scholarly journals Retraction: Effects of microRNA-146a on the proliferation and apoptosis of human osteoarthritis chondrocytes by targeting TRAF6 through the NF-κB signaling pathway

2021 ◽  
Vol 41 (6) ◽  
RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4441-4441
Author(s):  
Laura Fisher

Retraction of ‘Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signalling pathway in IL-1β-induced osteoarthritis chondrocytes’ by Bin Zhu et al., RSC Adv., 2018, 8, 36422–36429, DOI: 10.1039/C8RA02418A.


2018 ◽  
Vol 26 (7) ◽  
pp. 961-971 ◽  
Author(s):  
Fanfan Li ◽  
Yin Xie ◽  
Yuanyuan Wu ◽  
Mengzhou He ◽  
Meitao Yang ◽  
...  

Preeclampsia (PE) remains the leading cause of maternal and fetal morbidity and mortality. Excessive apoptosis of the placenta and poor remodeling of spiral arteries caused by insufficient invasion of trophoblast cells into uterus have been implicated in the pathogenesis of PE. Accumulating evidence showed that heat shock protein 20 (HSP20) is closely associated with the proliferation, apoptosis, and metastasis of tumor cells. However, little is known about whether HSP20 plays a role in the development of PE. In this study, we detected the apoptosis index and the expressions of HSP20 and apoptosis-associated proteins in the placentas from PE and normal pregnancies. We found that HSP20 was reversely related to the apoptosis rate and the levels of proapoptotic proteins. Moreover, we identified that HSP20 could suppress the proliferation and apoptosis of trophoblast cells, turning them into a more invasive phenotype. Additionally, H2O2-induced oxidative stress was significantly alleviated, and several key proteins on the Akt signaling pathway were upregulated in HSP20-overexpressing trophoblast cells. These findings strongly suggested that HSP20 might play a role in the remodeling of spiral arteries through affecting the invasiveness of extravillous trophoblast cells via Akt signaling pathway, and the dysregulation of it might contribute to the pathophysiology of PE.


2020 ◽  
Author(s):  
Hui Liu ◽  
Xiaobo Wang ◽  
Ouyang Jin ◽  
Denggang Fu ◽  
You Peng ◽  
...  

Abstract Background: Daidzein is one of the key bioactive substances of soybean isoflavones that has a wide range of health benefits includes antineoplastic. Epidemiological evidence suggests that soy glycogen is associated with the incidence and prognosis of lung cancer. we purposed to assess the effect and molecular mechanism of daidzein on lung cancer, and to maximize therapy outcome for individualized treatment. Methods: In this report, H1299 were cultured in a medium with 10 μM daidzein for 6 hours , we detected the expression level of apoptosis-related genes in H1299 by cDNA microarray analysis. The selected genes were further validated by using RT-PCR analysis and Western blot. Finally, We usedflow cytometry to detect cell cycle alterations, and apoptosis the proliferation and apoptosis in HELF and H1299 cells were detected by Cell counting kit-8 assays. Results: These results indicate that low concentrations of isoflavone crude extract and daidzein could significantly affect the proliferation of H1299 (Human lung adenocarcinoma) and HELF (Human embryonic lung fibroblast) cells. The results of microarray in our study suggest that apoptosis-related genes are up-regulated induced by daidzein in H1299 cells and verified by RT-qPCR, particularly TP53 and caspase9. Western blotting shows the effect of daidzein on P53 and caspase9 in HELF cells be more obvious than it in H1299 cells. While the expression of TP53 was suppressed by pifithrin-α (PFTα) in HELF and H1299 cells, the mRNA and protein expression of TP53 still increase induced by daidzein, also, the effect of apoptosis induced by daidzein is involved in the P53 apoptosis pathway through inhibition of TP53 gene expression by PFTα. Conclusions: In conclusion, daidzein affected proliferation and apoptosis in HELF and H1299 cells, and the mechanism of apoptosis involved in the P53 signaling pathway.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yong Li ◽  
Dapeng Wu ◽  
Pei Wang ◽  
Xiaohui Li ◽  
Gongning Shi

miR-195 is related to tumorigenesis and frequently inhibits cell proliferation and promotes apoptosis in various cancers, including esophageal carcinoma (EC). The mTOR/p70s6k signaling pathway, which is the major target pathway for HMGA2, regulates the survival and cell proliferation of many tumors and is commonly active in EC. The relationships of miR-195, HMGA2, and the mTOR/p70s6k signaling pathway in EC, however, remain unknown. In the present study, we found that the miR-195 level was significantly downregulated in EC tissues, while the mRNA expressions of HMGA2 were significantly upregulated. Dual-luciferase reporter assay demonstrated that HMGA2 is a target of miR-195. MTT assay and flow cytometry revealed that miR-195 overexpression inhibited cell proliferation and induced apoptosis by targeting HMGA2. We also found that HMGA2 restored the inhibitory effect of miR-195 on phosphorylation of mTOR and p70S6K. Furthermore, rapamycin, a specific inhibitor of the mTOR/p70S6K signaling pathway, decreased the levels of Ki-67 and Bcl-2/Bax ratio, inhibited cell proliferation, and promoted apoptosis in EC cells. In conclusion, upregulation of miR-195 significantly suppressed cell growth and induced apoptosis of EC cells via suppressing the mTOR/p70s6k signaling pathway by targeting HMGA2.


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