Journal of Cellular Physiology最新文献

Cancer stem cells (CSCs) are considered the major cause of the occurrence, progression, chemoresistance/radioresistance, recurrence, and metastasis of cancer. Increased interstitial fluid pressure (IFP) is a key feature of solid tumors. Our previous study showed that the distribution of liver cancer stem cells (LCSCs) correlated with the mechanical heterogeneity within liver cancer tissues. However, the regulation of liver cancer's mechanical microenvironment on the LCSC stemness is not fully understood. Here, we employed a cellular pressure-loading device to investigate the effects of normal IFP (5 mmHg), as well as increased IFP (40 and 200 mmHg) on the stemness of LCSCs. Compared to the control LCSCs (exposure to 5 mmHg pressure loading), the LCSCs exposed to 40 mmHg pressure loading exhibited significantly upregulated expression of CSC markers (CD44, EpCAM, Nanog), enhanced sphere and colony formation capacities, and tumorigenic potential, whereas continuously increased pressure to 200 mmHg suppressed the LCSC characteristics. Mechanistically, pressure loading regulated Yes-associated protein (YAP) activity and Bcl-2 modifying factor (BMF) expression. YAP transcriptionally regulated BMF expression to affect the stemness of LCSCs. Knockdown of YAP and overexpression of BMF attenuated pressure-mediated stemness and tumorgenicity, while YAP-deficient and BMF-deletion recused pressure-dependent stemness on LCSCs, suggesting the involvement of YAP/BMF signaling axis in this process. Together, our findings provide a potential target for overcoming the stemness of CSCs and elucidate the significance of increased IFP in cancer progression.

Alkaptonuria (AKU) is a progressive systemic inherited metabolic disorder primarily affecting the osteoarticular system, characterized by the degeneration of cartilage induced by ochronosis, ultimately leading to early osteoarthritis (OA). However, investigating AKU pathology in human chondrocytes, which is crucial for understanding the disease, encounters challenges due to limited availability and donor variability. To overcome this obstacle, an in vitro model has been established using homogentisic acid (HGA) to simulate AKU conditions. This model employed immortalized C20/A4 human chondrocytes and serves as a dependable platform for studying AKU pathogenesis. Significantly, the model demonstrates the accumulation of ochronotic pigment in HGA-treated cells, consistent with findings from previous studies. Furthermore, investigations into inflammatory processes during HGA exposure revealed notable oxidative stress, as indicated by elevated levels of reactive oxygen species and lipid peroxidation. Additionally, the model demonstrated HGA-induced inflammatory responses, evidenced by increased production of nitric oxide, overexpression of inducible nitric oxide synthase, and cyclooxygenase-2. These findings underscore the model's utility in studying inflammation associated with AKU. Moreover, analysis of serum amyloid A and serum amyloid P proteins revealed a potential interaction, corroborating evidence of amyloid fibril formation. This hypothesis was further supported by Congo red staining, which showed fibril formation exclusively in HGA-treated cells. Overall, the C20/A4 cell model provided valuable insights into AKU pathogenesis, emphasizing its potential for facilitating drug development and therapeutic interventions.

Histone lysine 2-hydroxyisobutyrylation (Khib) was identified as a novel posttranslational modification in 2014. Significant progress has been made in understanding its roles in reproduction, development, and disease. Although 2-hydroxyisobutyrylation shares some overlapping modification sites and regulatory factors with other lysine residue modifications, its unique structure suggests distinct functions. This review summarizes the latest advancements in Khib, including its regulatory mechanisms, roles in mammalian physiological processes, and its relationship with diseases. This provides direction for further research on Khib and offers new perspectives for developing treatment strategies for related diseases.

RETRACTION: C. Shi, T. Liu, J. Chi, H. Luo, Z. Wu, B. Xiong, S. Liu, Y. Zeng, “LINC00339 promotes gastric cancer progression by elevating DCP1A expression via inhibiting miR-377-3p,” Journal of Cellular Physiology 234, no. 12 (2019): 23667-23674, https://doi.org/10.1002/jcp.28934.

The above article, published online on 12 June 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Alexander Hutchison; and Wiley Periodicals LLC.

The retraction has been agreed upon the authors' request due to concerns related to the data presented in the article. In the following investigation performed by the journal, several inconsistencies between results presented and experimental methods described were found. Specifically, the experimental methods were found to lack or have unavailable supporting data, making the experiments not comprehensible to readers. Additionally, the raw data provided do not entirely support the results presented. Accordingly, the conclusions of this article are considered invalid by the editors.

This article corrects the following:

MitoNEET prevents iron overload-induced insulin resistance in H9c2 cells through regulation of mitochondrial iron.

