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OBJECTIVE: To investigate the role of microRNA-212-5p (miR-212-5p) in clear cell renal cell carcinoma (ccRCC) and to explore the potential underlying mechanisms. MATERIALS AND METHODS: 32 pairs of ccRCC clinical samples were collected. Renal ccRCC cells (786-O) and embryonic kidney cells (293T) were cultured in vitro. The ability of cell proliferation was detected by 3-(4,5)-dimethylthiazol(- z-y1)-3,5-diphenyl tetrazolium bromide (MTT) assay. Transwell migration assay was used to detect the abilities of cell invasion and migration. The relative protein and mRNA expressions of miR-212-5p were detected by Western blot and quantitative Real-time polymerase chain reaction (qRT-PCR) analysis, respectively. Furthermore, bioinformatics online sites and luciferase reporter gene assay were performed to predict and verify the potential targets of miR-212-5p, respectively. RESULTS: The expression level of miR-212-5p in ccRCC tissues and cell lines was significantly inhibited. Bioinformatics online sites and luciferase reporter gene assay confirmed that T-box transcription factor TBX15 (TBX15) was the potential target gene of miR-212-5p. In vitro experiments demonstrated that the proliferation, cell cycle, cell invasion and migration of ccRCC cells were obviously restricted after up-regulation of miR-212-5p. However, the above functional effects were significantly abolished in ccRCC cells after co-transfection with miR-212-5p mimics and LV-TBX15. CONCLUSIONS: MiR-212-5p acted as a tumor suppressor gene in ccRCC. Through targeting TBX15, miR-212-5p significantly inhibited the malignant behavior of ccRCC cells. Our findings revealed that miR-212-5p/TBX15 axis might be a potential therapeutic target for the treatment of ccRCC. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Long noncoding RNAs (lncRNAs) have been reported to be vital in tumor progression. Hepatocellular carcinoma (HCC) is a common type of fatal primary liver cancers worldwide. This study aims to determine whether lncRNA SNHG7 (small nucleolar RNA host gene 7) functions in the metastasis of HCC. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was conducted to detect the SNHG7 expression in HCC cells and tissue samples. Moreover, function assays were performed in vitro to identify the role of SNHG7 in metastasis of HCC cells. Western blot assay was used to explore the possible mechanism. RESULTS: SNHG7 expression was remarkably higher in HCC tissues than that in adjacent tissues. Moreover, HCC migration and invasion were suppressed after silence of SNHG7 in HCC cells. Moreover, after silence of SNHG7, RBM5 was upregulated in HCC cells. Besides, the expression of RBM5 in tumor tissues was negatively correlated to the expression of SNHG7. CONCLUSIONS: Our study suggests that SNHG7 could promote cell invasion and migration in HCC cells through downregulating RBM5, which may offer a new therapeutic intervention for HCC patients. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To examine the expression level of microRNA-485-5p (miRNA-485-5p) in acute myeloid leukemia (AML) and its biological function in regulating the proliferative ability of AML through targeting SALL4. PATIENTS AND METHODS: Serum level of miRNA-485-5p in AML patients and healthy controls was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). MiRNA-485-5p level in AML cell lines was detected by qRT-PCR as well. Proliferative and apoptotic changes in AML5 and U937 cells overexpressing miRNA-485-5p were assessed. Subsequently, the regulatory effect of miRNA-485-5p on SALL4 level was evaluated. Rescue experiments were conducted to uncover the role of miRNA-485-5p/SALL4 regulatory loop in regulating cellular behaviors of AML. RESULTS: Compared with healthy controls, serum level of miRNA-485-5p was lower in AML patients. MiRNA-485-5p was similarly downregulated in AML cell lines. Overexpression of miRNA-485-5p stimulated proliferation and alleviated apoptosis in AML. SALL4 level was downregulated by transfection of miRNA-485-5p mimics in AML5 and U937 cells. Overexpression of SALL4 could reverse the regulatory effect of miRNA-485-5p on proliferative and apoptotic abilities of AML. CONCLUSIONS: MiRNA-485-5p is downregulated in AML. Overexpression of miRNA-485-5p alleviates the malignant progression of AML through downregulating SALL4. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate the inhibitory role of microRNA- 1299 (miR-1299) in prostate cancer, and to explore the possible underlying mechanism. PATIENTS AND METHODS: The expression of miR-1299 in 35 PCa tissues and para-carcinoma tissues, as well as PCa cell lines (PC-3) and prostatic epithelial cell line (RWPE-1), was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Then, we explored the possible targets of miR-1299 by searching online databases. NIMA-related kinase 2 (NEK2) was identified as a direct target gene of miR-1299. Subsequently, qRT-PCR, Western blot (WB), and luciferase reporter gene assay were used to further verify the correlation between miR-1299 and NEK2. To better characterize the role of miR-1299 and NEK2 in PCa, we conducted functional experiments (MTT, flow cytometry, scratch-wound, and transwell assay) by transfecting PC-3 cells with miR-1299 mimics and si- NEK2 in different groups. RESULTS: The expression level of miR-1299 in PCa tissues was significantly lower than that of para-carcinoma tissues. Meanwhile, the expression of miR-1299 in PC-3 cells was also significantly downregulated when compared with RWPE-1 cells. Subsequent qRT-PCR, WB, and luciferase reporter gene assay verified that miR- 1299 transcriptionally repressed NEK2 by interacting with the essential binding sequence in 3'- UTR. Also, functional experiments demonstrated that decreased expression of NEK2 resulting from miR-1299 up-regulation could remarkably inhibit the proliferation, invasion, and migration of PCa cells. CONCLUSIONS: Our study indicated that miR-1299 was a novel suppressor in PCa through its negative regulation of NEK2. Moreover, our findings revealed that miR-1299/NEK2 axis might be a potential therapeutic target for the treatment of PCa. