LncRNA SNHG7 promotes the proliferation and inhibits apoptosis of renal cell cancer cells by downregulating CDKN1A.

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, "LncRNA SNHG7 promotes the proliferation and inhibits apoptosis of renal cell cancer cells by downregulating CDKN1A, by J.-S. Dong, B. Wu, B. Jiang, published in Eur Rev Med Pharmacol Sci 2019; 23 (23): 10241-10247-DOI: 10.26355/eurrev_201912_19661-PMID: 31841178" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19661.

Circ PSMC3 inhibits prostate cancer cell proliferation by downregulating DGCR8.

OBJECTIVE: The importance of circular RNAs in malignant tumors has attracted a lot of attention. Circular PSMC3 (CircPSMC3) is identified as a tumor suppressor in gastric cancer. The role of circPSMC3 in prostate cancer (PCa) remains unclear. Our study aims to uncover whether and how circPSMC3 functions in PCa development. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to determine the level of circPSMC3 in PCa tissues and cell lines. The relation between circPSMC3 expression and patients' prognosis was analyzed as well. CircPSMC3 lentivirus was constructed and transfected into PCa cells. Cell migration and invasion abilities were detected through wound healing assay, transwell assay, and Matrigel assay, respectively. Western blot assay was performed to detect the protein level of DGCR8. RESULTS: CircPSMC3 was lowly expressed in PCa tissues compared with adjacent normal tissues. Low expression of circPSMC3 was significantly downregulated in PCa cell lines as well. The migration and invasion abilities of PCa cells were significantly inhibited after circPSMC3 was overexpressed in vitro. Furthermore, DGCR8 expression increased remarkably via the overexpression of circPSMC3. CONCLUSIONS: CircPSMC3 could suppress PCa cell migration and invasion by upregulating DGCR8.

MicroRNA-588 regulates migration capacity and invasiveness of renal cancer cells by targeting EIF5A2.

OBJECTIVE: To investigate whether microRNA-588 was involved in the development and progression of renal cancer, and to explore its possible regulatory mechanisms. PATIENTS AND METHODS: Tumor tissues excised from renal carcinoma and adjacent normal tissues were selected for the experiment. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to analyze the expression level of microRNA-588 in tissue specimens. The relationship between the expression of microRNA-588 and the prognosis of patients with renal cell carcinoma was also evaluated. Subsequently, two renal cancer cell lines, including769-P and 786-O, were selected for functional experiments in vitro. Eukaryotic initiation factor 5A2 (pcDNA-EIF5A2) or microRNA-588 mimics was transfected into 769-P cells, respectively. Meanwhile, si-EIF5A2 or microRNA-588 inhibitor was transfected into 786-O cells. After that, the mRNA expression level of EIF5A2 was detected by qRT-PCR. The invasiveness and metastasis abilities of the two cell lines were evaluated via transwell assay. Furthermore, the levels of EIF5A2 and epithelial-mesenchymal transition (EMT)-related proteins were analyzed using Western blot. Luciferase reporter gene assay was used to confirm that microRNA-588 could directly regulate EIF5A2 expression. QRT-PCR and Western blot were performed to explore the mRNA and protein expressions of EIF5A2 in patients with highly or lowly-expressed microRNA-588. The correlation between the two molecules was evaluated using linear analysis. Through the above experiments, it was verified whether microRNA-588 could enhance the invasiveness and metastasis of renal cancer by targeting EIF5A2. RESULTS: MicroRNA-588 expression in tumor tissues of patients with renal carcinoma was significantly decreased with the increase of tumor diameter and stage. A higher level of microRNA-588 indicated significantly longer overall survival of patients. This suggested that microRNA-588 expression was negatively correlated with the prognosis of patients. Overexpression of microRNA-588 remarkably reduced the invasion and metastasis abilities of 769-P cells, as well as the expressions of EMT-related proteins. However, opposite results were observed in 786-O cells after knockdown of microRNA-588. Reporter gene assay confirmed that microRNA-588 could target bind to EIF5A2. In 769-P cells, up-regulated microRNA-588 significantly inhibited the mRNA and protein expressions of EIF5A2. However, down-regulated microRNA-588 in 786-O cells significantly enhanced the expressions of EIF5A2 at both mRNA and protein levels. Linear analysis verified that microRNA-588 was negatively correlated with EIF5A2 at the mRNA level. Additionally, the up-regulation of EIF5A2 in 769-P cells enhanced the malignancy of cancer cells and the expressions of EMT-related proteins. However, in 786-O cells, opposite results were observed after knockdown of EIF5A2. CONCLUSIONS: MicroRNA-588 was lowly expressed in renal cancer tissues and cell lines. This might lead to an increase in the protein level of EIF5A2, eventually promoting tumor invasion and metastasis.

LncRNA SNHG7 promotes the proliferation and inhibits apoptosis of renal cell cancer cells by downregulating CDKN1A.

OBJECTIVE: Recent studies have revealed that long non-coding RNAs (lncRNAs) have a crucial role in tumor progression. Renal cell cancer (RCC) is a common type of fatal gynecological cancer worldwide. This study aims to identify the role of lncRNA Small nucleolar RNA host gene 7 (SNHG7) in the progression of RCC. PATIENTS AND METHODS: Expression of lncRNA SNHG7 in both RCC cells and 50 pairs of tissue samples was detected by Real-time quantitative polymerase chain reaction (RT-qPCR). Moreover, the function of SNHG7 was identified by performing cell apoptosis assay, colony formation assay and proliferation assay in vitro. The underlying mechanism assays including RT-qPCR and Western blot assay were conducted. RESULTS: SNHG7 expression was remarkably upregulated in tumor tissues when compared with adjacent tissues. Moreover, RCC cell proliferation was inhibited and cell apoptosis was promoted after knockdown of SNHG7 in vitro. Moreover, after knockdown of SNHG7, CDKN1A was upregulated at mRNA and protein level in vitro. Furthermore, the expression of CDKN1A in tumor tissues was negatively correlated to the expression of SNHG7. CONCLUSIONS: These results above suggest that SNHG7 could promote cell proliferation and inhibit cell apoptosis in RCC through downregulating CDKN1A, which may offer a new therapeutic intervention for RCC patients.