Tam, Eddie, Hye K. Sung, and Gary Sweeney

Volume 238, Issue 8, Journal of Cellular Physiology

https://doi.org/10.1002/jcp.31044

First published online: 03 June 2023

In the original version of the article, the Mfn2 Western blot image in Figure 3g was not correctly displayed.

Please find corrected Figure 3g with correct display of Mfn2 Western blot image below.

RETRACTION: W. Li, S. Ma, X. Bai, W. Pan, L. Ai and W. Tan, “Long Noncoding RNA WDFY3-AS2 Suppresses Tumor Progression by Acting as a Competing Endogenous RNA of MicroRNA-18a in Ovarian Cancer,” Journal of Cellular Physiology 235, no. 2 (2020): 1141–1154, https://doi.org/10.1002/jcp.29028.

The above article, published online on 25 July 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Alexander Hutchison; and Wiley Periodicals LLC. The retraction has been agreed due to several instances of duplications of Western Blot bands found between Figures 3j, 5k and 7i of this article and figures from another article published elsewhere in the same year by different authors. The authors were invited to comment on the concerns raised but did not respond. The editors consider the results and conclusion reported in this article unreliable.

RETRACTION: M. Du, Y. Zhuang, P. Tan, Z. Yu, X. Zhang, A. Wang, “MicroRNA-95 Knockdown Inhibits Epithelial–mesenchymal Transition and Cancer Stem Cell Phenotype in Gastric Cancer Cells through MAPK Pathway by Upregulating DUSP5,” Journal of Cellular Physiology 235, no. 2 (2020): 944-956, https://doi.org/10.1002/jcp.29010.

The above article, published online on 15 July 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, the article makes use of unverifiable/unknown and/or contaminated cell lines. Additionally, the description of experimental methods is insufficient and relevant supporting data is unavailable, making the foundation of the study not comprehensible and/or reproducible to readers. Accordingly, the conclusions of this article are considered invalid by the editors. The authors have been informed of the decision of retraction but unavailable for a final confirmation.

RETRACTION: Ling Liu, Tan-Tan Yu, Chen-Chen Ren, Li Yang, Shi-Hong Cui, Xiao-An Zhang, “CP-31398 inhibits the progression of cervical cancer through reversing the epithelial mesenchymal transition via the downregulation of PAX2s,” Journal of Cellular Physiology 234, no. 3 (2019): 2929-2942, https://doi.org/10.1002/jcp.27109.

The above article, published online on 21 August 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Alexander Hutchison; and Wiley Periodicals LLC. The retraction has been agreed due to concerns related to the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Additionally, duplications affecting Figures 5a and 5c, and Figure 8a and 8c have been detected. Accordingly, the conclusions of this article are considered invalid by the editors.

Septic cardiomyopathy (SCM) is an acute cardiac dysfunction involving myocardial cell pyroptosis. TREM-1 is a known receptor on cell membrane that can amplify the inflammatory response. Our previous studies have shown that TREM-1 in cardiomyocytes is involved in the activation of NLRP3 through the SMC4/NEMO pathway. Here, we aimed to use Trem-1 and Nlrp3 knockout mice to verify the effect of TREM-1 through NLRP3 on cardiac function in septic mice. The results showed that TREM-1 knockout resulted in a decrease in the release of downstream cell signals, including SMC4 and NLRP3, resulting in a decrease in cytokine release and improvement of cardiac dysfunction. Knockout of NLRP3 also reduced cardiomyocyte pyroptosis and increased survival rate. The therapeutic targeting of TREM-1 activation of NLRP3 and its pathway may contribute to the treatment or prevention of SCM.

The transcription factor SOX9 is integral to tissue homeostasis and is implicated in skeletal malformation, campomelic dysplasia, and osteoarthritis (OA). Despite extensive research, the complete regulatory landscape of SOX9 transcriptional activity, interconnected with signaling pathways (TGFβ, WNT, BMP, IHH, NFκB, and HIF), remains challenging to decipher. This study focuses on elucidating SOX9 signaling in OA pathology using Fluorescence Recovery After Photobleaching (FRAP) to assess SOX9 activity directly in live human primary chondrocytes (hPCs). Single cell FRAP data revealed two distinct subpopulations with differential SOX9 dynamics, showing varied distribution between healthy and OA hPCs. Moreover, inherently elevated SOX9-DNA binding was observed in healthy hPCs compared to preserved and OA counterparts. Anabolic factors (BMP7 and GREM1) and catabolic inhibitors (DKK1 and FRZb) were found to modulate SOX9 transcriptional activity in OA-hPCs. These findings provide valuable insights into the intricate regulation of SOX9 signaling in OA, suggesting potential therapeutic avenues for modulating SOX9 activity in diseased states.