A Positive Feedback Loop of Long Noncoding RNA LINC00152 and KLF5 Facilitates Breast Cancer Growth.

The long noncoding RNA (lncRNA) LINC00152, also known as CYTOR, displays aberrant expression in various cancers. However, its clinical value and functional mechanisms in breast cancer remain insufficiently understood. Our study found that LINC00152 is significantly upregulated in breast cancer, and that it acts as an indicator of poor survival prognosis. Further studies revealed that LINC00152 knockdown suppresses cell proliferation and tumorigenicity in vitro and in vivo. Mechanistic analyses demonstrated that LINC00152 directly binds to KLF5 protein and increases KLF5 stability. Moreover, LINC00152 is also a KLF5-responsive lncRNA, and KLF5 activates LINC00152 transcription by directly binding to its promoter. Our study suggests that LINC00152 promotes tumor progression by interacting with KLF5. LINC00152 may be a valuable prognostic predictor for breast cancer, and the positive feedback loop of LINC00152-KLF5 could be a therapeutic target in pharmacological strategies.

LINC00152 Knock-down Suppresses Esophageal Cancer by EGFR Signaling Pathway.

AIM: This study aims to explain the role and mechanism of lncRNA LINC00152 in esophageal cancer. METHODS: The 30 pairs of esophageal cancer and adjacent normal tissues were collected and measuring the lncRNA LINC00152 expression by ISH and RT-qPCR assay. In the next cell experiment, Eca 109 and Kyse 150 cells were divided into 3 groups: NC group were treated with non-treatment; BL group were transfected with empty vector and lncRNA group were transfected with lncRNA LINC00152. The cells proliferation were measured by MTT assay; the cells apoptosis and cell cycle were evaluated by flow cytometry. The relative proteins expressions were measured by WB assay. RESULTS: Compared with NC groups, the cell proliferation rate of lncRNA groups were significantly suppressed (P<0.05, respectively); the cell apoptosis and G1 phase rates were significantly enhanced in the lncRNA groups (P<0.05, respectively). In the proteins expressions, the EGFR, PI3K and AKT proteins expressions of lncRNA group were significantly inhibited and the P21 proteins expressions were significantly stimulated in the lncRNA groups compared with those of NC groups in Eca 109 and Kyse 150 cells. CONCLUSION: The lncRNA LINC00152 had anti-tumor effects on esophageal cancer in the Eca 109 and Kyse 150 cells, the mechanisms were relative with EGFR pathway.

Down-regulation of lncRNA LINC00152 Suppresses Gastric Cancer Cell Migration and Invasion Through Inhibition of the ERK/MAPK Signaling Pathway.

PURPOSE: The aim of this study was to explore the regulatory role and mechanism of long noncoding RNA LINC00152 in gastric cancer (GC) cells. METHODS: LINC00152 expression in GC tissues and cells was detected by reverse transcription-polymerase chain reaction (qRT-PCR). MKN45 and MGC-803 cells were selected and assigned into different groups after transfection with si-LINC00152, activated ERK/MAPK signaling pathway (SA), or negative control. Cell proliferation, apoptosis, cycle, migration and invasion were assessed by CCK-8, flow cytometry, Transwell assay and Scratch test, respectively. Western blot analysis was conducted to detect the expression of E-cadherin, N-cadherin and ERK/MAPK signaling pathway protein. RESULTS: Compared with the normal tissues, higher expression of LINC00152 was found in GC tissues and LINC00152 was remarkably correlative with clinical stage and lymphatic metastasis. LINC00152 expression in GC cells was higher than that in GES-1 cells. Compared with the NC group, the cell proliferation rate, cells in G2/M phase, migration and invasion abilities as well as the expression of N-cadherin and p-ERK-1/2 were significantly decreased, and the expression of E-cadherin, cells in G0/G1 phase and cell apoptosis rate were significantly increased in the si-LINC00152-1 group. ERK/MAPK signaling pathway activator SA could reverse the biological role of LINC00152 in GC cells. CONCLUSION: These results demonstrated that the interference of LINC00152 expression may inhibit the invasion and migration of GC cells by inhibiting the ERK/MAPK signaling pathway.

lncRNA LINC00152 knockdown had effects to suppress biological activity of lung cancer via EGFR/PI3K/AKT pathway.

Accumulating evidence demonstrates that lncRNAs play important roles in regulating gene expression and are involved in various pathological processes. In our present study, we firstly evaluated lncRNA LINC00152 and EGFR expressions by ISH or IHC methods, and analyzed the correlation between LINC00152 and EGFR with RT-PCR. lncRNA LINC00152 of NSCLC tissues were significantly up-regulation compared with adjacent normal tissues and positively correlated with EGPR. The further cell experiments demonstrated that Linc00152 knockdown had effects of suppression cell proliferation, invasion and migration abilities and improving cell apoptosis and G1 phase rates in both A549 and H1299 cell lines. In the mechanism study, the results were shown that EGFR, PI3K, AKT, Fibronectin and Vimentin proteins expressions were significantly reduced and P21 protein expression was significantly increased in Linc00152 knockdown groups. Our results suggested lncRNA LINC00152 knock-down had anti-tumor effects via EGFR/PI3K/AKT pathway.