Wanglowe1799

LPIN1 was verified to be the target binding to miRNA-584 and its level was negatively regulated by miRNA-584. The overexpression of LPIN1 accelerated OCa cells to proliferate and migrate. Importantly, LPIN1 was responsible for OCa progression regulated by miRNA-584. CONCLUSIONS MiRNA-584 is downregulated in OCa tissues and cell lines. MiRNA-584 level is correlated with lymphatic metastasis, distant metastasis, and poor prognosis in OCa patients. By negatively regulating LPIN1, miRNA-584 suppresses the malignant progression of OCa.OBJECTIVE To elucidate the role of linc-UBC1 in regulating the metastasis and progression of ovarian cancer (OC) by downregulating the p53 level. PATIENTS AND METHODS Relative levels of linc-UBC1 in OC tissues and paracancerous tissues were determined by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Differential expressions of linc-UBC1 in OC tissues with different tumor staging or tumor sizes were detected as well. Receiver operating characteristic (ROC) curves were introduced for assessing the diagnostic value of linc-UBC1 in OC. After silence of linc-UBC1, proliferative and migratory abilities of HO8910 and HEY cells were evaluated. Subcellular distribution of linc-UBC1 was analyzed. The interaction between linc-UBC1 and p53 was explored through the RNA immunoprecipitation (RIP) assay. At last, rescue experiments were conducted to uncover the role of linc-UBC1/p53 regulatory loop in influencing the progression of OC. RESULTS Linc-UBC1 was upregulated in OC and its level negatively correlated to that of p53. Linc-UBC1 level was higher in OC patients with advanced TNM staging or larger tumor size. Linc-UBC1 was mainly distributed in the nucleus. Silence of linc-UBC1 attenuated proliferative and migratory abilities of HO8910 and HEY cells. RIP assay verified that linc-UBC1 could inhibit the transcription of p53. Knockdown of p53 could partially reverse the regulatory effects of linc-UBC1 on regulating the progression of OC. CONCLUSIONS Linc-UBC1 is upregulated in OC tissues and cells. It stimulates the proliferation and metastasis of OC by downregulating p53 level, thus exerting a carcinogenic role.OBJECTIVE Ovarian cancer is a highly invasive type of cancer. A previous study demonstrated that E-cadherin expression was upregulated in a human ovarian cancer cell line with a high expression of WW domain-containing oxidoreductase (WWOX), which is a tumor suppressor. Also, the migration and invasion ability of these cells was reduced. Snail family members are involved in the epithelial-to-mesenchymal transition (EMT) of ovarian cancer cells, and the expression of Snail family members is regulated by the transcription factor Elf5. The aim of the present research was to elucidate the role of WWOX in EMT of ovarian carcinoma cells through the Elf5/Snail pathway by gain and loss of function approaches in in vitro experiments. MATERIALS AND METHODS First, a WWOX gene expressing plasmid was transfected into CD133+CD117+ HO8910 ovarian carcinoma cells, and an Elf5 shRNA plasmid was transfected into these cells to assess the changes in EMT-related factors, including Snail1, and the invasive ability of tumor cells ability. Second, the human ovarian carcinoma cell lines HO8910 and SKOV3 were divided into six groups to detect the same indicators. RESULTS The results demonstrated that the high expression of WWOX resulted in an increased E-cadherin expression, decreased Snail1 activity, and decreased invasion ability in CD133+CD117+ HO8910 cells. Elf5 shRNA transfection did not affect the WWOX expression; however, it decreased the expression of E-cadherin and Elf5 activity, while increasing Snail1 activity and invasion ability in CD133+CD117+ HO8910 cells. It was also observed that WWOX overexpression in HO8910 and SKOV3 cells inhibited the expression of EMT-related proteins and inhibited cell migration and invasion. CONCLUSIONS Taken together, the results of the present report suggest that WWOX can decrease Snail1 activity by enhancing the activity of Elf5, thus upregulating E-cadherin expression and eventually inhibiting EMT of ovarian carcinoma.OBJECTIVE Recently, the vital role of circular RNAs is discovered in many diseases including tumor progression and metastasis. Hepatocellular carcinoma (HCC) is one of the most ordinary malignant tumors. The purpose of our study is to detect the potential function of hsa_circ_0011946 in HCC to offer new biomarkers and targets. PATIENTS AND METHODS The level of hsa_circ_0011946 in HCC tissues and cell lines was monitored by Real Time Quantitative Polymerase Chain Reaction (RT-qPCR). Pearson's Chi-square test was used to determine the association between hsa_circ_0011946 expression and several clinicopathological factors. Then, hsa_circ_0011946 was knocked down in HCC cells to uncover its function in metastasis of HCC. Cell migrated and invaded ability was measured through transwell assay, Matrigel assay and wound healing assay. Western blot assay was performed to analyze the effect of hsa_circ_0011946 on the epithelial-to-mesenchymal transition (EMT) process. RESULTS In this research, the expression level of hsa_circ_0011946 was significantly increased in HCC tissues compared to that in adjacent samples. The expression of hsa_circ_0011946 was also increased in HCC cell lines. The hsa_circ_0011946 expression was associated with lymphatic metastasis in HCC patients. this website Knockdown of hsa_circ_0011946 led to the inhibition of cell migration and invasion in HCC. In addition, results of further experiments revealed that the EMT-related proteins were regulated via the knockdown of hsa_circ_0011946 in HCC. CONCLUSIONS The hsa_circ_0011946 could enhance cell migration and invasion of HCC by inducing the EMT process.OBJECTIVE Abnormal expression of micro ribonucleic acids (miRNAs) has become an important marker of cancer. However, the exact molecular mechanisms of miRNAs were not very clear. Here, we decided to investigate the miR-19 effect and molecular mechanism on pancreatic cancer, which was blank until now. PATIENTS AND METHODS Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was applied for testing miR-19 and gene of phosphate and tensin homolog deleted on chromosome ten (PTEN) expression. Western blot was used for detecting the protein expression. Methyl thiazolyl tetrazolium (MTT) assay and transwell assay were carried out to measure cell proliferation, invasion, and migration. RESULTS We showed that miR-19 expression was increased in cancerous tissues and was associated with the survival of patients, tumor node metastasis (TNM) stage, tumor size, and lymph node metastasis. MiR-19 mimic enhanced cell proliferation, invasion, and migration, while suppressing miR-19 cell progression was suppressed.