17β-Estradiol Inhibits Mesenchymal Stem Cells-Induced Human AGS Gastric Cancer Cell Mobility via Suppression of CCL5- Src/Cas/Paxillin Signaling Pathway

Kuo, Chun Hong; Liu, Chung‐Jung; Lu, Chien Yu; Hu, Huang Ming; Kuo, Fu Chen; Liou, Yu Sen; Yang, Yuan; Hsieh, Ming Chia; Lee, Oscar K.; Wu, Deng Chyang; Wang, Sophie S.W.; Chen, Yao Li

doi:10.7150/ijms.6851

Cited by 16 publications

(9 citation statements)

References 32 publications

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“…Factors that influence both the proliferation rate and differentiation capacity of ADSCs, such as donor age, type, and location of adipose tissue (Lei et al, 2007), methods of cell isolation, and culturing conditions (Oedayrajsingh-Varma et al, 2006;Peptan et al, 2006) limit the success of ADSCs as therapeutic tool. For example, several studies have reported that hormones affect the proliferation and differentiation capacities of human or mouse MSCs (Kuo et al, 2013;Yazawa et al, 2014). Since the levels of sex hormones fluctuate during a woman's life, proliferation and differentiation of ADSCs might also be affected (Gallego et al, 2010;Hirschberg, 2012;Rossi et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Effect of pregnancy on the proliferation of rat adipose-derived stem cells

Zhang

Wang

et al. 2017

Genet. Mol. Res.

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ABSTRACT. Stem cell therapy faces many problems including poor survival rates and low viability. Enhancing the biological functions of stem cells improves efficacy of therapies. Estrogen, whose levels are elevated during pregnancy, affects the properties of bone marrow mesenchymal stem cells. Evidence suggests that adipose-derived stem cells (ADSCs), which are a type of adult mesenchymal stem cells, can be used in regenerative medicine. In fact, ADSCs from pregnant animals have been used in clinical therapies. However, the effect of the donor's reproductive status on proliferation of ADSCs is unknown. We investigated the effect of 17b-estradiol (E2) and progesterone (P) on the in vitro proliferation of ADSCs from laboratory rats. ADSCs were obtained from five different groups of 15 rats each -non-pregnant, pregnant, in perinatal period, non-pregnant and treated with E2, and non-pregnant and treated with P. Adhesion and viability of ADSCs were determined by MTT assay, and cell cycle was followed by flow cytometry. The proliferation rate of ADSCs from pregnant rats was significantly higher than those from the non-pregnant rats (P < 0.05); however, there was no statistically significant difference in proliferation rates during different phases of pregnancy (P > 0.05). Additionally, ADSCs from pregnant rats possess higher adhesion property in early stage (P1 passage) and higher proliferation rate than ADSCs from nonpregnant rats. Interestingly, ADSCs from non-pregnant rats that were treated with E2, but not those treated with P, showed higher proliferation rates than those from their untreated counterparts. These results suggest that the proliferative capacity and residence time in different cell cycle phases of ADSCs can be regulated by extrinsic factors such as estrogen concentration.

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Section: Introductionmentioning

confidence: 99%

Effect of pregnancy on the proliferation of rat adipose-derived stem cells

Zhang

Wang

et al. 2017

Genet. Mol. Res.

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“…Some previous studies tried to explain this gender difference from a physiological dimension. Speci cally, estrogen may play a large role in preventing gastric cancer [42][43][44]. Therefore, this evidence may explain to a certain extent that men (estrogen-de cient) patients with gastric cancer have a higher risk of death than women.…”

Section: Discussionmentioning

confidence: 99%

Cancer-Specific Survival Analysis in Patients with Gastric Cancer: Based on Competing Risk Model

