The Expression of Concern has been published due to concerns raised by a third party regarding duplicated Western blot bands between the Figure 5 Slug and Figure 6 Integrin 3 subpanels.A subsequent investigation by the journal team identified further inconsistencies regarding duplication of the -actin control bands in Figures 1A and3A,B.The authors were informed about the concerns but they remained unresponsive.In the absence of a satisfactory explanation and/or the original raw data, the journal team could not verify the authenticity of these figures and could not exclude that these concerns affect the conclusions of the article.Therefore, the journal has decided to issue an Expression of Concern to inform and alert the readers.

U. K. Misra and S. V. Pizzo, "Upregulation of mTORC2 Activation by the Selective Agonist of EPAC, 8-CPT-2Me-cAMP, in Prostate Cancer Cells: Assembly of a Multiprotein Signaling Complex," Journal of Cellular Biochemistry 113, no. 5 (2011): 1488-1500, https://doi.org/10.1002/jcb.24018. The above article, published online on 15 December 2011 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, duplication of image elements has been detected between Figures 4C and 7B, between Figure 7A and 7B, and within Figure 6C. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.

ABSTRACTGenerating new and efficient drugs through machine learning‐assisted quantitative structure–activity relationships (ML‐QSAR) has become a promising strategy for addressing multidrug‐resistant gram‐negative bacterial infections. We developed robust ML‐QSAR models using Genetic Function Approximation (GFA), Support Vector Machine (SVM), and Artificial Neural Network (ANN) methods to predict the activity of experimentally known quinoline‐based MsbA inhibitors, aiming to create more effective antibacterial drugs. The ML models were built using eight significant molecular descriptors: B09[N‐Cl], CATS3D_04_AA, F06[N‐O], G2i, molecular weight (MW), Mor04p, VE1sign_B(s), and VE1sign_Dz(i), along with 279 molecular fingerprints to predict the MsbA inhibition activity of quinoline‐based compounds. The molecular descriptor‐based SVM model achieved an R² of 0.9891 and a q² cross‐validation correlation of 0.9388. In contrast, the molecular fingerprint‐based SVM model had an R² of 0.9981 and a q² cross‐validation correlation of 0.7584, making it the best‐performing model. The robustness of these developed models was further validated through various internal, external, and applicability domain analyses. The most active compounds identified in this data set, compounds 31 and 40, were subsequently used to generate 62 new quinoline‐based compounds. Additionally, three modelled quinoline‐based inhibitors, M28, N7, and N23, demonstrated excellent bioactivity, binding affinity, and pharmacokinetic profiles. To support further research, the fingerprint‐based ML‐QSAR model is available as a web application, MsbA‐Pred (https://msba-mohan-amrita.streamlit.app/), which allows users to predict MsbA inhibitory activity from any device.

L. Zhang, X. Luo, F. Chen, W. Yuan, X. Xiao, X. Zhang, Y. Dong, Y. Zhang, and Y. Liu, "LncRNA SNHG1 Regulates Cerebrovascular Pathologies as a Competing Endogenous RNA Through HIF-1α/VEGF Signaling in Ischemic Stroke, " Journal of Cellular Biochemistry 119, no. 7 (2018): 5460-5472, https://doi.org/10.1002/jcb.26705. The above article, published online on 27 January 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Image elements within Figures 3 C and 6 F were found to have been published previously by different authors in different scientific contexts. The authors were invited to comment on these concerns but did not respond. Accordingly, the article is retracted as the editors have lost confidence in the integrity and reliability of the full body of data presented in the article and consider its conclusions invalid. The authors were informed of the retraction.

