This study is performed to elucidate the role of long non-coding RNA myocardial infarction associated transcript (lncRNA MIAT) in vulnerable plaque formation in rats with atherosclerosis (AS) through the regulation of the PI3K/Akt signaling pathway. The mice model of AS was established, and the successful modeled AS mice were treated with overexpressed MIAT and silenced MIAT. The levels of blood lipids, atherosclerotic plaques (AP) formation, the lipid content, collagen content, apoptosis of aortic cells, angiogenesis as well as the expression of inflammatory factors, such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were determined through a series of experiments. MIAT was found to be upregulated in AS. Additionally, MIAT up-regulated the levels of blood lipids, promoted AP formation, increased the lipid content and decreased the collagen content of AP, promoted the apoptosis of aortic cells in AS mice by activating the PI3K/Akt signaling pathway. Meanwhile, MIAT was determined to promote angiogenesis as well as the expression of inflammatory factors (IL-1β, IL-6, and TNF-α) in AS mice through the activation of the PI3K/Akt signaling pathway. Furthermore, MIAT activated the PI3K/Akt signaling pathway to participate in AS progression. Our study suggests that upregulation of MIAT can aggravate AS injury in AS mice via the activation of the PI3K/Akt signaling pathway, which could provide a novel target for the treatment of AS.

No abstract

Bortezomib is a novel proteasome inhibitor that has promising antitumor activity against various cancer cells. We have assessed its antitumor activity in non-small cell lung cancer (NSCLC) A549 and H157 cells in vitro where it inhibited cell growth and induced apoptosis, which was associated with cytochrome c release and caspase-3 activation. Bortezomib upregulated autophagic-related proteins, the Atg12-Atg5 complex and LC3-II, which indicated autophagy had occurred. The combination of bortezomib with autophagic inhibitor 3-methyladenine or chloroquine significantly enhanced suppression of cell growth and apoptosis induced by bortezomib in A549 and H157 cells. Our study indicated that inhibition of both proteasome and autophagy has great potential for NSCLC treatment.

No abstract

No abstract