MicroRNA‑638 expression change in osteosarcoma patients via PLD1 and VEGF expression

Xue, Mei; Shen, Jinhu; Cui, Jie; Wu, Jinxia; Qiao, Wei; Ding, Ningding; Song, Chengjie; Shan, Bin

doi:10.3892/etm.2019.7429

Cited by 7 publications

(8 citation statements)

References 22 publications

(47 reference statements)

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“…VEGF activates pro-survival signaling pathways leading to tumor growth and ultimately malignancy [5][6][7][8][9][10]. Therefore, a number of studies have been performed to investigate VEGF expression from solid tumors; it is critical and necessary to understand the intricate balance between pro-survival and anti-survival tendencies of tumors and detect potential malignancy [4,9,[11][12][13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

“…Currently, studies of VEGF secretion from the spheroids using microfluidic systems are limited to qualitative or semi-quantitative analysis based on analysis of RNA [ 7 , 16 , 17 , 43 ] rather than direct measurement of the protein itself. Several studies using anti-cancer agents on spheroid systems have concluded that physical properties of spheroids are related to drug efficacy [ 50 , 51 ].…”

Section: Introductionmentioning

confidence: 99%

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Comparison of VEGF-A secretion from tumor cells under cellular stresses in conventional monolayer culture and microfluidic three-dimensional spheroid models

2020

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Vascular endothelial growth factor (VEGF) is a major cytokine in tumor biology affecting tumor survival, aggressiveness and pro-angiogenetic activities. In addition, cellular stresses often result in aggressive pro-angiogenetic behavior in tumors. For in vitro study, conventional monolayer cell culture has been broadly exploited; however, it often provides limited information due to its different microenvironment from that in vivo. Recently, three-dimensional (3D) cell spheroid culture provides in vivo-like microenvironments to study tumor biology and their survival mechanisms with better predictive power. In this work, vascular endothelial growth factor of type A (VEGF-A) secretion from osteosarcoma (MG-63) cells cultured using monolayer and 3D spheroid models under two stress conditions: nutrient deficiency (reduced serum culture) and hypoxia-inducible factor (HIF) inhibition (HIF inhibitor, YC-1) are characterized and systematically compared. In order to obtain ample sample size for consistent characterization of cellular responses from cancer spheroids under the stresses and compare the responses to those from the conventional monolayer model, a microfluidic spheroid formation and culture device is utilized in the experiments. In the analysis, cell viability is estimated from captured images, and quantification of VEGF-A secreted from the cells is achieved using enzyme-linked immunosorbent assay (ELISA). The experimental results show that the viabilities decrease when the cells face higher stress levels in both monolayer and 3D spheroid culture models; however, the VEGF-A secretion profiles between the cell culture models are different. The VEGF-A secretion decreases when the cells face higher stress conditions in the monolayer cell culture. In contrast, for the 3D spheroid culture, the VEGF-A concentration decreases for low stress levels but increases while the stress level is high. The VEGF-A regulation in the 3D models mimics in vivo cases of tumor survival and can provide insightful information to investigate tumor angiogenesis in vitro. The approach developed in this paper provides an efficient method to quantitatively and statistically study tumor growth kinetics and stress responses from highly uniform samples and it can also be applied to compare the underlying biomolecular mechanisms in monolayer and 3D spheroid culture models to elucidate the effects of microenvironments on cellular response in cancer research.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Comparison of VEGF-A secretion from tumor cells under cellular stresses in conventional monolayer culture and microfluidic three-dimensional spheroid models

2020

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“…For instance, Hu et al reported that the expression of miR-1285-3p in OS tissues and cell lines was downregulated and associated with patients' overall survival [21]. Xue et al focused on the role of miR-638 in OS progression and demonstrated that miR-638 could enhance OS cell apoptosis and inhibit cell proliferation and invasion [22]. miR-1826 has been studied in some human cancers, such as melanoma [14], colorectal carcinoma [13], renal cancer [15], and bladder cancer [23].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR-1826 Indicates a Poor Prognosis for Osteosarcoma Patients and Regulates Tumor Cell Proliferation, Migration, and Invasion

