Fosterbynum4770

1, CD27-AS1, EIF3J-DT, LINC01011, LINC01063, LINC02381, AC073896.3, and SNHG16) were identified to be significantly different, which made up an autophagy-related lncRNA signature. The signature divided patients with colon adenocarcinoma into the low-risk group and the high-risk group. A risk score based on the signature was a significantly independent factor for the patients with colon adenocarcinoma (HR = 1.088, 95%CI = 1.057 - 1.120; P less then 0.001). Additionally, the ten lncRNAs were significantly enriched in autophagy process, metabolism, and tumor classical pathways. In conclusion, the ten autophagy-related lncRNAs and their signature might be molecular biomarkers and therapeutic targets for the patients with colon adenocarcinoma.Several studies have demonstrated that brain and muscle Arnt-like protein-1 (Bmal1) acts as a core clock gene for maintaining normal cell function, including hepatocytes and cardiomyocytes. Loss of Bmal1 is associated with type 2 diabetes due to pancreatic β-cell failure. However, little information is available about its role and mechanism in pancreatic β-cell. To address this, we investigated the consequences of Bmal1 inhibition in an insulinoma cell line (INS-1) by using small interfering RNA (siRNA). We observed that knockout of Bmal1 impaired glucose-stimulated insulin secretion in β-cell. Meanwhile, the depletion of Bmal1 in β-cell caused an adverse change in mitochondrial membrane potential and mitochondrial architecture. Deletion of Bmal1 attenuated mRNA and protein expression of mitofusin 1 (Mfn1) and mitofusin 2 (Mfn2) and enhanced the expression of fission 1 (Fis1). In summary, the deletion of Bmal1 impaired β-cell function may be via the mitochondrial signaling pathway in INS-1 cells.

Phosphoinositides play a regulatory role in clathrin-mediated endocytosis. However, their involvement in clathrin-independent endocytosis termed rapid endocytosis (RE), which is the mode of vesicle recycling during neurotransmitter release by transient fusion (known as kiss-and-run), has not been investigated. Here, we used patch-clamp recording of whole-cell membrane capacitance in adrenal chromaffin cells (ACC) to monitor changes of RE kinetics in response to pharmacological alteration of phosphatidylinositol-4,5-biphosphate (PI(4,5)P

) level by phenylarsine oxide (PAO) or antibody against phosphatidylinositol 4-kinase (Ab

).

We found that PAO and Ab

significantly abrogated RE kinetics. Infusion of PI(4,5)P

through the patch pipette potentiated RE kinetics and reversed PAO- and Ab

-induced blockade of RE. Similarly, the application of the bifunctional thiol dithiothreitol (DTT) to PAO-treated cells completely prevented the inhibitory effect of PAO on RE. These findings indicate that PI(4,5)P

is implicated in the signaling (mechanistic) process of RE in ACC.

We found that PAO and AbPI4K significantly abrogated RE kinetics. check details Infusion of PI(4,5)P2 through the patch pipette potentiated RE kinetics and reversed PAO- and AbPI4K-induced blockade of RE. Similarly, the application of the bifunctional thiol dithiothreitol (DTT) to PAO-treated cells completely prevented the inhibitory effect of PAO on RE. These findings indicate that PI(4,5)P2 is implicated in the signaling (mechanistic) process of RE in ACC.

Increasing evidence highlights the significance of microRNAs (miRNAs) in the progression of atherosclerosis (AS). Our aim was to probe out the role and regulatory mechanism of miR-29a-3p in AS.

An in vivo model of AS was conducted by high-fat diet ApoE

mice. Oxidized low-density lipoprotein- (ox-LDL-) exposed vascular smooth muscle cells (VSMCs) were utilized as an in vitro of AS. Serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were detected. Hematoxylin and eosin (H&E) and Masson's staining was presented to investigate the pathological changes. miR-29a-3p and TNFRSF1A expression was detected by RT-qPCR. Proliferative, migrated, and invaded abilities of VSMCs were determined via a series of assays. The interaction between miR-29a-3p and TNFRSF1A was verified through luciferase reporter assay.

Upregulated miR-29a-3p and downregulated TNFRSF1A were found both in vitro and in vivo models of AS. miR-29a-3p mimic distinctly decreased the serum levels of TC, TG, and LDL-C and increased serum HDL-C levels. Moreover, its overexpression could ameliorate plaque formation of AS mice. In ox-LDL-induced VSMCs, miR-29a-3p overexpression notably decreased cell proliferation, migration, and invasion, which was reversed by TNFRSF1A overexpression. Also, miR-29a-3p could directly target the 3'UTR of TNFRSF1A.

miR-29a-3p overexpression ameliorated plaque formation of AS and suppressed proliferation, migration, and invasion of ox-LDL-induced VSMCs via TNFRSF1A, which offered novel insights into the progression of AS.

miR-29a-3p overexpression ameliorated plaque formation of AS and suppressed proliferation, migration, and invasion of ox-LDL-induced VSMCs via TNFRSF1A, which offered novel insights into the progression of AS.

The purpose of this study was to investigate the regulatory mechanisms of ceRNAs in breast cancer (BC) and construct a new five-mRNA prognostic signature.

The ceRNA network was constructed by different RNAs screened by the edgeR package. The BC prognostic signature was built based on the Cox regression analysis. The log-rank method was used to analyse the survival rate of BC patients with different risk scores. The expression of the 5 genes was verified by the GSE81540 dataset and CPTAC database.

A total of 41 BC-adjacent tissues and 473 BC tissues were included in this study. A total of 2,966 differentially expressed lncRNAs, 5,370 differentially expressed mRNAs, and 359 differentially expressed miRNAs were screened. The ceRNA network was constructed using 13 lncRNAs, 267 mRNAs, and 35 miRNAs. Kaplan-Meier (K-M) methods showed that two lncRNAs (AC037487.1 and MIR22HG) are related to prognosis. Five mRNAs (

,

,

,

, and

) in the ceRNA network were used to establish a prognostic signature. Survival analysis showed that the prognosis of patients in the low-risk group was significantly better than that in the high-risk group (

= 0.