CD36 enrichment in HER2-positive mesenchymal stem cells drives therapy refractoriness in breast cancer by Lorenzo Castagnoli, Alma Franceschini, Valeria Cancila, Matteo Dugo, Martina Bigliardi, Claudia Chiodoni, Paolo Toneguzzo, Viola Regondi, Paola A. Corsetto, Filippo Pietrantonio, Serena Mazzucchelli, Fabio Corsi, Antonio Belfiore, Antonio Vingiani, Giancarlo Pruneri, Francesca Ligorio, Mario P. Colombo, Elda Tagliabue, Claudio Tripodo, Claudio Vernieri, Tiziana Triulzi, Serenella M. Pupa

“…We provided evidence of a consistent enrichment of CD36 in HER2 + epithelial-mesenchymal transition (EMT)-like CSCs from all tested resistant cell models that mechanistically occurs via Wnt signaling pathway activation. Consistently, both in vitro and in vivo dual blockade of CD36 and HER2 increased the anti-CSC efficacy of anti-HER2 drugs favoring the transition of the therapy resistant mesenchymal CSCs into therapy-sensitive mesenchymal-epithelial transition (MET)-like epithelial state. …”
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Mesenchymal stem cells from perinatal tissues promote diabetic wound healing via PI3K/AKT activation by Jiawei Huang, Qingwen Deng, Lai Ling Tsang, Guozhu Chang, Jinghui Guo, Ye Chun Ruan, Chi Chiu Wang, Gang Li, Hon Fai Chan, Xiaohu Zhang, Xiaohua Jiang

“…Mass spectrometry revealed a conserved set of proteins including THBS1 (thrombospondin 1), SERPINE1 (serpin family E member 1), ANXA1 (annexin A1), LOX (lysyl oxidase), and ITGB1 (integrin beta-1) which are involved in extracellular matrix (ECM) organization and wound healing, with the PI3K/AKT signaling pathway playing a central role. The PEGDA/SA/Col-I hydrogel demonstrated a unique balance of mechanical and biological properties and an optimal environment for MSC viability and function. …”
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RECQL4 affects MHC class II‐mediated signalling and favours an immune‐evasive signature that limits response to immune checkpoint inhibitor therapy in patients with malignant melan... by Sara Egea‐Rodriguez, Renáta Váraljai, Thierry M. Nordmann, Restuan Lubis, Manuel Philip, Florian Rambow, Alexander Roesch, Michael Flaig, Susanne Horn, Raphael Stoll, Fang Zhao, Annette Paschen, Bert Klebl, Ian D. Hickson, Dirk Schadendorf, Matthias Mann, Iris Helfrich

“…We performed gene set enrichment analysis to identify RECQL4‐dependent signalling pathways and explored the association between RECQL4 levels and immunoscores. …”
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ZC3H15 suppression ameliorates bone cancer pain through inhibiting neuronal oxidative stress and microglial inflammation by Li-Quan Huang, Ting-Xuan Yan, Bao-Sheng Wang, Hao Li, Nai-Bao Zhou

“…Additionally, microglial activation and inflammatory response in spinal cord tissues of BCP mice were also attenuated by AAV-shZC3H15, which was verified in LPS-treated microglial cells in vitro by blocking the inhibitory protein κBα (IκBα)/nuclear factor κB (NF-κB) signaling pathway. Conclusions: Our results provide evidence that suppressing ZC3H15 can alleviate BCP by restricting neuronal oxidative stress and microglial activation, contributing to the improvement of nociceptive behaviors. …”
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PreS1 deletions in genotype C HBV leads to severe hepatic inflammation and hepatocarcinogenesis via the IRE1-JNK axis by Yu-Min Choi, Junghwa Jang, Dong Hyun Kim, Ziyun Kim, Eunseo Kim, Won Hyeok Choe, Bum-Joon Kim

“…This leads to enhanced HBV replication and production of tumor-promoting inflammatory cytokines and IL6 and COX2 via the IRE1-JNK signaling pathway. Furthermore, in vivo data showed that the activation of IRE1-JNK signaling consequently leads to lipid accumulation and apoptosis within 21Del-HBV-infected hepatocytes, collectively driving severe tumorigenesis in the liver. …”
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T Cell-Derived Apoptotic Extracellular Vesicles Ameliorate Bone Loss via CD39 and CD73-Mediated ATP Hydrolysis by Yang X, Zhou Y, Zhou F, Bao L, Wang Z, Li Z, Ding F, Kuang H, Liu H, Tan S, Qiu X, Jing H, Liu S, Ma D

“…The adenosine generated by ApoEVs inhibits the inflammatory response and promotes osteogenesis through A2BR and downstream PKA signaling.Conclusion: T cell-derived ApoEVs are enriched with CD39 and CD73, enabling them to hydrolyze extracellular ATP to adenosine, thereby promoting bone regeneration via A2BR and PKA signaling pathway. Our data underscore the substantive role of T cell-derived ApoEVs to treat osteoporosis, thus providing new ideas for the development of ApoEVs-based therapies in tissue regeneration. …”
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The prognosis and metabolite changes of NSCLC patients receiving first‐line immunotherapy combined chemotherapy in different M1c categories according to 9th edition of TNM classifi... by Liang Zheng, Fang Hu, Wei Nie, Jun Lu, Bo Zhang, Jianlin Xu, Shuyuan Wang, Ying Li, Xiaoxuan Zheng, Wei Zhang, Yinchen Shen, Runbo Zhong, Tianqing Chu, Baohui Han, Hua Zhong, Xueyan Zhang

“…In comparison to M1c1 patients, M1c2 patients exhibited alterations in various pathways pretreatment, including platelet activation, linoleic acid metabolism, and the VEGF signaling pathway. Diminished levels of lipid‐associated metabolites (diacylglycerol, sphingomyelin) were correlated with adverse outcomes. …”
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Non-lethal sonodynamic therapy mitigates hypertensive renal fibrosis through the PI3K/AKT/mTORC1-autophagy pathway by DanDan Liu, Hui Wang, Jialong Li, Siqi Sheng, Shu Wang, Ye Tian

“…NL-SDT inhibited the transition of epithelial cells into myofibroblasts by activating PI3K-AKT-mTORC1-autophagy pathway in TGF-β1-induced NRK-52E cells. (3) The administration of the pathway inhibitors showed a reciprocal effect on NL-SDT-inhibited epithelial-mesenchymal transition (EMT). (1) NL-SDT reduced blood pressure temporarily in mice model of hypertensive renal fibrosis induced by Ang II. (2) NL-SDT alleviated renal fibrosis in mice model of hypertensive renal fibrosis induced by Ang II. (3) NL-SDT promoted autophagy by inhibiting PI3K-AKT-mTORC1 signaling pathway and alleviated renal fibrosis in mice model of hypertensive renal fibrosis induced by Ang II. …”
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