer effects of training, as indicated by the significant group*introversion interactions on the post-training 1-back efficiency and TS switching cost. Our results suggested that attention control training with the MFT-M showed a broad transfer scope, and the transfer effect was influenced by the form of training task. Introversion facilitated the transfer to working memory and hindered the transfer to flexibility.

Cancer­associated fibroblast­derived LRRC15 promotes the migration and invasion of triple­negative breast cancer cells via Wnt/ß­catenin signalling pathway regulation.

Triple­negative breast cancer (TNBC) is a highly aggressive tumour subtype associated with poor prognosis. The function of leucine­rich repeat­containing protein 15 (LRRC15), a member of the leucine­rich repeat superfamily, in TNBC has not yet been elucidated. The aim of this study was to identify the combined role of LRRC15 and Wnt/ß­catenin signalling pathway in the development of TNBC. The expression of LRRC15 in TNBC tissues was analysed using data from The Cancer Genome Atlas. Cell migration and invasion assays were conducted to study the function of LRRC15 in TNBC. The expression of Wnt/ß­catenin signalling proteins was analysed via western blotting. The effect of LRRC15 on ß­catenin nuclear localisation was measured by performing western blotting and luciferase assays. It was found that high LRRC15 expression was associated with poor prognosis in patients with TNBC. High expression of LRRC15 in cancer­associated fibroblasts (CAFs) promoted cell migration and invasion in TNBC cells. In addition, TNBC cells with LRRC15 overexpression in CAFs showed an aberrant increase in ß­catenin activity concomitant with nuclear localisation of ß­catenin, which inhibited its degradation. These results showed that LRRC15 promoted tumour migration and invasion in TNBC cells by regulating the Wnt/ß­catenin signalling pathway.

Actin-Like Protein 8 Promotes the Progression of Triple-Negative Breast Cancer via Activating PI3K/AKT/mTOR Pathway.

OBJECTIVE: The purpose of this study was to investigate the function of actin-like protein 8 (ACTL8) on triple-negative breast cancer (TNBC) and its potential mechanisms. METHODS: In our study, ACTL8 expression and the prognostic values of ACTL8 were evaluated via the dataset from the Cancer Genome Atlas (TCGA). At the same time, the expression of ACTL8 in TNBC cells was measured by Western blot and qRT-PCR. Then, the effects of ACTL8 on the growth and metastasis of TNBC were investigated by using 5-ethynyl-20-deoxyuridine (EdU), colony formation, flow cytometry, wound healing and transwell assays. Mechanistically, Western blot was performed to confirm the interaction between ACTL8 and phosphatidylinositol 3'-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway in TNBC. RESULTS: ACTL8 expression was upregulated in TNBC and associated with the poor prognosis of TNBC. Silencing ACTL8 suppressed the proliferation, migration and invasion, also promoted the apoptosis in MDA-MB-231 and BT-549 cells. Moreover, we found that silencing ACTL8 could inhibit the activation of PI3K/AKT/mTOR signaling pathway in MDA-MB-231 and BT-549 cells. Meanwhile, the impact of silencing ACTL8 on the proliferation, apoptosis, migration and invasion was enhanced by PI3K/AKT/mTOR pathway inhibitor (Wortmannin) and reversed by PI3K/AKT/mTOR pathway activator (740Y-P). CONCLUSION: Our data demonstrated that ACTL8 may facilitate the proliferation, migration and invasion, while inhibiting apoptosis through activating PI3K/Akt/mTOR signaling pathway in TNBC.