Secretion of interleukin-6 by bone marrow mesenchymal stem cells promotes metastasis in hepatocellular carcinoma

Mi, Fei; Gong, Lan

doi:10.1042/bsr20170181

Cited by 51 publications

(39 citation statements)

References 43 publications

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“…which promoted POSTN expression in HNC. [33][34][35] The current study also showed that the POSTN-activated PI3K/Akt/mTOR pathway In conclusion, our work showed the relationship between BMMSC and HNC. We showed that BMMSC promoted proliferation, invasion, survival, tumorigenicity and migration of HNC through POSTN-mediated PI3K/Akt/mTOR activation.…”

Section: Discussionsupporting

confidence: 69%

“…In this study, we found that MSC‐CM could promote the expression of POSTN possibly because BMMSC could secrete many kinds of cytokines into MSC‐CM such as interleukin‐6 (IL‐6), interleukin‐10 (IL‐10), vascular endothelial growth factor (VEGF), transforming growth factor beta (TGF‐β) etc. which promoted POSTN expression in HNC . The current study also showed that the POSTN‐activated PI3K/Akt/mTOR pathway played important roles on the effect of BMMSC on HNC cells.…”

Section: Discussionsupporting

confidence: 63%

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Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/Akt/mammalian target of rapamycin

et al. 2018

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Bone marrow mesenchymal stem cells (BMMSC) have been shown to be recruited to the tumor microenvironment and exert a tumor‐promoting effect in a variety of cancers. However, the molecular mechanisms related to the tumor‐promoting effect of BMMSC on head and neck cancer (HNC) are not clear. In this study, we investigated Periostin (POSTN) and its roles in the tumor‐promoting effect of BMMSC on HNC. In vitro analysis of HNC cells cultured in BMMSC‐conditioned media (MSC‐CM) showed that MSC‐CM significantly promoted cancer progression by enhancing cell proliferation, migration, epithelial‐mesenchymal transformation (EMT), and altering expression of cell cycle regulatory proteins and inhibition of apoptosis. Moreover, MSC‐CM promoted the expression of POSTN and POSTN promoted HNC progression through the activation of the phosphoinositide 3‐kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway. In a murine model of HNC, we found that BMMSC promoted tumor growth, invasion, metastasis and enhanced the expression of POSTN and EMT in tumor tissues. Clinical sample analysis further confirmed that the expression of POSTN and N‐cadherin were correlated with pathological grade and lymph node metastasis of HNC. In conclusion, this study indicated that BMMSC promoted proliferation, invasion, survival, tumorigenicity and migration of head and neck cancer through POSTN‐mediated PI3K/Akt/mTOR activation.

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Section: Discussionsupporting

confidence: 69%

Section: Discussionsupporting

confidence: 63%

Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/Akt/mammalian target of rapamycin

et al. 2018

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“…Indeed, our array data reveals that young Sca-1 + stem cells upregulate several genes related to development, cytoskeleton reorganization, and induction of growth factors. Although it remains unclear whether healthy young BM stem cells could directly contribute to tumour formation, BM stem cells have been previously documented in promoting the growth of existing cancer cells [78,79]. Moreover, processes such as cytoskeleton remodelling have been implicated in malignant cell metastasis and tumour formation [80,81].…”

Section: Discussionmentioning

confidence: 99%

Rectification of radiotherapy-induced cognitive impairments in aged mice by reconstituted Sca-1+ stem cells from young donors

