RESUMO
We detected some serious inaccuracies and mistakes. Therefore, the article "Long non-coding RNA LINP1 promotes the malignant progression of prostate cancer by regulating p53, by H.-F. Wu, L.-G. Ren, J.-Q. Xiao, Y. Zhang, X.-W. Mao, L.-F. Zhou, published in Eur Rev Med Pharmacol Sci 2018; 22 (14): 4467-4476-DOI: 10.26355/eurrev_201807_15498-PMID: 30058678" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/15498.
RESUMO
OBJECTIVE: We aim to investigate the expression of long non-coding RNA-LINP1 (lncRNA LINP1) in prostate cancer (PCa) and its potential mechanism. PATIENTS AND METHODS: The expression of lncRNA LINP1 in 74 pairs of PCa and normal tissues were detected by quantitative Real-time polymerase chain reaction (qRT-PCR); the relationship between its expression and the pathological features and prognosis of PCa was also analyzed. The expression of lncRNA LINP1 in the PCa cell line was verified by qRT-PCR. Knockdown of LINP1 was constructed by transfection of small interfering RNA (siRNA) in two PCa cell lines (Lncap and PC-3). The biological function of LINP1 was evaluated by cell counting kit-8 (CCK-8) assay, colony formation assay, migration and invasion assay, respectively. Finally, the potential mechanism of LINP1 was explored by Western blot and qRT-PCR. RESULTS: qRT-PCR results showed a higher expression of LINP1 in PCa than that of normal tissues. Compared with PCa patients with a lower expression of LINP1, those with higher expression had a higher tumor stage, lymphatic metastasis and distant metastasis rate, and lower overall survival rate. Proliferation, invasion and metastasis in cells transfected with si-LINP1 were remarkably decreased than those transfected with negative control (si-NC). Moreover, the expressions of the key proteins in the p53 signaling pathway, including p53, PTEN, Akt and CDK2 were remarkably decreased in cells after knockdown of LINP1. In addition, a negative correlation between LINP1 and p53 was confirmed by rescue experiments. CONCLUSIONS: Up-regulated LINP1 in PCa was correlated with a higher PCa stage, lymphatic metastasis, distant metastasis, and worse prognosis. Furthermore, LINP1 could promote the proliferative, migratory and invasive abilities of PCa by regulating the p53-signaling pathway.
Assuntos
Regulação Neoplásica da Expressão Gênica , Neoplasias da Próstata/genética , RNA Longo não Codificante/metabolismo , Proteína Supressora de Tumor p53/metabolismo , Progressão da Doença , Técnicas de Silenciamento de Genes , Humanos , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Prognóstico , Próstata/patologia , Neoplasias da Próstata/mortalidade , Neoplasias da Próstata/patologia , RNA Longo não Codificante/genética , RNA Interferente Pequeno , Transdução de Sinais/genética , Regulação para CimaRESUMO
Chronic obstructive parotitis (COP) is a common disease of the parotid gland. A total of 104 patients with COP were identified and randomized into a treatment group (52 cases) and a control group (52 cases). All patients underwent sialography and salivary gland scintigraphy (SGS) examinations before surgery. The patients in the treatment group received chymotrypsin combined with gentamicin via interventional sialendoscopy to irrigate the duct, and the control group received gentamicin alone. All patients were asked to record their pain on a visual analogue scale (VAS) before treatment and at 1 week, 2 weeks, 1 month, 3 months, and 6 months after surgery. The VAS score for pain intensity was decreased at 1 week post-treatment in both groups (P<0.05). Compared to the control group, the VAS score was lower in the treatment group at 1 week, 2 weeks, and 1 month post-treatment (P<0.05). The 6-month postoperative SGS results showed improved uptake and excretion in both groups (P<0.05). The treatment group exhibited higher scores for postoperative SGS excretion than the control group (P<0.05). The administration of chymotrypsin combined with gentamicin by sialendoscopy is effective for the treatment of non-stone-related COP and specifically improves the excretion function of the parotid gland.
