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Background/aims: CINN is the main ingredient of the traditional Chinese medicine cinnamon. The purpose of the present study was to investigate the effects of CINN on the proliferation and apoptosis of NPC cells and to elucidate the underlying molecular mechanisms., Materials and Methods: CNE2 human NPC cells were treated with various CINN concentrations. The effects of CINN on the proliferation and apoptosis of CNE2 NPC cells were examined using the MTT assay and flow cytometric analysis. Additionally, western blotting was performed to analyze the expression of a number of cell cycle- and apoptosis-related proteins., Results: The proliferation of CNE2 cells was significantly inhibited after treatment with different CINN concentrations for various lengths of time. The inhibitory effect of CINN was concentration-and time-dependent. Flow cytometric analysis showed that 2 mmol/L CINN displayed a significant apoptosis-inducing effect. The western blot analysis results showed that KLF6, Fas-L, Bax, P53 and caspase-3 protein expression was drastically increased in the CNE2 cells after treatment with 2 mmol/L CINN, whereas Bcl-2 and cyclin D1 protein expression was markedly reduced., Conclusion: CINN inhibits the proliferation and induces the apoptosis of CNE2 cells. Therefore, CINN possesses a potential anti-tumor effect., (© 2016 The Author(s) Published by S. Karger AG, Basel.)

This document is a correction notice for an article titled "Inhibition of GSK3β activity alleviates acute liver failure via suppressing multiple programmed cell death." The correction addresses errors in Figures 3, 5, and 7 of the original article. The errors include inverted images and a change in the vertical coordinate of the graph to better illustrate the results of the experiments. The original article has been updated by the authors. The document also provides contact information for the corresponding author and licensing information for the article. [Extracted from the article]

Background: Acute liver failure (ALF) is one of the most common life-threatening diseases in adults without previous liver disease. Glycogen synthase kinase 3β (GSK3β) is a serine/threonine protein kinase that is widely distributed in the cells. Inhibition of its activity can inhibit cell death and promote autophagy through various pathways, thus providing a protective effect. In this study, we aimed to investigate the effect on ALF after inhibition of GSK3β and its potential mechanisms. Methods: D- galactosamine(D-Gal) in combination with lipopolysaccharide(LPS) was used to induce ALF in vitro and in vivo. And then GSK3β inhibitor TDZD-8 was used to explore the protective effect against ALF. After TDZD-8 treatment TUNEL staining and flow techniques were used to detect the proportion of apoptosis in liver tissues and cells respectively, while western blotting and immunofluorescence assays were performed to detect the expression levels of apoptosis, pyroptosis and necroptosis-related proteins in tissues and cells. In addition, western blotting was performed to explore the specific mechanism of hepatoprotective effect after GSK3β inhibition to detect the expression levels of TAK1, TRAF6 and HDAC3 after TRAF6 and HDAC3 inhibition alone. The co-localization of TRAF6 and HDAC3 in vitro was detected by immunofluorescence, while the interaction between TRAF6 and HDAC3 was detected by immunoprecipitation assay. Results: Both in vivo and in vitro experiments, GSK3β inhibitor TDZD-8 can significantly alleviate the progression of ALF. Inhibition of GSK3β activity could significantly reduce the level of hepatocyte apoptosis, pyroptosis, necroptosis and improve liver dysfunction and tissue damage. Furthermore, we found that hepatocyte TAK1 and TRAF6 levels decreased and HDAC3 levels increased in ALF, whereas inhibition of GSK3β upregulated TAK1 and TRAF6 levels and decreased HDAC3 expression. Conclusion: GSK3β inhibitor TDZD-8 can prevent the progression of ALF, and its action may involve the TRAF6/HDAC3/TAK1 pathway. [ABSTRACT FROM AUTHOR]

PANoptosis is a new cell death proposed by Malireddi et al in 2019, which is characterized by pyroptosis, apoptosis and necroptosis, but cannot be explained by any of them alone. The interaction between pyroptosis, apoptosis and necroptosis is involved in PANoptosis. In this review, from the perspective of PANoptosis, we focus on the relationship between pyroptosis, apoptosis and necroptosis, the key molecules in the process of PANoptosis and the formation of PANoptosome, as well as the role of PANoptosis in diseases. We aim to understand the mechanism of PANoptosis and provide a basis for targeted intervention of PANoptosis-related molecules to treat human diseases. [ABSTRACT FROM AUTHOR]

