Long non-coding DANCR targets miR-185-5p to upregulate LIM and SH3 protein 1 promoting prostate cancer via the FAK/PI3K/AKT/GSK3β/snail pathway.

Long non-coding RNA differentiation antagonizing non-protein coding RNA (DANCR) acts as an oncogene in different cancers, although its roles in prostate cancer are not fully reported. We aimed to explore its mechanism in facilitating the malignancy of prostate cancer. The expression of DANCR, microRNA (miR)-185-5p and LIM and SH3 protein 1 (LASP1) in 40 pairs of prostate cancer tissues and normal tissues, five prostate cancer cell lines and one epithelial cell line was assessed by a quantitative real-time polymerase chain reaction, western blotting and immunohistochemistry, respectively. In transfected PC3 and C4-2 cells, cell proliferation, migration, invasion, cell cycle distribution and epithelial-mesenchymal transition (EMT) protein expression were tested via cell counting kit-8, wound healing, transwell, flow cytometry and western blot assays, respectively. The interactions between DANCR, miR-185-5p and LASP1 were verified by a dual-luciferase reporter assay. Rescue experiments were conducted to determine the roles of DANCR on the malignant properties of PC3 and C4-2 cells. The involvement of the signaling pathway was examined using a p-FAK inhibitor. DANCR and LASP1 expression was enhanced, whereas miR-185-5p expression was diminished in prostate cancer tissues and cell lines. Knockdown of DANCR suppressed cell proliferation, migration, invasion, G1-S transition and expression of EMT proteins of the transfected PC3 and C4-2 cells. DANCR sponged miR-185-5p to upregulate LASP1 expression. DANCR-miR-185-5p-LASP1 axis activates the FAK/PI3K/AKT/GSK3β/Snail pathway to promote the malignant properties of PC3 and C4-2 cells. These findings suggest that DANCR exerts oncogenic roles in prostate cancer via the miR-185-5p/LASP1 axis activating the FAK/PI3K/AKT/GSK3β/Snail pathway. It can be a potential biomarker in the diagnosis and monitoring of prostate cancer.

Sun W ，Zu S ，Shao G ，Wang W ，Gong F ... -  《-》

LIM and SH3 protein 1 induces glioma growth and invasion through PI3K/AKT signaling and epithelial-mesenchymal transition.

This study investigated the underlying mechanism of LIM and SH3 protein 1 (LASP1)-induced malignant glioma growth and invasion. We compared the expression of LASP1 in malignant glioma tumor tissues and low-grade glioma tissues by immunohistochemistry. We also compared LASP1 overexpression and LASP1 knockout glioma cell proliferation and invasion in vitro and in vivo. We detected activation of the PI3K/AKT signaling pathway and epithelial-mesenchymal transition (EMT) process in tumor cells by western blotting or immunofluorescence. Glioma-bearing mice were used to investigate the anticancer effects of PI3K/AKT inhibitors in combination with temozolomide. We observed the enhanced expression of LASP1 in malignant glioma tumor tissues compared to low-grade glioma tissues, and LASP1 overexpression in glioma cells revealed an elevated capability of proliferation and invasion in vitro and in vivo. LASP1 overexpression also facilitated PI3K/AKT signaling and the EMT process through the downstream transcription factor Snail, which resulted in the intensive invasion of cancer cells. We combined PI3K/AKT inhibitors and temozolomide to block the LASP1/PI3K/AKT/Snail signaling pathway, which dramatically enhanced tumor suppression and provides an innovative approach for clinical glioma treatment. LASP1 is upregulated in malignant glioma and facilitates glioma cell proliferation and invasion by activation the PI3K/AKT/Snail signaling pathway. Blockade of the PI3K/AKT signal efficiently enhanced the anticancer effects of chemotherapeutic agents, which provides an innovative target in glioma treatment.

Zhong C ，Li X ，Tao B ，Peng L ，Peng T ，Yang X ，Xia X ，Chen L ... -  《-》

Downregulation of long noncoding RNA breast cancer anti-estrogen resistance 4 inhibits cell proliferation, invasion, and migration in esophageal squamous cell carcinoma by regulating the microRNA-181c-5p/LIM and SH3 protein 1 axis.

Ke S ，Fang M ，Li R ，Wang J ，Lu J ... -  《-》

Long non-coding RNA LINC01207 promotes prostate cancer progression by downregulating microRNA-1972 and upregulating LIM and SH3 protein 1.

Prostate cancer is a heritable and clinically heterogeneous cancer. Both long non-coding RNAs (lncRNAs) and microRNAs (miRs) have been implicated in the pathogenesis and development of prostate cancer. Analysis of microarray data indicated that the lncRNA LINC01207 was differentially expressed in prostate cancer. In silico analysis predicted the interaction between LINC01207 and miR-1972 as well as the interaction between miR-1972 and the mRNAs LIM and SH3 protein 1 (LASP1). Thus, we explored the role of LINC01207 and miR-1972 in the growth and progression of prostate cancer. Quantitative real-time polymerase chain reaction revealed that LINC01207 and LASP1 were highly expressed in prostate cancer, while miR-1972 expression was lower. The interaction among LINC01207, miR-1972, and LASP1 was confirmed by RNA-fluorescence in situ hybridization, RNA immunoprecipitation, and dual luciferase reporter assay, which verified that LINC01207 could bind to miR-1972 and downregulate miR-1972, and miR-1972 targeted LASP1 and negatively regulated its expression. Both in vitro and in vivo experiments found that silencing LINC01207 inhibited cell proliferation, migration, invasion and tumor formation and enhanced apoptosis in prostate cancer cells, suggesting that LINC01207 functioned as a tumor promoter in prostate cancer and that it may represent a novel therapeutic target.

Wang S ，Qiu J ，Wang L ，Wu Z ，Zhang X ，Li Q ，Jiang F ... -  《-》

LINC01123 Promotes the Progression of Colorectal Cancer via miR-625-5p/LASP1 Axis.

Shang T ，Zhou X ，Chen W 《-》