PANoptosis is involved in various pathological processes, but its role in acute myocardial infarction (AMI) remains unclear. This study aimed to explore the mechanism by which PANoptosis is involved in AMI. GSE172270 was used as an internal test set, and GSE159657 served as an external validation set to identify disease targets for AMI. WGCNA was performed to identify potential hub genes associated with AMI. Then, genes related to PANoptosis among the disease targets of AMI were screened. Additionally, human cardiomyocytes AC16 and mouse cardiomyocytes HL-1 were cultured in sugar-free and serum-free medium for 4 h and 12 h, and the expression of key genes regulating PANoptosis was detected by qRT-PCR. Finally, mRNA interference and overexpression experiments were conducted to verify the expression of key mRNAs. A total of 45 upregulated and 125 downregulated differentially expressed genes (DEGs) were identified in the GSE172270 data set. WGCNA identified 891 potential hub genes associated with AMI. In the GSE159657 data set, 695 upregulated and 552 downregulated DEGs were identified. Four genes related to AMI-PANoptosis (PRDX1, MMACHC, BLVRB, and TXNL1) were screened. Through qRT-PCR verification, PRDX1 was identified as the most specific and significant gene. The expression of the PANoptosis positive regulator ZPB1 was upregulated, while the PANoptosis negative regulator TAK1 was downregulated. Additionally, key cell death genes (MLKL, p-MLKL, Caspase-3, Caspase-7, and GSDMD) were upregulated in sugar-free and serum-free culture. However, PRDX1 interference reversed these effects. Our study demonstrated that PRDX1 is a key regulator of PANoptosis in AMI.

Y. Hou, L. Li, Y. Ju, Y. Lu, L. Chang, and X. Xiang, "MiR-101-3p Regulates the Viability of Lung Squamous Carcinoma Cells via Targeting EZH2," Journal of Cellular Biochemistry 118, no. 10 (2017): 3142-3149, https://doi.org/10.1002/jcb.25836. The above article, published online on 14 December 2016 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, duplication of multiple image elements within Figure 3 C and 3E has been identified. Additional flaws and inconsistencies between methodology described and results presented were found. The authors were not able to provide comprehensive raw data. Accordingly, the article is retracted as the editors have lost confidence in the integrity and reliability of the full body of data presented in the article and consider its conclusions invalid.

Lythrum anceps (Koehne) Makino (Japanese common name: "Misohagi") is an edible plant belonging to the Lythraceae family. It is mainly distributed in Asia, Northern Africa, and Europe. Plants of the genus Lythrum exhibit a broad range of biological activities including anti-inflammatory and antimicrobial activities. Because of this, the plants are used in traditional medicine to treat hemorrhage, infected wounds, and dysentery. The activation of peroxisome proliferator-activated receptor-gamma (PPARγ) is an effective target for improving insulin resistance and anti-inflammatory activity. However, PPARγ activation by the genus Lythrum remains unclear. Aiming to evaluate PPARγ activation by L. anceps, we generated a reporter cell line using an artificial chromosome vector that stably expresses dual-color beetle luciferases. Dual-color real-time bioluminescence monitoring revealed marked PPARγ activation in L. anceps extracts. Moreover, ellagic acid was identified as a PPARγ activator present in L. anceps by a bioassay-guided fractionation approach.

Glioblastoma multiforme (GBM), a highly heterogeneous CNS tumor known for its highest incidence rates and poor prognosis has shown limited success in the therapies due to hypoxia-driving immune-suppression in the tumor microenvironment (TME). Emerging evidence highlights the involvement of tumor cell-derived exosomes in tumor-associated microglia polarization via transfer of exosomal onco-proteins and miRNAs. Although the regulatory role of long noncoding RNAs (lncRNAs) in immune signaling are known, its mechanism in microglial polarization via exosomes in GBM still remains poorly understood. In our study, we found that in comparison to the normoxic GBM-derived exosomes lncRNA H19 was significantly upregulated in hypoxic GBM-derived exosomes. Hypoxic GBM-derived exosomes and secretome (conditioned media) caused the reduction in the % phagocytosis of microglia as compared with the control group. Moreover, GBM secretome caused increase in the M2-specific genes (IL10, STAT-3, CD163, CD206) in microglia indicating its polarization to the protumorigenic (M2) phenotype. LncRNA H19 knocked down GBM-secretome treatment in microglia further reduced the STAT-3 expression indicating H19 mediated signaling. Overall, our results suggest the involvement of hypoxic exosomes and lncRNA H19 in microglial polarization and H19 as a potential target.