Wlodarek

Cao

Alibhai

et al. 2020

J Neuroinflammation

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Background: Radiotherapy is widely used and effective for treating brain tumours, but inevitably impairs cognition as it arrests cellular processes important for learning and memory. This is particularly evident in the aged brain with limited regenerative capacity, where radiation produces irreparable neuronal damage and activation of neighbouring microglia. The latter is responsible for increased neuronal death and contributes to cognitive decline after treatment. To date, there are few effective means to prevent cognitive deficits after radiotherapy.Methods: Here we implanted hematopoietic stem cells (HSCs) from young or old (2-or 18-month-old, respectively) donor mice expressing green fluorescent protein (GFP) into old recipients and assessed cognitive abilities 3 months post-reconstitution.Results: Regardless of donor age, GFP + cells homed to the brain of old recipients and expressed the macrophage/ microglial marker, Iba1. However, only young cells attenuated deficits in novel object recognition and spatial memory and learning in old mice post-irradiation. Mechanistically, old recipients that received young HSCs, but not old, displayed significantly greater dendritic spine density and long-term potentiation (LTP) in CA1 neurons of the hippocampus. Lastly, we found that GFP + /Iba1 + cells from young and old donors were differentially polarized to an anti-and pro-inflammatory phenotype and produced neuroprotective factors and reactive nitrogen species in vivo, respectively. Conclusion: Our results suggest aged peripherally derived microglia-like cells may exacerbate cognitive impairments after radiotherapy, whereas young microglia-like cells are polarized to a reparative phenotype in the irradiated brain, particularly in neural circuits associated with rewards, learning, and memory. These findings present a proof-of-principle for effectively reinstating central cognitive function of irradiated brains with peripheral stem cells from young donor bone marrow.

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“…In another study, . CAM, chick chorioallantoic membrane; FGF, fibroblast growth factors; GP130, glycoprotein 130; mRNA, messenger RNA; NP, nanoparticles; SEM, standard error of the mean; siRNA, small interfering RNA; STAT3, signal transducer and activator of transcription 3; S1PR1, sphingosine-1-phosphate receptor 1; TGF-β, transforming growth factor-β; TMC, N,N,N-trimethyl chitosan; VEGF, vascular endothelial growth factor it was shown that the IL-6/STAT3 pathway could promote cell invasion and metastasis (Mi & Gong, 2017).…”

Section: Discussionmentioning

confidence: 99%

Coinhibition of S1PR1 and GP130 by siRNA‐loaded alginate‐conjugated trimethyl chitosan nanoparticles robustly blocks development of cancer cells

Rostami

Nikkhoo

Khazaei-Poul

et al. 2020

Journal Cellular Physiology

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There is an interconnected network between S1P/sphingosine‐1‐phosphate receptor 1 (S1PR1), IL‐6/glycoprotein 130 (GP130), and signal transducer and activator of transcription 3 (STAT3) signaling pathways in the tumor microenvironment, which leads to cancer progression. S1P/S1PR1 and IL‐6/GP130 signaling pathways phosphorylate and activate STAT3, and it then induces the expression of S1PR1 and interleukin‐6 (IL‐6) in a positive feedback loop leading to cancer progression. We hypothesized that blockade of this amplification loop can suppress the growth and development of cancer cells. Therefore, we silenced STAT3 upstream molecules including the S1PR1 and GP130 molecules in cancer cells using small interfering RNA (siRNA)‐loaded alginate‐conjugated trimethyl chitosan (ATMC) nanoparticles (NPs). The generated NPs had competent properties including the appropriate size, zeta potential, polydispersity index, morphology, high uptake of siRNA, high rate of capacity, high stability, and low toxicity. We evaluated the effects of siRNA loaded ATMC NPs on tumor hallmarks of three murine‐derived cancer cell lines, including 4T1 (breast cancer), B16‐F10 (melanoma), and CT26 (colon cancer). The results confirmed the tumor‐suppressive effects of combinational targeting of S1PR1 and GP130. Moreover, combination therapy could potently suppress tumor growth as assessed by the chick chorioallantoic membrane assay. In this study, we targeted this positive feedback loop for the first time and applied this novel combination therapy, which provides a promising approach for cancer treatment. The development of a potent nanocarrier system with ATMC for this combination was also another aspect of this study, which should be further investigated in cancer animal models in further studies.

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Secretion of interleukin-6 by bone marrow mesenchymal stem cells promotes metastasis in hepatocellular carcinoma

Cited by 51 publications

References 43 publications

Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/Akt/mammalian target of rapamycin

Bone marrow mesenchymal stem cells promote head and neck cancer progression through Periostin‐mediated phosphoinositide 3‐kinase/Akt/mammalian target of rapamycin

Rectification of radiotherapy-induced cognitive impairments in aged mice by reconstituted Sca-1+ stem cells from young donors

Coinhibition of S1PR1 and GP130 by siRNA‐loaded alginate‐conjugated trimethyl chitosan nanoparticles robustly blocks development of cancer cells

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