Silencing of Perilipin 3 Inhibits Lung Adenocarcinoma Cell Immune Resistance by Regulating the Transcription of PD-L1 Through c-Myc.

Background: Perilipin 3 (PLIN3), a lipid droplet-associated protein, is found to be highly expressed in human cancers. This study aimed to investigate the biological functions and underlying mechanism of PLIN3 in lung adenocarcinoma (LUAD).

Methods: To analyse PLIN3 expression in normal and cancerous tissues, relevance between PLIN3 expression and survival prognosis, and to predict the pathways related to PLIN3, bioinformatic analysis was performed.

MicroRNA-325 facilitates atherosclerosis progression by mediating the SREBF1/LXR axis via KDM1A.

Aims: MicroRNA-325 (miR-325) was significantly upregulated in diabetic atherosclerosis, while its specific role in atherosclerosis has not been established. The present study was set to probe the effects of miR-325 on the atherosclerosis progression and to explore the mechanisms.

Materials And Methods: The ApoE mouse with atherosclerosis was developed to detect the miR-325 expression in atherosclerotic plaques.

Negative feedback of NF-κB signaling by long noncoding RNA MALAT1 controls lipopolysaccharide-induced inflammation injury in human lung fibroblasts WI-38.

The study was designed to elucidate the regulatory mechanism of long noncoding RNA human metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in lipopolysaccharides (LPS)-caused inflammation injury in human lung fibroblasts WI-38. WI-38 cells were stimulated with LPS to construct acute pneumonia cell model. MALAT1 in LPS-stimulated WI-38 cells was examined.

Cullin7 is required for lung cancer cell proliferation and is overexpressed in lung cancer.

Ubiquitin ligase Cullin7 has been identified as an oncogene in some malignant diseases such as choriocarcinoma and neuroblastoma. However, the role of Cullin7 in lung cancer carcinogenesis remains unclear. In this study, we explored the functional role of Cullin7 in lung cancer cell proliferation and tumorigenesis and determined its expression profile in lung cancer.

Variance of TNFAIP8 expression between tumor tissues and tumor-infiltrating CD4+ and CD8+ T cells in non-small cell lung cancer.

Tumor necrosis factor alpha-induced protein 8 (TNFAIP8) has been recently documented in various malignancies, but its role in non-small cell lung cancer (NSCLC) remains uncertain. In the current study, we investigated the level of TNFAIP8 in NSCLC tissues, adjacent noncancerous lung tissues, healthy lung tissues, CD4+ T cells, and CD8+ T cells by real-time reverse transcription PCR (RT-PCR) and Western blot analysis. Results revealed that the mRNA level of TNFAIP8 was significantly increased in cancer tissue than in healthy lung tissue from donors (p < 0.