LINC01605 regulates proliferation, migration and invasion of colorectal cancer cells via targeting miR-3960/SOX11.

OBJECTIVE: We aimed to determine the expression level of long intergenic non-coding ribonucleic acid 1605 (LINC01605) in colorectal cancer (CRC), and to explore the effects of the LINC01605/microRNA (miR)-3960/sex-determining region Y-box 11 (SOX11) regulatory axis on the biological behaviors of CRC cells and the molecular mechanism therein. PATIENTS AND METHODS: Tissue specimens were collected from 38 patients with CRC, and the relative expression level of LINC01605 in the CRC tissues and CRC cells was measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Then, the effects of LINC01605 on the proliferation, apoptosis, invasion and metastasis of CRC cells were observed via in vitro assays [cell counting kit (CCK)-8 assay, flow cytometry and transwell assay]. Besides, the possible miRNAs binding to LINC01605 were predicted by the bioinformatics method, and they were screened and verified using qRT-PCR and Dual-Luciferase reporter gene assay. Finally, the downstream target genes of miR-3960 were predicted by means of bioinformatics, and they were also screened and confirmed via qRT-PCR and Dual-Luciferase reporter gene assay. RESULTS: According to the results of qRT-PCR, the expression of LINC01605 was up-regulated in 31 out of 38 cases of CRC tissue specimens, and its expression in CRC cells was higher than that in normal colorectal cells. The results of in vitro assays revealed that the proliferation, migration and invasion abilities of CRC cells were weakened, with an increased apoptosis rate after interference with LINC01605 expression. Based on the results of qRT-PCR and Dual-Luciferase reporter gene assay, miR-3960 was the target of LINC01605, while SOX11 was the target of miR-3960. Moreover, the expression of miR-3960 rose, but that of SOX11 declined after interference with LINC01605 expression. It was found through Western blotting that the protein expression of SOX11 was lowered after interference with LINC01605 expression. CONCLUSIONS: LINC01605 has an up-regulated expression in CRC, and accelerates the proliferation, migration and metastasis of CRC cells by the miR-3960/SOX11 regulatory axis.

Upregulation of lncRNA NCK1-AS1 predicts poor prognosis and contributes to non-small cell lung cancer proliferation by regulating CDK1.

OBJECTIVE: To detect the expression of long non-coding ribonucleic acid (lncRNA) NCK1-AS1 in non-small cell lung cancer (NSCLC), analyze the association between its expression and the clinicopathological characteristics of NSCLC patients, and study the biological function of NCK1-AS1 in vitro. PATIENTS AND METHODS: The relative expression of NCK1-AS1 in NSCLC tissues and cells was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The association between the expression of NCK1-AS1 and the clinicopathological characteristics of NSCLC was statistically analyzed. The effects of interference in the expression of NCK1-AS1 on the biological behaviors of NSCLC cells were detected via in vitro experiments, including Cell Counting Kit-8 (CCK-8) assay, colony formation assay and flow cytometry. After interference in the expression of NCK1-AS1, the expression of cyclin-dependent kinase 1 (CDK1) was determined using Western blotting. RESULTS: The results of qRT-PCR showed that the expression of NCK1-AS1 was up-regulated in 50 out of 64 cases of NSCLC tissues. It was found via statistical analysis that highly expressed NCK1-AS1 was positively correlated with tumor size, TNM stage and lymph node metastasis. The results of qRT-PCR revealed that the expression of NCK1-AS1 was also up-regulated in NSCLC cells. After interference in the expression of NCK1-AS1, the proliferation of NSCLC cells was inhibited, and the cell cycle was arrested at G2/M phase. The results of Western blotting manifested that the expression of CDK1 was suppressed after interference in the expression of NCK1-AS1. CONCLUSIONS: The expression of NCK1-AS1 is up-regulated in NSCLC, which indicates a poor prognosis. Highly expressed NCK1-AS1 promotes the proliferation of NSCLC cells through activating CDK1.

Inhibition of miR-221 influences bladder cancer cell proliferation and apoptosis.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Inhibition of miR-221 influences bladder cancer cell proliferation and apoptosis, by H. Liu, J.-K. Chang, J.-Q. Hou, Z.-H. Zhao, L.-D. Zhang, published in Eur Rev Med Pharmacol Sci 2017; 21 (14): 3193-3199-PMID: 28770966" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/13140.

Over-expression of mir-124 inhibits MMP-9 expression and decreases invasion of renal cell carcinoma cells.

