Tumor xenograft animal models for esophageal squamous cell carcinoma

Lee, Nikki P.; Chan, Chung Man; Tung, Lai Nar; Wang, Hector K.; Law, Simon

doi:10.1186/s12929-018-0468-7

Cited by 58 publications

(36 citation statements)

References 37 publications

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“…Although certain variables, such as the site of implantation, the properties of cell lines, and the growth properties of the xenograft, can affect the stability and reproducibility of xenograft formation 35 , 36 , cell line-derived xenograft models have been widely used in cancer research attribute to its high accessibility in laboratory settings 37 . Here, based on the results of our preliminary experiments, HCT116 cells were chosen to produce stable xenograft in mice in our system.…”

Section: Discussionmentioning

confidence: 99%

TAp63α targeting of Lgr5 mediates colorectal cancer stem cell properties and sulforaphane inhibition

et al. 2020

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Cancer stem cells (CSCs) have an established role in cancer progression and therapeutic resistance. The p63 proteins are important transcription factors which belong to the p53 family, but their function and mechanism in CSCs remain elusive. Here, we investigated the role of TAp63α in colorectal CSCs and the effects of sulforaphane on TAp63α. We found that TAp63α was upregulated in spheres with stem cell properties compared to the parental cells. Overexpression of TAp63α promoted self-renewal capacity and enhanced CSC markers expression in colorectal sphere-forming cells. Furthermore, we showed that TAp63α directly bound to the promoter region of Lgr5 to enhance its expression and activate its downstream β-catenin pathway. Functional experiments revealed that sulforaphane suppressed the stemness of colorectal CSCs both in vitro and in vivo. Upregulation of TAp63α attenuated the inhibitory effect of sulforaphane on colorectal CSCs, indicating the role of TAp63α in sulforaphane suppression of the stemness in colorectal cancer. The present study elucidated for the first time that TAp63α promoted CSCs through targeting Lgr5/β-catenin axis and participated in sulforaphane inhibition of the stem cell properties in colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

TAp63α targeting of Lgr5 mediates colorectal cancer stem cell properties and sulforaphane inhibition

et al. 2020

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“…These findings indicate that PLOD2 directly promotes breast cancer metastasis and mediates adipocyte-driven migration and invasion. In this study, We chose the xenograft model to study the tumor microenvironment interactions which is stable and most commonly used model at present [39, 40]. But actually, Using a xenograft model in this experiment has some disadvantages, for instance, the tumor component is human while the environment is mouse that will lead to insufficiently reflect the physiological environment in humans.…”

Section: Discussionmentioning

confidence: 99%

Adipocyte-derived IL-6 and leptin promote breast Cancer metastasis via upregulation of Lysyl Hydroxylase-2 expression

Wei

et al. 2018

Cell Commun Signal

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BackgroundAdipocytes make up the major component of breast tissue, accounting for 90% of stromal tissue. Thus, the crosstalk between adipocytes and breast cancer cells may play a critical role in cancer progression. Adipocyte-breast cancer interactions have been considered important for the promotion of breast cancer metastasis. However, the specific mechanisms underlying these interactions are unclear. In this study, we investigated the mechanisms of adipocyte-mediated breast cancer metastasis.MethodsBreast cancer cells were cocultured with mature adipocytes for migration and 3D matrix invasion assays. Next, lentivirus-mediated loss-of-function experiments were used to explore the function of lysyl hydroxylase (PLOD2) in breast cancer migration and adipocyte-dependent migration of breast cancer cells. The role of PLOD2 in breast cancer metastasis was further confirmed using orthotopic mammary fat pad xenografts in vivo. Clinical samples were used to confirm that PLOD2 expression is increased in tumor tissue and is associated with poor prognosis of breast cancer patients. Cells were treated with cytokines and pharmacological inhibitors in order to verify which adipokines were responsible for activation of PLOD2 expression and which signaling pathways were activated in vitro.ResultsGene expression profiling and Western blotting analyses revealed that PLOD2 was upregulated in breast cancer cells following coculture with adipocytes; this process was accompanied by enhanced breast cancer cell migration and invasion. Loss-of-function studies indicated that PLOD2 knockdown suppressed cell migration and disrupted the formation of actin stress fibers in breast cancer cells and abrogated the migration induced by following coculture with adipocytes. Moreover, experiments performed in orthotopic mammary fat pad xenografts showed that PLOD2 knockdown could reduce metastasis to the lung and liver. Further, high PLOD2 expression correlated with poor prognosis of breast cancer patients. Mechanistically, adipocyte-derived interleukin-6 (IL-6) and leptin may facilitate PLOD2 upregulation in breast cancer cells and promote breast cancer metastasis in tail vein metastasis assays. Further investigation revealed that adipocyte-derived IL-6 and leptin promoted PLOD2 expression through activation of the JAK/STAT3 and PI3K/AKT signaling pathways.ConclusionsOur study reveals that adipocyte-derived IL-6 and leptin promote PLOD2 expression by activating the JAK/STAT3 and PI3K/AKT signaling pathways, thus promoting breast cancer metastasis.Electronic supplementary materialThe online version of this article (10.1186/s12964-018-0309-z) contains supplementary material, which is available to authorized users.

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“…They are not true tumors: this is exemplified by the fact that no one has been able to produce a satisfactory xenograft animal model of keloids, whereas such models are readily created for neoplasms. 116 However, they do share some quasi-neoplastic features, as follows. First, at the clinical level, they demonstrate continuous growth in volume, gradually invade into the adjacent healthy skin, recur easily after surgery, respond to radiotherapies, chemotherapies and immunotherapies that are effective for tumors, 38 and occasionally, after frequent ulceration, exhibit malignant transformation and metastasis.…”

Section: Effect Of Exercisementioning

confidence: 99%

Systemic factors that shape cutaneous pathological scarring

Huang

Ogawa

2020

FASEB j.

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Cutaneous pathological scars are fibrotic lesions that grow continuously, invade the adjacent skin, and are erythematous, itchy, and painful. Their etiology remains unclear but may involve genetic, local mechanical, and systemic factors. Here, we will summarize the main systemic factors that shape cutaneous pathological scarring, especially keloid formation and aggravation. They include circulating cytokines, chemokines, growth factors, particular cell types, sex hormones, the systemic renin‐angiotensin system, and vitamin D, all of which directly shape the angiogenesis, inflammation, fibrosis, and remodeling in pathological scars. There are also several environmental factors that more indirectly influence pathological scar formation or progression, namely diet, smoking, psychological stress, and exercise. Notably, much of the evidence on these systemic factors focus on their effects on one pathological scar characteristic, namely their fibrosis. However, systemic factors probably also shape other pathological scar characteristics. We describe two new avenues of keloid research that may greatly improve our understanding of pathological scarring and the systemic factors that affect it. One is the multiple similarities between keloids and tumors; the other is the different stem‐cell populations in keloids. We expect this research will greatly aid the development of diagnostic biomarkers for cutaneous pathological scars and drugs/techniques/regimens that prevent, improve, or cure these scars.

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Tumor xenograft animal models for esophageal squamous cell carcinoma

Cited by 58 publications

References 37 publications

TAp63α targeting of Lgr5 mediates colorectal cancer stem cell properties and sulforaphane inhibition

TAp63α targeting of Lgr5 mediates colorectal cancer stem cell properties and sulforaphane inhibition

Adipocyte-derived IL-6 and leptin promote breast Cancer metastasis via upregulation of Lysyl Hydroxylase-2 expression

Systemic factors that shape cutaneous pathological scarring

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