Long noncoding RNA SOX2-OT facilitates prostate cancer cell proliferation and migration via miR-369-3p/CFL2 axis.

Accepted as crucial participators in human malignancies, long noncoding RNAs (lncRNAs) have been proven to exert significant function on the complicated processes of cancer progression. Although existing investigations have revealed the oncogenic role of lncRNA SOX2 overlapping transcript (SOX2-OT) in different kinds of cancers, such as osteosarcoma and cholangiocarcinoma, the potential role of it in prostate cancer (PC) is poorly understood. This study was the first attempt to decipher the underlying regulatory mechanism of SOX2-OT in PC. According to the data from this study, SOX2-OT expression was conspicuously elevated in PC tissues and cells. Silenced SOX2-OT could repress PC cell proliferation and migration. Besides, mechanism assays manifested that SOX2-OT bound with miR-369-3p and negatively correlated with miR-369-3p in PC. Additionally, miR-369-3p was confirmed to elicit suppressive impact on PC progression. What's more, cofilin 2 (CFL2) was testified to be a downstream target gene of miR-369-3p. Final rescue tests uncovered that CFL2 upregulation or miR-369-3p inhibition could largely restore SOX2-OT knockdown-mediated function on PC progression. To sum up, SOX2-OT accelerates cell proliferation and migration by targeting miR-369-3p/CFL2 axis in PC.

Wo Q ，Zhang D ，Hu L ，Lyu J ，Xiang F ，Zheng W ，Shou J ，Qi X ... -  《-》

miR-3189-3p Mimics Enhance the Effects of S100A4 siRNA on the Inhibition of Proliferation and Migration of Gastric Cancer Cells by Targeting CFL2.

Bian Y ，Guo J ，Qiao L ，Sun X ... -  《INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES》

Long Noncoding RNA SOX2-OT Knockdown Inhibits Proliferation and Metastasis of Prostate Cancer Cells Through Modulating the miR-452-5p/HMGB3 Axis and Inactivating Wnt/β-Catenin Pathway.

Song X ，Wang H ，Wu J ，Sun Y ... -  《-》

Long non-coding RNA SOX2-OT enhances cancer biological traits via sponging to tumor suppressor miR-122-3p and miR-194-5p in non-small cell lung carcinoma.

The oncogenic role of long non-coding RNA SOX2 overlapping transcript (SOX2-OT) has been demonstrated as a miRNA decay system that sponges tumor suppressor miRNA, including miR-122-3p in glioblastoma and miR-194-5p in glioblastoma, gastric, and colorectal cancers. However, the molecular function of SOX2-OT remains unknown in most cancers, including lung cancer. In the current study, we aimed to evaluate the downstream regulatory function of SOX2-OT in A549 and Calu-3 lung cancer cell lines. We knocked down SOX2-OT expression using an RNA interference system, which significantly decreased expression in A549 and Calu-3 cells. The expression of down-regulating miRNAs (miR-122-3p and miR-194-5p) was evaluated, revealing increased expression of miR-122-3p and miR-194-5p. Additionally, the expression of miRNAs downstream mRNA, including FOXO1 (Forkhead Box O1) and FOXA1 (Forkhead Box O1), changed. Recently, critical roles of FOXO1 and FOXA1 proteins in pathways involved in proliferation, metastasis and apoptosis have been demonstrated. Downstream changes in cellular traits were assessed using MTT, flow cytometry, metastasis and apoptosis assays. These assessments confirmed that the biological behaviors of lung cancer cells were influenced after SOX2-OT knockdown. In summary, the present study highlights the oncogenic role of SOX2-OT through the regulation of miR-122-3p/FOXO1 and miR-194-5p/FOXA1 pathways.

Dodangeh F ，Sadeghi Z ，Maleki P ，Raheb J ... -  《-》

CTCF-induced upregulation of HOXA11-AS facilitates cell proliferation and migration by targeting miR-518b/ACTN4 axis in prostate cancer.

Testified as crucial participators in different types of human malignancies, long noncoding RNAs (lncRNAs) have been revealed to exert a significant effect on the complicated courses of tumor progression. Although existing literatures have revealed the oncogenic role of lncRNA homeobox A11 antisense RNA (HOXA11-AS) in multiple cancers, the underlying role of HOXA11-AS in prostate cancer (PCa) and its potential molecular mechanism remains poorly understood. To decipher the molecular performance of HOXA11-AS in PCa. The expression of HOXA11-AS, miR-518b and actinin alpha 4 (ACTN4) was detected by a real-time quantitative polymerase chain reaction. Colony formation, EdU, flow cytometry, wound healing, and transwell assays were utilized to explore the biological role of HOXA11-AS in PCa. The interaction between RNAs (CCCTC-binding factor [CTCF], HOXA11-AS, miR-518b, and ACTN4) was tested via chromatin immunoprecipitation, luciferase reporter and RNA immunoprecipitation assays. HOXA11-AS in PCa cells was expressed at high levels. Silenced HOXA11-AS in PCa cells could lead to a significant elevation in the abilities of cell proliferation and migration whereas a remarkable declination in cell apoptosis capability. Subsequent molecular mechanism assays confirmed that HOXA11-AS bound with miR-518b and negatively regulates miR-518b expression. Besides, HOXA11-AS could regulate the expression of ACTN4 by sponging miR-518b. Moreover, rescued-function assays revealed that miR-518b inhibition or ACTN4 upregulation reversed the repressive effect of HOXA11-AS knockdown on PCa progression. Furthermore, CTCF was validated to activate HOXA11-AS transcription in PCa cells. CTCF-induced upregulation of HOXA11-AS facilitates PCa progression via miR-518b/ACTN4 axis, providing a new target for PCa treatment.

Xing Z ，Li S ，Liu Z ，Zhang C ，Bai Z ... -  《-》