OBJECTIVE: JAK-STAT3 signaling pathway is related to tumor invasion and metastasis that can regulate matrix metalloproteinase-9 (MMP-9) expression. MicroRNA-124 (MiR-124) was found downregulated in renal cell carcinoma. Bioinformatics analysis revealed the complementary binding site between miR-124 and 3'-UTR of signal transducers and activators of transcription 3 (STAT3). This study investigated the role of miR-124 in regulating Janus kinase (JAK)-STAT3 activity, MMP-9 expression, and renal cell carcinoma invasion. MATERIALS AND METHODS: Luciferase assay was used to test the targeting regulatory effect of miR-124 on STAT3. MiR-124, STAT3, phosphorylated STAT3 (p-STAT3), and MMP-9 expressions were compared in HK-2, 769-P, and OS-RC-2 cells. Transwell assay was applied to evaluate cell invasion. OS-RC-2 cells were divided into control, miR-NC, miR-124 mimic, STAT3 inhibition, and miR-124 mimic+Stattic groups. RESULTS: MiR-124 targeted inhibited STAT3 expression. OS-RC-2 cells exhibited the strongest invasive ability, followed by 769-P and HK-2 cells. STAT3, p-STAT3, and MMP-9 expressions were highest in OS-RC-2 cells, followed by 769-P and HK-2 cells. MiR-124 demonstrated the opposite expression trend. MiR-124 mimic and/or Stattic treatment attenuated cell invasion through reducing STAT3, p-STAT3, and MMP-9 levels. CONCLUSIONS: MiR-124 down-regulation was associated with renal cancer cell OS-RC-2 invasion enhancement. Over-expression of miR-124 attenuated OS-RC-2 cell invasion by down-regulating STAT3 and MMP-9.

Inhibition of miR-221 influences bladder cancer cell proliferation and apoptosis.

OBJECTIVE: Janus kinase (JAK) - signal transducer and activator of transcription (STAT) signaling pathway participate in cell proliferation and apoptosis. Suppressors of cytokine signaling 3 (SOCS3) are negative regulators of JAK-STAT3. SOCS3 was found significantly declined, while microRNA-221 (miR-221) obviously up-regulated in bladder cancer tissue. Bioinformatics analysis revealed the complementary binding site between miR-221 and 3'-UTR of SOCS3. This study investigated the role of miR-221 in regulating SOCS3/JAK-STAT3 signaling pathway and bladder cancer cell proliferation and apoptosis. PATIENTS AND METHODS: Bladder cancer tumor tissue and para-carcinoma tissue were collected from patients to test miR-221 and SOCS3 expressions. Dual luciferase assay was used to test the targeting regulatory effect of miR-221 on SOCS3. MiR-221, SOCS3, p-JAK1, p-JAK2, and survivin expressions were compared in T24 and HBEC cells. T24 cells were divided into miR-NC, miR-221 inhibitor, pSicoR-blank, pSicoR-SOCS3, and miR-221 inhibitor + pSicoR-SOCS3 groups. Flow cytometry was applied to detect cell apoptosis. EdU staining was adopted to evaluate cell proliferation. RESULTS: MiR-221 significantly increased, while SOCS3 obviously reduced in bladder cancer tissue compared with para-carcinoma tissue. MiR-221 targeted inhibited SOCS3 expression. MiR-221, phosphorylated JAK1 (p-JAK1), phosphorylated JAK2 (p-JAK2), phosphorylated STAT3 (p-STAT3), and survivin levels markedly up-regulated, whereas SOCS3 expression apparently declined in T24 cells compared with that in HBEC cells. MiR-221 inhibitor and/or pSicoR-SOCS3 elevated SOCS3 expression, decreased p-JAK1, p-JAK2, p-STAT3, and survivin levels, enhanced cell apoptosis, and attenuated cell proliferation. CONCLUSIONS: MiR-221 elevated, while SOCS3 reduced in bladder cancer tissue. Inhibition of miR-221 suppressed T24 cell proliferation and induced apoptosis by up-regulating SOCS3 expression, lowering JAK-STAT3 signaling pathway activity, and attenuating survivin expression.

Random Lasing Action from Randomly Assembled ZnS Nanosheets.

Lasing characteristics of randomly assembled ZnS nanosheets are studied at room temperature. Under 266-nm optical excitation, sharp lasing peaks emitted at around 332 nm with a linewidth less than 0.4 nm are observed in all directions. In addition, the dependence of lasing threshold intensity with the excitation area is shown in good agreement with the random laser theory. Hence, it is verified that the lasing characteristics of randomly assembled ZnS nanosheets are attributed to coherent random lasing action.

Rapid inhibitory effect of corticosterone on histamine release from rat peritoneal mast cells.

Glucocorticoids are steroids endowed with powerful anti-inflammatory properties, which are routinely believed to require several hours to take effect through modulation of gene expression. Our recent report has shown that glucocorticoids could inhibit allergic reaction within 10 minutes, which the classical genomic mechanism could not explain. Histamine is thought to be one of major mediators in the allergic reaction, and IgE-mediated histamine release from mast cells plays a pivotal role in allergic diseases. Here, we have determined a rapid effect of corticosterone on histamine release from rat peritoneal mast cells, using fluorometric assay. The results showed that corticosterone could inhibit antigen-induced histamine release from rat peritoneal cells within 15 minutes (p<0.05), which could be mimicked by membrane-impermeable BSA conjugated corticosterone (p<0.05). Neither glucocorticoid nuclear receptor antagonist nor protein synthesis inhibitor could block the rapid action (p<0.05). The study provided evidence that nongenomic mechanism might be involved in rapid effect of glucocorticoids on mast cells in allergic disease.