Wei

Zhu

2020

International Journal of Genomics

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Background. Osteosarcoma (OS) is the most frequent bone tumor with high metastasis. This study is aimed at assessing the expression and prognostic significance of microRNA-1826 (miR-1826) in OS patients, as well as its biological function in tumor progression. Methods. Quantitative Real-Time PCR was employed to measure the expression of miR-1826 in OS tissues and cell lines. Kaplan-Meier survival analysis and Cox regression model were used to evaluate the prognostic value of miR-1826. CCK-8 and Transwell assay were conducted to investigate the effect of miR-1826 on OS cell proliferation, migration, and invasion. Results. miR-1826 expression was downregulated in OS tissues and cell lines and associated with OS patients’ clinical stage and distant metastasis. Low levels of miR-1826 were related with shorter survival time and determined as an independent prognostic indicator for the overall survival of OS patients. The overexpression of miR-1826 in OS cells led to inhibited cell proliferation, migration, and invasion. Conclusion. The decreased expression of miR-1826 predicts a poor prognosis in OS patients, and its overexpression inhibits OS cell proliferation, migration, and invasion. This newly identified miR-1826 provides a novel sight into the pathogenesis of OS and offers a candidate prognostic biomarker and therapeutic target for OS treatment.

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“…In addition, high doses of chemotherapeutic agents have side effects (9). Therefore, understanding the molecular mechanism underlying the occurrence and development of Os could aid in the discovery of novel targets for Os treatment (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

TRIP6 regulates the proliferation, migration, invasion and apoptosis of osteosarcoma cells by activating the NF‑κB signaling pathway

Liu

Cheng

et al. 2020

Exp Ther Med

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Thyroid hormone receptor-interacting protein 6 (TRIP6), a member of the zyxin family of Lin-Isl-Mec (LIM) proteins, is an adaptor protein primarily expressed in epithelial cells. TRIP6 can regulate a variety of cellular responses, such as actin cytoskeletal reorganization and cell adhesion. However, to the best of our knowledge, the role of TRIP6 in osteosarcoma (Os) has not been previously reported. Therefore, the present study investigated the role of TRIP6 in the occurrence and development of Os, and the potential of utilizing TRIP6 as a therapeutic target in Os. The present results suggested that the expression levels of TRIP6 were significantly increased in Os cells and clinical tissue specimens compared with normal osteoblasts and adjacent non-tumor tissue. Moreover, the present results suggested that overexpressing TRIP6 significantly increased proliferation, migration and invasion, while inhibiting apoptosis in Os cells. However, silencing TRIP6 decreased proliferation, migration and invasion, while activating apoptosis in Os cells. The present results suggested that overexpression of TRIP6 increased NF-κB activation by decreasing the protein expression levels of inhibitor of κBα, and increasing total and phosphorylated P65 levels. The present results indicated that TRIP6 silencing decreased NF-κB activation. Collectively, the present results suggested that TRIP6 may play a role in promoting Os cell proliferation, migration and invasion, while inhibiting cell apoptosis. Furthermore, TRIP6 may be utilized as a novel prognostic biomarker and therapeutic target in Os.

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MicroRNA‑638 expression change in osteosarcoma patients via PLD1 and VEGF expression

Cited by 7 publications

References 22 publications

Comparison of VEGF-A secretion from tumor cells under cellular stresses in conventional monolayer culture and microfluidic three-dimensional spheroid models

Comparison of VEGF-A secretion from tumor cells under cellular stresses in conventional monolayer culture and microfluidic three-dimensional spheroid models

Downregulation of miR-1826 Indicates a Poor Prognosis for Osteosarcoma Patients and Regulates Tumor Cell Proliferation, Migration, and Invasion

TRIP6 regulates the proliferation, migration, invasion and apoptosis of osteosarcoma cells by activating the NF‑κB signaling pathway

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