Long non-coding RNA MIR503HG inhibits the proliferation, migration and invasion of colon cancer cells via miR-107/Par4 axis.

Colon cancer is a common caner with high death rate in the world. The study aimed to detect the effect and mechanism of long non-coding RNA (LncRNA) MIR503HG on colon cancer. The MIR503HG expression was measured in colon cancer tissues and cell lines by qRT-PCR. The proliferation, apoptosis, migration and invasion of colon cancer cells were measured by MTT, flow-cytometry, wound healing and transwell assay. The protein expression of E-cadherin, N-cadherin, and Vimentin was detected by Western blot. The target relationships among MIR503HG, miR-107 and Par4 were predicted by StarBase and TargetScan, and verified by luciferase reporter and RNA pull-down assay. The xenograft tumor model was constructed in mice to verify the inhibitory effect of MIR503HG in vivo. The expression of MIR503HG was decreased in colon cancer tissues and cell lines. MIR503HG overexpression inhibited cell proliferation, migration and invasion, promoted cell apoptosis, down-regulated N-cadherin and Vimentin, and up-regulated E-cadherin in colon cancer. MIR503HG negatively regulated its target miR-107. MiR-107 overexpression reversed the anti-tumor effects of MIR503HG overexpression on colon cancer cells. Par4 was a target of miR-107, which was positively regulated by MIR503HG. The promoting effects of MIR503HG silencing on colon cancer cells were eliminated by Par4 overexpression. MIR503HG regulated Par4 via sponging miR-107 in colon cancer, which promoting a new idea for the treatment of colon cancer.

Han H ，Li H ，Zhou J 《-》

LncRNA LINC00662 promotes colon cancer tumor growth and metastasis by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway.

Cheng B ，Rong A ，Zhou Q ，Li W ... -  《JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH》

lncRNA MIR503HG functioned as a tumor suppressor and inhibited cell proliferation, metastasis and epithelial-mesenchymal transition in bladder cancer.

Bladder cancer is the most common malignancy with high recurrence. Currently, the long noncoding RNAs (lncRNAs) have been suggested to play vital roles in the pathogenesis of bladder cancer. The present study investigated the role of lncRNA MIR503 host gene (MIR503HG) in the pathogenesis of bladder cancer by using both in vitro and in vivo functional assays. The expression of MIR503HG was downregulated in bladder cancer tissues and cell lines. Low expression of MIR503HG was associated with advanced tumor stage, advanced histological grade, and lymph node metastasis. Ectopic expression of MIR503HG inhibited cell proliferation, cell growth, cell invasion, and migration, and also promoted cell apoptosis and inhibited cell cycle progression in SW780 cells. In parallel, T24 cells were used for loss-of-function studies. Knockdown of MIR503HG promoted the cancer cell proliferation and increased the migration and invasion abilities of T24 cells. In addition, knockdown of MIR503HG reduced the cell apoptotic rate in cancer cells and promoted cell cycle progression. Furthermore, MIR503HG overexpression decreased the epithelial-mesenchymal transition-related mRNA and protein levels of ZEB1, Snail, N-cadherin, and vimentin, with an increase in E-cadherin level. Consistently, knockdown of MIR503HG showed the opposite effects. In vivo xenograft, nude mice results showed that overexpression of MIR503HG suppressed the tumor growth and tumor metastasis. In conclusion, our results identified a novel lncRNA MIR503HG that exhibited significant antiproliferation, antimigration/invasion effects on bladder cancer cells both in vitro and in vivo, which may hold a therapeutic promise to treat bladder cancer.

Qiu F ，Zhang MR ，Zhou Z ，Pu JX ，Zhao XJ ... -  《-》

LINC00342 regulates cell proliferation, apoptosis, migration and invasion in colon adenocarcinoma via miR-545-5p/MDM2 axis.

Colon adenocarcinoma (COAD) is the third most common cancer in the world. We aimed to explore the functional mechanism of LINC00342 in COAD. The LINC00342 expressions in COAD tissues were detected via qRT-PCR and in situ hybridization analysis. Statistical analysis was performed to analyze the relationship between LINC00342 expression and COAD clinical features. Small interfering LINC00342 (siLINC00342)/siCtrl were synthesized and then transfected into COAD cells. Cell apoptosis and proliferation were respectively assessed by flow cytometry and cell counting kit-8 assay. Cell migration and invasion were both measured using transwell assay. The target miRNA of LINC00342 were predicted and verified by online bioinformatics tools and luciferase reporter assay and RNA pull-down assay. Mice COAD models were constructed to explore the effects of LINC00342 on COAD in vivo. LINC00342 was over-expressed in COAD tissues and LINC00342 overexpression was related to the poor prognosis of COAD patients. LINC00342 knockdown inhibited cell proliferation, migration and invasion and promoted apoptosis of COAD cells. LINC00342 targeted to miR-545-5p/murine double minute 2 (MDM2) in COAD. In COAD tissues and cell lines, LINC00342 expression was positively correlated to MDM2 expression, while it was negatively correlated to miR-545-5p expression. Both miR-545-5p-mimic and siMDM2 transfection could recover the changes of cell biological activities which were induced by LINC00342 overexpression. LINC00342 knockdown suppressed COAD tumor growth in vivo. LINC00342 affected cell biological activities of COAD in vivo and in vitro via regulating miR-545-5p/MDM2. It might a novel target in COAD therapy.

Miao Z ，Liu S ，Xiao X ，Li D ... -  《-》

Long non-coding RNA CRNDE promotes the proliferation, migration and invasion of hepatocellular carcinoma cells through miR-217/MAPK1 axis.

Hepatocellular carcinoma (HCC) is an invasive malignant tumour and the second major cause of cancer-related deaths over the world. CRNDE and miR-217 are non-coding RNAs which play critical roles in cell growth, proliferation, migration. Mitogen-activated protein kinase 1 (MAPK1) also participates in cancer cell process. Hence, this study aimed at investigating the effect of CRNDE on migration and invasion of HCC and figuring out the role of miR-217 and MAPK1 in this process. The overexpression of CRNDE was demonstrated by a microarray-based lncRNA profiling study. CRNDE expression in HCC was verified by qRT-PCR. MTT assay and BrdU staining were applied to detect cell proliferation level. Transwell assay was utilized to examine cell migration and invasiveness abilities. Wound healing assay was performed for further exploration of cell migration capacity. MiR-217 was predicted by bioinformatics. The dual luciferase reporter assay was performed to corroborate the targeting relationship between CRNDE, miR-217 and MAPK1. MAPK1, the downstream target of miR-217, was predicted using bioinformatics and was further confirmed by qRT-PCR and Western blot. The interaction between CRNDE, miR-217 and MAPK1 was studied by qRT-PCR, Western blot, MTT, BrdU, transwell assay and wound healing assay. CRNDE was up-regulated in HCC tissues and HCC cell lines. The high expression of CRNDE facilitated cell proliferation, migration and invasion, while the inhibited one affected on the contrary. MiR-217, negatively correlated with CRNDE expression, was the target of CRNDE and was more lowly expressed in HCC. With the high expression of miR-217, HCC cell proliferation, migration and invasion were suppressed. MAPK1, the possible target of miR-217, was negatively correlated with miR-217 but positively correlated with CRNDE and had the same effect in HCC formation process as CRNDE. Long non-coding RNA CRNDE promotes the proliferation, migration and invasion of HCC cells through miR-217/MAPK1 axis.

Wang H ，Ke J ，Guo Q ，Barnabo Nampoukime KP ，Yang P ，Ma K ... -  《-》