MiR-101 affects proliferation and apoptosis of cervical cancer cells by inhibition of JAK2.

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, "MiR-101 affects proliferation and apoptosis of cervical cancer cells by inhibition of JAK2, by H. Wei, W.-R. He, K.-M. Chen, X.-W. Wang, C.-J. Yi, published in Eur Rev Med Pharmacol Sci 2019; 23 (13): 5640-5647-DOI: 10.26355/eurrev_201907_18299-PMID: 31298355" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18299.

MiR-101 affects proliferation and apoptosis of cervical cancer cells by inhibition of JAK2.

OBJECTIVE: JAK2 expression and dysfunction play a role in tumor pathogenesis. Bioinformatics analysis revealed a targeted binding site between miR-101 and the 3'-UTR of JAK2 mRNA. This study investigated the role of miR-101 in regulating JAK2 expression and affecting the proliferation and apoptosis of cervical cancer cells. PATIENTS AND METHODS: The tumor tissues and adjacent tissues of patients with cervical cancer were collected. The expression of miR-101 and JAK2 was detected by qRT-PCR. The dual luciferase reporter gene assay validated the targeting relationship between miR-101 and JAK2. The cervical cancer Caski cells were cultured in vitro, and divided into miR-NC group and miR-101 mimic group. The expression of JAK2 and p-JAK2 was detected by Western blot, cell apoptosis was detected by flow cytometry, and cell proliferation was detected by EdU staining. RESULTS: Compared with adjacent tissues, miR-101 expression was significantly decreased, and JAK2 expression was increased in cervical cancer tissues. There was a targeted regulatory relationship between miR-101 and JAK2. Compared with HcerEpic cells, miR-101 expression in HeLa and Caski was significantly decreased, and the expression of JAK2 and p-JAK2 was significantly increased. Transfection of miR-101 mimic significantly reduced the expression of JAK2 and p-JAK2 in Caski cells, reduced cell proliferation and increased cell apoptosis. CONCLUSIONS: The decrease of miR-101 expression and the increase of JAK2 expression play a role in cervical cancer, while the increase of miR-101 expression can inhibit the proliferation and promote the apoptosis of cells by inhibiting the expression of JAK2.

Cationic amino acid transporter-2 mRNA induction by tumor necrosis factor-alpha in vascular endothelial cells.

Nitric oxide (NO) synthesis may be coupled to the activity of the cellular L-arginine transporter, namely the cationic amino acid transporter. The present study examined tumor necrosis factor (TNF)-alpha-induced alterations in the gene expression of the cationic amino acid transporter (CAT) and NO production in human umbilical vein endothelial cells. In quiescent endothelial cells, CAT-1 mRNA expression, determined by reverse transcription-polymerase chain reaction, was dominant to that of CAT-2. TNF-alpha (10 ng/ml for 1-24 h) induced a time-dependent increase in CAT-2 but not CAT-1 expression. Moreover, TNF-alpha (1-30 ng/ml) treatment for 6 h induced a concentration-dependent increase in CAT-2 mRNA expression. The upregulation of CAT-2 expression by TNF-alpha was associated with enhanced nitrite accumulation in the culture medium (70% increase compared with vehicle-treated cells at 24 h). Thus, induction of the cationic amino acid transporter may constitute one mechanism for the TNF-alpha-induced NO production in human umbilical vein endothelial cells.