The patient recovered uneventfully from surgery and showed satisfactory improvements in pain and ankle motion.

Ankle synovium is a potential source of MSCs for the treatment of OLT. We developed a novel harvesting technique that was simple, convenient and had no complications.

Ankle synovium is a potential source of MSCs for the treatment of OLT. We developed a novel harvesting technique that was simple, convenient and had no complications.

The purpose of this study was to explore the effect of micro ribonucleic acid (miR)-145 on the apoptosis of chondrocytes in osteoarthritis (OA), and to research the association between its targeting on B-cell lymphoma-2 (Bcl-2)/adenovirus E1B 19 kDa interacting protein 3 (BNIP3) and Notch signaling pathway and chondrocyte apoptosis.

The mouse model of OA was established via surgery, and chondrocytes were isolated and cultured in vitro. Then, the chondrocytes were transfected with miR-145 inhibitor, miR-145 mimics, miR-negative control (NC), BNIP3-siRNA and BNIP3-vector, respectively, with those normally cultured as the control. After that, the expression levels of miR-145 and BNIP3 in cells were detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR), the apoptosis rate was detected via flow cytometry, and the apoptosis level was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the target gene sequences were predicted).

MiR-145 can reduce OA-induced chondrocyte apoptosis through targeted inhibition on BNIP3 and regulation on Notch signaling pathway.

MiR-145 can reduce OA-induced chondrocyte apoptosis through targeted inhibition on BNIP3 and regulation on Notch signaling pathway.

Intervertebral disc (IVD) degeneration (IDD) is a well-known consequence of low back pain, as characterized by aberrant cell proliferation and apoptosis of nucleus pulposus (NP) cells. In the present study, we aimed to investigate the effect of lncRNA small nucleolar RNA host gene 6 (SNHG6) on deregulated functions of degenerative NP cells.

After the establishment of rat IDD models, the mRNA and protein levels of collagen-I (Col-I) and collagen II (Col-II), and mRNA level of SNHG6 were detected by using reverse transcription quantitative Real Time-PCR (RT-qPCR) and Western blot. We further investigated the role and molecular mechanisms of SNHG6 by overexpressing or silencing it in degenerative NP cells. PMX205 Cell proliferation was measured by MTT assay and EdU staning, and apoptosis was measured by flow cytometry. The target of SNHG6 was identified by starBase and Dual-Luciferase reporter assay.

Upregulation of SNHG6 was found in IDD NP cells than in normal cells, associated with higher level of Col-I and lower level of Col-II. Overexpression of SNHG6 inhibited cell proliferation and enhanced apoptosis, accompanied by increased expression of Bax, caspase-3, and p21, as well as decreased expression of Bcl-2, which was in reverse to the treatment of SNHG6 silencing. Moreover, miR-101-3p was indicated as a target of SNHG6, and inhibition of miR-101-3p reversed the effects on proliferation and apoptosis induced by SNHG6.

SNHG6 suppressed cell proliferation and induced apoptosis by increasing expression of Bax, caspase-3, p21 and decreasing Bcl-2 through targeting miR-101-3p, which suggested that SNHG6 could be a potential target in the treatment of IDD.

SNHG6 suppressed cell proliferation and induced apoptosis by increasing expression of Bax, caspase-3, p21 and decreasing Bcl-2 through targeting miR-101-3p, which suggested that SNHG6 could be a potential target in the treatment of IDD.The article “LncRNA FEZF1-AS1 promoted chemoresistance, autophagy and epithelial-mesenchymal transition (EMT) through regulation of miR-25-3p/ITGB8 axis in prostate cancer, by Z.-H. Wang, J.-H. Wang, K.-Q. Wang, Y. Zhou, J. Wang, published in Eur Rev Med Pharmacol Sci 2020; 24(5) 2281-2293-DOI 10.26355/eurrev_202003_20494-PMID 32196579” has been withdrawn from the authors. The Publisher apologizes for any inconvenience this may cause. https//www.europeanreview.org/article/20494.The article “Long non-coding RNA PVT1 regulates glioma proliferation, invasion, and aerobic glycolysis via miR-140-5p, by Y. Shao, H.-T. Chen, Q.-R. Ma, Y.-W. Zhang, Y.-Q. He, J. Liu published in Eur Rev Med Pharmacol Sci 2020; 24(1) 274-283-DOI 10.26355/eurrev_202001_19922-PMID 31957841” has been withdrawn from the authors. The Publisher apologizes for any inconvenience this may cause. https//www.europeanreview.org/article/19922.The article “Clinical significance of a new oncogenic factor P5CR1 in gastric cancer, by C.-X. Zhang, Y. Li, W.-H. Gong, J. Zhang, published in Eur Rev Med Pharmacol Sci 2020; 24(5) 2421-2427-DOI 10.26355/eurrev_202003_20509-PMID 32196593” has been withdrawn from the authors. The Publisher apologizes for any inconvenience this may cause. https//www.europeanreview.org/article/20509.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, “Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1, by Z.-B. Zhong, Y.-J. Wu, J.-N. Luo, X.-N. Hu, Z.-N. Yuan, G. Li, Y.-W. Wang, G.-D. Yao, X.-F. Ge, published in Eur Rev Med Pharmacol Sci 2019; 23(24) 10867-10873-DOI 10.26355/eurrev_201912_19790-PMID 31858555” has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https//www.europeanreview.org/article/19790.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, “Long non-coding RNA PCAT-1 promotes cardiac fibroblast proliferation via upregulating TGF-β1, by Q. Chen, C. Feng, Y. Liu, Q.-F. Li, F.-Y. Qiu, M.-H. Wang, Z.-D. Shen, G.-S. Fu, published in Eur Rev Med Pharmacol Sci 2019; 23(23) 10517-10522-DOI 10.26355/eurrev_201912_19692-PMID 31841207” has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https//www.europeanreview.org/article/19692.