Mesenchymal stem cells promote chemoresistance by activating autophagy in intrahepatic cholangiocarcinoma

Gan, Linhe; Shen, Hao; Li, Xinduo; Han, Zhipeng; Jing, Yingying; Yang, Xue; Wu, Mengchao; Xia, Yong

doi:10.3892/or.2020.7838

Cited by 10 publications

(6 citation statements)

References 45 publications

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“…This was impressively confirmed for MSCs, as recently summarized with a focus on tumor biology [222]. Importantly, MSCs were found to release relatively high amounts of exosomes [223]. MSC-derived exosomes are of particular interest, because they can have immune suppressive properties [224].…”

Section: Msc-derived Exosomes With Protective Anti-inflammatory and A...mentioning

confidence: 67%

Melatonin and the Programming of Stem Cells

Hardeland

2022

IJMS

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Melatonin interacts with various types of stem cells, in multiple ways that comprise stimulation of proliferation, maintenance of stemness and self-renewal, protection of survival, and programming toward functionally different cell lineages. These various properties are frequently intertwined but may not be always jointly present. Melatonin typically stimulates proliferation and transition to the mature cell type. For all sufficiently studied stem or progenitor cells, melatonin’s signaling pathways leading to expression of respective morphogenetic factors are discussed. The focus of this article will be laid on the aspect of programming, particularly in pluripotent cells. This is especially but not exclusively the case in neural stem cells (NSCs) and mesenchymal stem cells (MSCs). Concerning developmental bifurcations, decisions are not exclusively made by melatonin alone. In MSCs, melatonin promotes adipogenesis in a Wnt (Wingless-Integration-1)-independent mode, but chondrogenesis and osteogenesis Wnt-dependently. Melatonin upregulates Wnt, but not in the adipogenic lineage. This decision seems to depend on microenvironment and epigenetic memory. The decision for chondrogenesis instead of osteogenesis, both being Wnt-dependent, seems to involve fibroblast growth factor receptor 3. Stem cell-specific differences in melatonin and Wnt receptors, and contributions of transcription factors and noncoding RNAs are outlined, as well as possibilities and the medical importance of re-programming for transdifferentiation.

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Section: Msc-derived Exosomes With Protective Anti-inflammatory and A...mentioning

confidence: 67%

Melatonin and the Programming of Stem Cells

Hardeland

2022

IJMS

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“…NanoDrop 2000 was used to measure protein concentration. After that, the protein was prepared with a 5x loading buffer in proportion, and the sample was performed using publishing protocols [ 16 , 17 ] with antibodies directed against α -smooth muscle actin ( α -SMA, ab5694, Abcam, Cambridge, UK), E-cadherin (ab212059, Abcam), N-cadherin (AF4039, Affinity), Slug (ab51772, Abcam), Snail (ab216347, Abcam), and Vimentin (ab92547, Abcam); the dilution of these antibodies was 1 : 1000, and β -actin (ab8227, Abcam) and GAPDH (ab9485, Abcam) ratio of these two antibodies was 1 : 100000.…”

Section: Methodsmentioning

confidence: 99%

No Effect on Tumorigenesis in MG63 Cells Induced by Co-Cultured Mesenchymal Stem Cells

Xing

Wang

et al. 2022

Journal of Oncology

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Osteosarcoma is a kind of bone tumor with an extremely high malignant degree and often occurs in adolescents. Mesenchymal stem cells are believed to play an important role in the microenvironment of osteosarcoma, but whether they promote or inhibit the development of osteosarcoma is controversial. In this study, the coexpression of mesenchymal stem cells (MSCs) with osteosarcoma cell MG63 was used to explore the effect of MSCs on MG63. We found that co-culture of MSCs with MG63 did not affect the proliferation, invasion, and migration of MG63 cells, nor did it significantly affect the epithelial- and glial-mesenchymal transformation of MG63 cells. Therefore, in this study, we obtained a new concept that MSCs neither promote nor inhibit the occurrence and development of osteosarcoma.

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“…(5) Highly activated mTOR pathway: High activation of the mTOR pathway may increase protein synthesis, leading to protein accumulation in Treg cells ( 331 ), enhancing cell metabolism, promoting the autophagy system of Treg cells, and leading to dysfunction and reduced differentiation of Treg cells ( 332 , 333 ). A study demonstrated that mTORC2 plays a proinflammatory role in blocking Treg generation in SLE.…”

Section: Renal Microenvironmentmentioning

confidence: 99%

“…The activities of these enzymes reduce the availability of amino acids (for example, tryptophan, arginine, histidine, and threonine) to surrounding T cells, inhibiting mTOR signaling via the lipid phosphatase PTEN and blocking the proliferation of Teff cells, thus promoting Treg cell induction (183). ( 5) Highly activated mTOR pathway: High activation of the mTOR pathway may increase protein synthesis, leading to protein accumulation in Treg cells (331), enhancing cell metabolism, promoting the autophagy system of Treg cells, and leading to dysfunction and reduced differentiation of Treg cells (332,333). A study demonstrated that mTORC2 plays a proinflammatory role in blocking Treg generation in SLE.…”

Section: The Role Of Treg Cell Metabolism In Lupus Nephritismentioning

confidence: 99%

A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives

Han

Tao

et al. 2022

Front. Immunol.

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Kidney disease encompasses a complex set of diseases that can aggravate or start systemic pathophysiological processes through their complex metabolic mechanisms and effects on body homoeostasis. The prevalence of kidney disease has increased dramatically over the last two decades. CD4+CD25+ regulatory T (Treg) cells that express the transcription factor forkhead box protein 3 (Foxp3) are critical for maintaining immune homeostasis and preventing autoimmune disease and tissue damage caused by excessive or unnecessary immune activation, including autoimmune kidney diseases. Recent studies have highlighted the critical role of metabolic reprogramming in controlling the plasticity, stability, and function of Treg cells. They are also likely to play a vital role in limiting kidney transplant rejection and potentially promoting transplant tolerance. Metabolic pathways, such as mitochondrial function, glycolysis, lipid synthesis, glutaminolysis, and mammalian target of rapamycin (mTOR) activation, are involved in the development of renal diseases by modulating the function and proliferation of Treg cells. Targeting metabolic pathways to alter Treg cells can offer a promising method for renal disease therapy. In this review, we provide a new perspective on the role of Treg cell metabolism in renal diseases by presenting the renal microenvironment、relevant metabolites of Treg cell metabolism, and the role of Treg cell metabolism in various kidney diseases.

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Mesenchymal stem cells promote chemoresistance by activating autophagy in intrahepatic cholangiocarcinoma

Cited by 10 publications

References 45 publications

Melatonin and the Programming of Stem Cells

Melatonin and the Programming of Stem Cells

No Effect on Tumorigenesis in MG63 Cells Induced by Co-Cultured Mesenchymal Stem Cells

A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives

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