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The article titled "Retraction Note: A New Porous Metal–Organic Framework Constructed from 2, 5-Thiophenedicarboxylate and Melamine Ligands: Catalysis Dye Degradation and Anti-tumor Activity in Myocardioma" has been retracted by the Editor-in-Chief and the Publisher of the Journal of Cluster Science. The retraction was prompted by evidence of systematic manipulation of the publication process, including issues with citations, phrasing, figures, and ethics approval statements. The authors have not responded to correspondence regarding the retraction. Springer Nature, the publisher, remains neutral in regards to jurisdictional claims and institutional affiliations. [Extracted from the article]

With the discovery of magnetoreceptor mechanisms in animals, it materialized the novel applications of controlling cell and animal behaviors using magnetic fields. T cells have shown to be sensitive to magnetic fields. Here, we reported that exposure to moderate SMFs (static magnetic fields) led to increased granule and cytokine secretion as well as ATP production and mitochondrial respiration from CD8+ T cells. These effects were inhibited by knocking down the Uqcrb and Ndufs6 genes of mitochondrial respiratory chain, whose transcriptions were regulated by candidate magnetoreceptor genes Isca1 and Cry1/Cry2. SMF exposure also promoted CD8+ T cell granule and cytokine secretion and repressed tumor growth in vivo. SMFs enhanced CD8+ T cell cytotoxicity, and the adoptive transfer into tumor-bearing mice resulted in enhanced antitumor effects. Collectively, our study suggests that moderate SMFs enhance CD8+ T cell cytotoxicity by promoting mitochondrial respiration and promoted the antitumor function of CD8+ T cells. [ABSTRACT FROM AUTHOR]

Glycine plays a key role in rapidly proliferating cancer cells such as A549 cells. Targeting glycine metabolism is considered as a potential means for cancer treatment. However, the drug-induced alterations in glycine metabolism have not yet been investigated. Herein, a total of 34 glycine metabolites were examined in A549 cells with or without anticancer drug treatment. This work showed all tested anticancer agents could alter glycine metabolism in A549 cells including inhibition of pyruvate metabolism and down-regulation of betaine aldehyde and 5′-phosphoribosylglycinamide. Principal component analysis and orthogonal partial least-squares discrimination analysis exhibited the difference between control and each drug-treated group. In general, cisplatin, camptothecin, and SAHA could induce the significant down-regulation of more metabolites, compared with afatinib, gefitinib, and targretin. Both glycine, serine and threonine metabolism, and purine metabolism were significantly disturbed by the treatment with afatinib, gefitinib, and targretin. However, the treatment using cisplatin, camptothecin, and SAHA was considered to be highly responsible for the perturbation of glycine, serine and threonine metabolism, and cysteine and methionine metabolism. Finally, multivariate analysis for control and all drug-treated groups revealed 11 altered metabolites with a significant difference. It implies anti-cancer agents with different mechanisms of action might induce different comprehensive changes of glycine metabolomics. The current study provides fundamental insights into the acquisition of the role of anti-cancer agents in glycine metabolism while suppressing cancer cell proliferation, and may aid the development of cancer treatment targeting glycine metabolism. [ABSTRACT FROM AUTHOR]

Purpose: The mechanisms underlying the oncogenic properties of WW domain binding protein 2 (WBP2) in breast cancer have not been fully understood. In this study, we explored the role of WBP2 in cell cycle regulation in ER+ breast cancer cells and how it is regulated in the cancer cells.Methods: The association between WBP2 expression and prognosis in ER+ breast cancer was assessed by data mining in Breast Cancer Gene-Expression Miner v4.0. Cell cycle was assessed by PI staining and flow cytometry. EdU staining was applied to visualize cells in S phase. The binding between miR-206 and WBP2 were verified by dual luciferase assay. CCK-8 assay and flow cytometric analysis were applied to assess the functional role of WBP2 and miR-206 in the cancer cells.Results: High WBP2 expression correlates with higher risk of any events (AE) and metastatic relapse (MR) and also indicates shorter AE-free survival and MR-free survival in ER+ breast cancer patients. In both MCF-7 and BT474 cells, WBP can influence the expression of G1/S-related cell cycle proteins, including p21, CDK4, and cyclin D1. In addition, WBP2 overexpression resulted in facilitated G1/S transition, while WBP2 knockdown impaired the transition. The 3'UTR of WBP2 has a conserved miR-206 binding site. Functionally, miR-206 knockdown decreased tamoxifen sensitivity in tamoxifen-sensitive (TamS) MCF-7 cells, while miR-206 overexpression and WBP2 knockdown enhanced the sensitivity in tamoxifen-resistant (TamR) MCF-7 cells.Conclusion: Based on these findings, we infer that the miR-206/WBP2 axis can modulate tamoxifen sensitivity via regulating G1/S progression in ER+ breast cancer. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study was to investigate the effect of Ki67-ZD55-IL-24 with temozolomide (TMZ) against melanoma in mice. Methods: Seventy-eight mice with subcutaneous injection of A375 cells (2 × 10) into the right flank were randomized to receive phosphate buffered saline (PBS), Ki67-ZD55, Ki67-ZD55-IL-24, TMZ, TMZ + Ki67-ZD55, and TMZ + Ki67-ZD55-IL-24. Six mice were killed in each group 10 days after intervention for detecting IL-24 mRNA and protein expression. The remaining mice were monitored to draw the body weight change curve and tumor growth curve, and killed 30 days after intervention. Tumors were excised and weighted. The morphology of tumor tissues was determined by hematoxylin and eosin (HE) staining, and the apoptosis index and rate of apoptotic cells were determined by TUNEL assay and AnnexinV-FITC/PI double staining, respectively. Results: The Ki67-ZD55-IL-24-treated group generated much more reactive oxygen species than the untreated group. There was no significant difference in IL-24 expression between Ki67-ZD55-IL-24 and TMZ + Ki67-ZD55-IL-24 groups. Immunohistochemical analysis and Western blot revealed that both the Ki67-ZD55 and Ki67-ZD55-IL-24 could significantly reduce the expression of MGMT. Toxicity assessments demonstrated that mice in the three groups that received TMZ exhibited significant body weight loss following treatment. HE staining showed that TMZ + Ki67-ZD55-IL-24 group had much fewer karyokinesis in the tumors, compared with other groups. The apoptosis index of tumor tissues and the rate of apoptotic cells were significantly higher in TMZ + Ki67-ZD55-IL-24 group than in other groups (all P < 0.05). Conclusions: These findings indicate this novel strategy holds promising potentials for treatment of malignant melanoma. [ABSTRACT FROM AUTHOR]