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To elucidate the biological functions of long non-coding RNA (lncRNA) SNHG7 in breast cancer (BC), and its underlying mechanism in the occurrence and progression of BC. PATIENTS AND METHODS: The expression of SNHG7 in 72 pairs of BC tissues and paracancerous tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). Correlation between SNHG7 expressions with pathological indicators of BC patients was analyzed. Similarly, SNHG7 expression in BC cell lines was determined by qRT-PCR as well. After constructing the small inference RNA of SNHG7, cell proliferation, migration and invasion were determined by cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and transwell assay. MicroRNA-186 expression in BC tissues and cells was accessed. Dual-luciferase reporter gene assay was conducted to verify the binding condition between SNHG7 and microRNA-186. RESULTS: SNHG7 expression was higher in BC tissues than that of paracancerous tissues. High expression of SNHG7 was positively correlated to tumor stage, lymph node metastasis and distant metastasis, whereas not correlated to age, sex and tumor location of BC. Kaplan-Meier curves revealed that higher expression of SNHG7 is correlated to the worse prognosis of BC patients. SNHG7 was highly expressed in BC cells as well. Knockdown of SNHG7 inhibited proliferative, invasive and migratory abilities of BC cells. QRT-PCR data showed that microRNA-186 is lowly expressed in BC tissues compared with that of paracancerous tissues. MicroRNA-186 was lowly expressed in BC cells as well. Both mRNA and protein levels of microRNA-186 were negatively correlated to SNHG7 in BC tissues. Finally, the dual-luciferase reporter gene assay demonstrated that SNHG7 could be directly targeted by microRNA-186. CONCLUSIONS: SNHG7 is highly expressed in BC, which is correlated to tumor stage, lymph node metastasis and distant metastasis of BC patients. SNHG7 could promote malignant progression of BC by regulating microRNA-186. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Hepatocarcinoma is a great threat to global health. MicroRNA-23a was suggested to regulate growth and apoptosis in certain cell lines. Our study was focused on growth, proliferation, and apoptosis of hepatocarcinoma cell line MHCC97H under the influence of microRNA-23a, and explored the mechanism of pro-apoptosis microRNA-23a. MATERIALS AND METHODS: MicroRNA-23a and control microRNA (scramble miRNA, for short as miRNA) were synthesized with the routine protocol. Lipofection transfection was performed in hepatocarcinoma cell line MHCC97H. 3-(4,5-dimethyl- 2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, caspase-3 activity detection, and flow cytometry were performed to examine growth, proliferation, and apoptosis of hepatocarcinoma cell line MHCC97H, respectively. Kidney inhibitor of apoptosis protein (KIAP) and small interfere RNA (siRNA) was synthesized for inhibition of KIAP. KIAP plasmid was established for activation of KIAP. Western blot was performed to examine the protein expression of KIAP and caspase protein family after transfection of KIAP siRNA or KIAP plasmid. RESULTS: Compared with miRNA transfection, microRNA-23a transfection significantly reduced the growth of MHCC97H cells, and decreased the expression of KIAP (p < 0.05). Enhanced translocation of phosphatidylserine and activation of caspase-3 were observed in microRNA-23a transfection cells. Moreover, inhibition of KIAP enhanced the pro-apoptosis effect of microRNA-23a, while activation of KIAP abrogated pro-apoptosis effect of microRNA- 23a. CONCLUSIONS: MicroRNA-23a inhibits growth and proliferation of MHCC97H cells, and induces apoptosis of MHCC97H cells via down-regulating KIAP. KIAP could be a potential therapeutic target for hepatocarcinoma treatment. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To evaluate the plaque distribution and composition pattern in the left main coronary artery (LMCA) disease using intracoronary ultrasound. PATIENTS AND METHODS: Intravascular ultrasound data of 50 patients from the January 2010 to December 2015 with significant LMCA bifurcation lesions, with angiographic diameter stenosis >50%, and requiring revascularization, were evaluated. Plaque burden and percentage of necrotic core (% NC) at the minimal lumen area site and maximal % NC site were measured in different segments. The segments that were included in the study are as follows: segment 1: proximal LMCA, segment 2: left anterior descending (LAD) ostium, segment 3: left circumflex branch (LCX) ostium, segment 4: proximal LAD, segment 5: proximal LCX. According to its relationship with the bifurcation ridge, the blood vessel wall was divided into the contralateral bifurcation ridge blood vessel wall and bifurcation ridge blood vessel wall. RESULTS: Plaque burden results showed that the plaque eccentricity index of segment 2 and segment 3 was significantly higher than that of the other segments at sites of the minimal lumen area and maximal % NC with a statistically significant difference (p<0.05). Plaque eccentricity index of contralateral bifurcation ridge was significantly higher than that of the bifurcation ridge, and the difference was statistically significant (p<0.05). Analysis of plaque composition showed the fibrous tissue percentage of segment 2 and segment 3 was significantly higher than the other segments that at the sites of minimal lumen area and the maximal % NC site. The fibrous percentage of the contralateral bifurcation ridge was significantly lower than that of the bifurcation ridge. CONCLUSIONS: Intravascular ultrasound is an effective way for detecting the distribution and composition of the atherosclerotic plaque at the left main coronary artery bifurcation and is of great significance to adjuvant interventional therapy. [ABSTRACT FROM AUTHOR]

A correction is presented to the article "Long noncoding RNA SNHG7 represses the expression of RBM5 to strengthen metastasis of hepatocellular carcinoma" which appeared in the 2020 issue.