Upregulation of lncRNA SUMO1P3 promotes proliferation, invasion and drug resistance in gastric cancer through interacting with the CNBP protein.

Gastric cancer (GC) is one type of the most common malignancies in the world. In the process of exploring the pathological mechanism of GC and searching for treatment methods, long non-coding RNAs (lncRNAs) display significant participation. Small ubiquitin-like modifier 1 pseudogene 3 (SUMO1P3) is a newly identified lncRNA, of which the biological role and underlying mechanism in GC progression have not been elucidated.

PCAT-1 contributes to cisplatin resistance in gastric cancer through miR-128/ZEB1 axis.

Increasing evidence suggests that dysregulation of long non-coding RNAs (lncRNAs) is implicated with chemoresistance in cancers. However, their function and molecular mechanisms in gastric cancer (GC) chemoresistance remain not well elucidated. In this study, we aimed to investigate the functional role and the underlying molecular mechanism of lncRNA prostate cancer-associated transcript 1 (PCAT-1) in cisplatin (DDP) resistance of GC.

LncRNA MEG3 enhances I sensitivity in thyroid carcinoma via sponging miR-182.

Background: Long non-coding RNA (LncRNA) MEG3 has been demonstrated as a tumor suppressor in various cancers, including thyroid carcinoma (TC). However, the detail functions and possible mechanisms of MEG3 in I resistance of TC remain to be uncovered.

Methods: qRT-PCR was performed for the detection of MEG3 and miR-182 levels.