Zhu

et al. 2020

Preprint

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BackgroundCompeting risk events are prone to cause bias in the estimation of all-cause mortality. In order to eliminate the impact of competing events on survival analysis, we constructed a competing risk model. Besides, we attempted to build nomograms to predict gastric cancer-specific mortality (GCSM) and other-cause mortality (OCM).MethodsThe competing risk model was constructed to evaluate all-cause mortality, GCSM and OCM, by using the gastric cancer data from 2004 to 2013 in the Surveillance, Epidemiology, and End Results Program (SEER) dataset. Nomograms were used to predict the risk of individual dying from gastric cancer and other causes based on competing risk model.ResultsA total of 15299 cases were screened out. The 1-year, 5-year, and 8-year survival probabilities were 48.9 %, 22.1 %, and 16.4 % for all-cause mortality, respectively. Univariate and multivariate analyses showed that sex, race, marital status, age at diagnosis, malignant, tumor diameter and TNM staging were all significant prognostic factors of gastric cancer. The GCSM and OCM models showed the risk of death treated by radiotherapy decreased from 0.689 to 0.494 after considering competing risk events. Furthermore, the nomograms showed good accuracy for GCSM prediction of the 1-,5-,8-year, the AUC values of the nomograms were 0.801 [95% CI, 0.793–0.808], 0.820 [95% CI, 0.810–0.829] and 0.823 [95% CI, 0.808–0.844]. The AUC values of the nomograms for predicting 1-, 5-, and 8-year OCM were 0.784 [95% CI, 0.778–0.792], 0.755 [95% CI, 0.748–0.765] and 0.747 [95% CI, 0.739–0.759].ConclusionsOverall, the prognosis of patients with Gastric cancer is poor. The competing risk model could accurately evaluate the probability of dying from gastric cancer and other causes. Nomograms showed relatively good performance and could be considered as convenient individualized predictive tools for predicting GCSM and OCM.

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“…Curcumin is a bioactive compound and found to abrogate the NF-κB signaling and VEGF production to attenuate the GC-MSC-triggered tumor angiogenesis ( 64 ). In addition to these, several researchers have successfully adopted specific neutralizing antibodies of IL-8, IL-6, and CCL-5 to inhibit MSC-mediated GC invasive motility, and 17β- estradiol also impair the functions of IL-8, IL-6, and CCL-5 under the same context via ceasing the activation of their downstream Src/Cas/Paxillin signaling pathway, thus hormonal therapy might be anticipated based on MSC activity ( 82 , 83 , 91 ).…”

Section: The Prospects Of Msc In Targeted Therapymentioning

confidence: 99%

Mesenchymal Stem Cells in Gastric Cancer: Vicious but Hopeful

Zhong

Zhang

et al. 2021

Front. Oncol.

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Tumor progression depends on the collaborative interactions between tumor cells and the surrounding stroma. First-line therapies direct against cancer cells may not reach a satisfactory outcome, such as gastric cancer (GC), with high risk of recurrence and metastasis. Therefore, novel treatments and drugs target the effects of stroma components are to be promising alternatives. Mesenchymal stem cells (MSC) represent the decisive components of tumor stroma that are found to strongly affect GC development and progression. MSC from bone marrow or adjacent normal tissues express homing profiles in timely response to GC-related inflammation signals and anchor into tumor bulks. Then the newly recruited “naïve” MSC would achieve phenotype and functional alternations and adopt the greater tumor-supporting potential under the reprogramming of GC cells. Conversely, both new-comers and tumor-resident MSC are able to modulate the tumor biology via aberrant activation of oncogenic signals, metabolic reprogramming and epithelial-to-mesenchymal transition. And they also engage in remodeling the stroma better suited for tumor progression through immunosuppression, pro-angiogenesis, as well as extracellular matrix reshaping. On the account of tumor tropism, MSC could be engineered to assist earlier diagnosis of GC and deliver tumor-killing agents precisely to the tumor microenvironment. Meanwhile, intercepting and abrogating vicious signals derived from MSC are of certain significance for the combat of GC. In this review, we mainly summarize current advances concerning the reciprocal metabolic interactions between MSC and GC and their underlying therapeutic implications in the future.

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17β-Estradiol Inhibits Mesenchymal Stem Cells-Induced Human AGS Gastric Cancer Cell Mobility via Suppression of CCL5- Src/Cas/Paxillin Signaling Pathway

Cited by 16 publications

References 32 publications

Effect of pregnancy on the proliferation of rat adipose-derived stem cells

Effect of pregnancy on the proliferation of rat adipose-derived stem cells

Cancer-Specific Survival Analysis in Patients with Gastric Cancer: Based on Competing Risk Model

Mesenchymal Stem Cells in Gastric Cancer: Vicious but Hopeful

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