Upregulated UCA1 contributes to oxaliplatin resistance of hepatocellular carcinoma through inhibition of miR-138-5p and activation of AKT/mTOR signaling pathway.

Hepatocellular carcinoma (HCC) inevitably developed oxaliplatin (OXA) resistance after long-term treatment, but the mechanism remains unclear. Here, we found that LncRNA UCA1 was upregulated in most of OXA-resistant HCC tissues and cells (HepG2/OXA and SMMC-7721/OXA). Follow-up analysis and online Kaplan-Meier Plotter revealed that HCC patients with high UCA1 level had a shorter survival compared with those with low expression.

A novel metastatic promoter CEMIP and its downstream molecular targets and signaling pathway of cellular migration and invasion in SCLC cells based on proteome analysis.

Purpose: Metastasis is an unavoidable event happened among almost all small cell lung cancer (SCLC) patients. However, the molecular driven factors have not been elucidated. Recently, a novel hydrolase called cell migration inducing hyaluronidase (CEMIP) triggered both migration and invasion in many tumors but not SCLC.

Differential long noncoding RNAs expression in cancer-associated fibroblasts of non-small-cell lung cancer.

Aim: The aim of this study was to investigate the role of long noncoding RNAs (lncRNAs) profiles in cancer-associated fibroblasts (CAFs) during non-small-cell lung cancer (NSCLC) progression.

Materials & Methods: Differentially expressed lncRNAs and mRNAs were detected by lncRNA microarray between three patient-paired CAFs and the adjacent normal fibroblasts, which were obtained from tumoral and nontumoral portions of surgically resected lung tissue from three primary NSCLCs. Bioinformatic analyses including gene ontology and pathway analysis were applied to these differentially expressed mRNAs.

Cancer-Associated Fibroblasts Accelerate Malignant Progression of Non-Small Cell Lung Cancer via Connexin 43-Formed Unidirectional Gap Junctional Intercellular Communication.

Background/aims: Gap junctions, which are assembled by connexins, can directly connect the cytoplasm of adjacent cells and enable gap junctional intercellular communication (GJIC) as well as metabolic coupling between neighboring cells. Here, we investigated the role of connexin 43 (Cx43) and its derived GJIC in the interplay between non-small cell lung cancer (NSCLC) cells and cancer-associated fibroblasts (CAFs).

Methods: CAFs and NSCLC cells were co-cultured with direct contact and separated using flow cytometry.