LINC01140 (Long Intergenic Non-Protein Coding RNA 1140)

LINC01140, miR-140-5p and FGF9 form a lncRNA-miRNA-mRNA axis that modulates the gastric cancer phenotypes and in turn affects gastric cancer cell aggressiveness.

Overall, LINC01140 prevents BC development via the miR-200b-3p-DMD axis. These findings support the latent potential and usefulness of the LINC01140-miR-200b-3p-DMD network as a target for BC therapy.

Besides, there was a significant negative association between expression levels of FAM13A-AS1, KCNIP2-AS1and LIPE-AS1 genes in tumor tissues and different mitotic rates. Taken together, PPARγ-related lncRNAs might be regarded as potential contributors to the pathogenesis of breast cancer.

In addition, exosomal LINC01140 hindered the activation of the Wnt/β-catenin signaling pathway, leading to a decrease in the growth of breast cancer cells in vivo. The presence of exosomal LINC01140 impedes the initiation of Wnt/β-catenin and reduces the cancerous characteristics of BC cells.

LINC01140 functioned as an antitumor agent in BC by sponging miR-452-5p to release RGS2. This hints that LINC01140 is a promising therapeutic target for BC.

To summarize, LINC01140 regulates the radiosensitivity of NPC cells through the competing endogenous RNA (ceRNA) mode. Our study aims to identify novel biomarkers for regulating the radiosensitivity of NPC.

Our results indicate that LINC01140 downregulation inhibits the invasion, proliferation, and EMT in osteosarcoma cells through targeting the miR-139-5p/HOXA9 axis. Therefore, LINC01140 is a potential therapeutic target for osteosarcoma.

AMPK (involved LIPE and LEP) and PPAR (involved PLIN1) were two significantly enriched pathways in luminal A breast cancer. This study could be helpful in unraveling the pathogenesis and providing novel therapeutic strategies for luminal A breast cancer.