Simple Summary: Liver receptor homolog-1 (LRH-1) is highly observed in tissues with secretory function, such as the ovaries, suggesting that LRH-1 may play an essential role in the ovarian endocrine. In particular, ovarian granulosa cells (GCs) are the functional cells that produce steroid hormones. The fate of GCs directly affects follicular development or atresia. These effects were lost in granulosa-specific LRH-1-knockout mice, showing that LRH-1 is a central modulator of ovarian function. However, the underlying mechanism LRH-1 in the bovine ovaries remains unclear. We aimed to detect the effect of LRH-1 on steroid hormones in bovine GCs and explore the potential relationship between LRH-1 and the fate of GCs. The results show that LRH-1 was specifically highly expressed in GCs of atretic follicles. Mechanistically, LRH-1 induced the apoptosis of bovine GCs by the progestogen receptor signaling pathway. While this finding provided new ideas for the study of follicular atresia, it also provided a theoretical basis for the clinical diagnosis and treatment for infertility in cow. The purpose of the present investigation was to assess the function of LRH-1 on GCs and the mechanisms involved. Here, LRH- was highly expressed in the bovine GCs of atretic follicles. Treatment with 50 μM of LRH-1 agonist (DLPC) significantly induced the expression of LRH-1 (p < 0.05). In particular, LRH-1 activation blocked the progestogen receptor signaling pathway via downregulating progesterone production and progestogen receptor levels (p < 0.05), but had no effect on 17 beta-estradiol synthesis. Meanwhile, LRH-1 activation promoted the apoptosis of GCs and increased the activity of caspase 3 (p < 0.05). Importantly, upregulating the progestogen receptor signaling pathway with progestogen could attenuate the LRH-1-induced proapoptotic effect. Moreover, treatment with progestogen decreased the activity of the proapoptotic gene caspase 3 and increased the expression of antiapoptotic gene Bcl2 in LRH-1 activated GCs (p < 0.05). Taken together, these results demonstrate that LRH-1 might be dependent on the progestogen receptor signaling pathway to modulate bovine follicular atresia. [ABSTRACT FROM AUTHOR]

In monocarpic plants, stem cells are fated to die. However, the potential mechanism of stem cell death has remained elusive. Here, we reveal that the levels of two forms of reactive oxygen species (ROS), superoxide anion free radical ( O 2 · − ) and hydrogen peroxide (H2O2), show dynamic changes in the shoot apex during the plant life cycle of Arabidopsis thaliana. We found that the level of O 2 · − decreased and disappeared at four weeks after bolting (WAB), while H2O2 appeared at 3 WAB and showed a burst at 5 WAB. The timing of dynamic changes in O 2 · − and H2O2 was delayed for approximately three weeks in clv3-2, which has a longer lifespan. Moreover, exogenous application of H2O2 inhibited the expression of the stem cell determinant WUSCHEL (WUS) and promoted the expression of the developmentally programmed cell death (dPCD) marker gene ORESARA 1 (ORE1). These results indicate that H2O2 triggers an important signal inducing dPCD in stem cells. Given that O 2 · − plays roles in maintaining WUS expression and stem cell activity, we speculate that the dynamic shift from O 2 · − to H2O2 in the shoot apex results in stem cell death. Our findings provide novel insights for understanding ROS-mediated regulation during plant stem cell death. [ABSTRACT FROM AUTHOR]

Monocarpic plants have a single reproductive phase, in which their longevity is developmentally programmed by molecular networks. In the reproductive phase of Arabidopsis thaliana , the inflorescence meristem (IM) maintains a central pool of stem cells and produces a limited number of flower primordia, which result in seed formation and the death of the whole plant. In this study, we observed morphological changes in the IM at cellular and intracellular resolutions until the end of the plant life cycle. We observed four biological events during the periods from 1 week after bolting (WAB) till the death of stem cells: (1) the gradual reduction in the size of the IM, (2) the dynamic vacuolation of IM cells, (3) the loss of the expression of the stem cell determinant WUSCHEL (WUS), and (4) the upregulation of the programmed cell death marker BIFUNCTIONAL NUCLEASE1 (BFN1) in association with the death of stem cells. These results indicate that the stem cell population gradually decreases in IM during plant aging and eventually is fully terminated. We further show that the expression of WUS became undetectable in IM at 3 WAB prior to the loss of CLAVATA3 (CLV3) expression at 5 WAB; CLV3 is a negative regulator of WUS. Moreover, clv3 plants showed delayed loss of WUS and lived 6 weeks longer compared with wild-type plants. These results indicated that the prolonged expression of CLV3 at 4–5 WAB may be a safeguard that inhibits the reactivation of WUS and promotes plant death. Finally, through transcriptome analysis, we determined that reactive oxygen species (ROS) are involved in the control of plant longevity. Our work presents a morphological and physiological framework for the regulation of plant longevity in Arabidopsis. [ABSTRACT FROM AUTHOR]

The transcription factor signal transducer and activator of transcription 3 (STAT3) contributes to cell proliferation, apoptosis and motility in human cancer cells. We aim to elucidate the function of STAT3 in esophageal carcinogenesis process and molecular mechanisms. We showed that hyperactivated STAT3 in esophageal carcinogenesis tissues correlated with the overexpression of octamer transcription factor-1 (Oct-1). High STAT3 phosphorylation correlated with shorter survival compared with low STAT3 phosphorylation. STAT3 and Oct-1 expression levels affected the proliferation and colony formation of Eca-109 esophageal squamous cell carcinoma cells by altering Erk and Akt activation. Nevertheless, STAT3 regulated the migration and invasion of esophageal squamous cell carcinoma cells independent of Oct-1. In conjunction with Oct-1, STAT3 inhibited apoptosis in esophageal squamous cell carcinoma cells. Constitutively activated STAT3 in normal human esophageal epithelium cells (HET-1A) elevated Oct-1 expression,and promoted proliferation and decreased apoptosis. STAT3 activated HET-1A cells to form tumors in vivo, suggesting that overactivated STAT3 is sufficient for carcinogenesis. We further confirmed the colocalization of STAT3 and Oct-1 in the nucleus and found that STAT3 regulates the transcription and expression of Oct-1 by directly targeting its promoter. Activated STAT3 also upregulated many genes associated with Oct-1. Together, our results indicate that STAT3 plays a crucial role in esophageal carcinogenesis by regulating the cell proliferation and apoptosis in conjunction with Oct-1. [ABSTRACT FROM AUTHOR]