microRNA-128 plays a critical role in human non-small cell lung cancer tumourigenesis, angiogenesis and lymphangiogenesis by directly targeting vascular endothelial growth factor-C

Hu, Jing; Cheng, Yi; Li, Yuezhen; Jin, Zaishun; Pan, Yanming; Liu, Guibo; Fu, Songbin; Zhang, Yafang; Feng, Kai; Feng, Yukuan

doi:10.1016/j.ejca.2014.06.005

Cited by 148 publications

(132 citation statements)

References 43 publications

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“…Flow cytometry detection. Cells (5x10 6 ) were harvested, and an apoptosis detection kit (Biosea, Beijing, China) was used to examine the apoptosis rate in accordance with the manufacturer's instructions. Next, the cells were read by flow cytometry (BD Biosciences, Franklin Lakes, NJ, USA) (Ex, 488 nm; Em, 635 nm), and the obtained numerical values were analyzed with CellQuest 3.0 software (BD Biosciences).…”

Section: Methodsmentioning

confidence: 99%

“…They exhibit an abnormal expression and function in various types of malignancies, and act as different types of tumor-related gene (4,5). miR-128 is an anti-oncogene which is expressed at low levels in certain malignant tumors, including glioma (6,7). miR-128 specifically inhibits a number of target genes related to tumor cell characteristics, including apoptosis and proliferation (8,9).…”

Section: Introductionmentioning

confidence: 99%

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miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

et al. 2015

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Abstract. In this study, we investigate whether miR-128 is capable of regulating the apoptosis and proliferation of human U251 glioma cells by downregulating RhoE. The expression of miR-128 was assessed by quantitative polymerase chain reaction in normal brain tissue and glioma samples. A significant downregulation of the expression of miR-128 was detected in glioma in contrast to normal brain tissue. Following the transfection of pre-miR-128 and anti-miR-128 into U251 cells, the high expression of miR-128 could inhibit proliferation and induce apoptosis in U251 cells, and those effects could be restored by miR-128 knockdown. To analyze the regulation mechanism of miR-128, TargetScan, miRanda and PicTar were used to ascertain whether RhoE was a potential target gene. Next, luciferase activity assay and western blot analysis confirmed that RhoE was a direct and specific target gene of miR-128. The advanced effects of pre-miR-128 on the apoptosis and proliferation of U251 cells were reversed by the upregulation of RhoE expression. In summary, aberrantly expressed miR-128 regulates apoptosis and proliferation in human glioma U251 cells partly by directly targeting RhoE. This finding may offer a new potential therapeutic strategy for the treatment of glioma.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

et al. 2015

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“…Tumor suppressor microRNAs, miR-1862, miR27b, and miR128 [63][64][65] have been found to target VEGF-C and inhibit tumor progression. While there is no putative hypoxia responsive binding site on the VEGF-C promoter and a previous study showed that VEGF-C mRNA does not change under hypoxic conditions, 54 a very recent study demonstrated that VEGF-C protein is increased in tumors and this is mediated in an internal ribosome entry site (IRES)-dependent manner.…”

Section: Cytokines Growth Factors and Extracellular Matrix (Ecm)mentioning

confidence: 99%

The non-canonical role of vascular endothelial growth factor-C axis in cancer progression

Wang

Tsai

2015

Exp Biol Med (Maywood)

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It has been shown in many clinical studies that the level of vascular endothelial growth factor-C (VEGF-C) positively correlates with lymph node metastasis. Nevertheless, beyond the canonical role of VEGF-C in stimulating lymphangiogenesis and thus promoting lymph node/distant metastasis, emerging evidence indicates that expression of VEGF-C contributes to various aspects of carcinogenicity via autocrine regulation. The newly identified functions of VEGF-C include but are not limited to proliferation, migration, invasion, and chemo-resistance. Besides tumor cell autocrine regulation, VEGF-C can also modulate the immune system such that tumor cells more easily escape immune surveillance. Therefore, understanding the functional roles and regulatory mechanisms related to the VEGF-C axis may lead to alternative strategies for cancer treatment. This mini-review will focus on summarizing recent discoveries regarding the unconventional functions of VEGF-C in cancer progression.

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“…Low‐level expression of miR‐128‐3p also correlates with poor clinical outcome of patients with breast cancer (Qian et al ., 2012; Zhu et al ., 2011). Other studies have shown that miR‐128‐3p is also lower expressed in other tumor tissues and that its overexpression inhibits tumor cell proliferation, angiogenesis, and invasion (Evangelisti et al ., 2009; Hu et al ., 2014; Palumbo et al ., 2013). Hence, we define TGFβ1 as a regulator of MET expression in breast cancer by upregulating C‐ets‐1 and downregulating miR‐128‐3p expression, which results in cell migration, invasion, and metastasis in a HGF‐dependent manner (Fig.…”

Section: Discussionmentioning

confidence: 99%

TGFβ1 regulates HGF‐induced cell migration and hepatocyte growth factor receptor MET expression via C‐ets‐1 and miR‐128‐3p in basal‐like breast cancer

et al. 2018

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Breast cancer is the most common cancer in women worldwide. The tumor microenvironment contributes to tumor progression by inducing cell dissemination from the primary tumor and metastasis. TGFβ signaling is involved in breast cancer progression and is specifically elevated during metastatic transformation in aggressive breast cancer. In this study, we performed genomewide correlation analysis of TGFBR2 expression in a panel of 51 breast cancer cell lines and identified that MET is coregulated with TGFBR2. This correlation was confirmed at the protein level in breast cancer cell lines and human tumor tissues. Flow cytometric analysis of luminal and basal‐like breast cancer cell lines and examination of 801 tumor specimens from a prospective cohort of breast cancer patients using reverse phase protein arrays revealed that expression of TGFBR2 and MET is increased in basal‐like breast cancer cell lines, as well as in triple‐negative breast cancer tumor tissues, compared to other subtypes. Using real‐time cell analysis technology, we demonstrated that TGFβ1 triggered hepatocyte growth factor (HGF)‐induced and MET‐dependent migration in vitro. Bioinformatic analysis predicted that TGFβ1 induces expression of C‐ets‐1 as a candidate transcription factor regulating MET expression. Indeed, TGFβ1‐induced expression of ETS1 and breast cancer cell migration was blocked by knockdown of ETS1. Further, we identified that MET is a direct target of miR‐128‐3p and that this miRNA is negatively regulated by TGFβ1. Overexpression of miR‐128‐3p reduced MET expression and abrogated HGF‐induced cell migration of invasive breast cancer cells. In conclusion, we have identified that TGFβ1 regulates HGF‐induced and MET‐mediated cell migration, through positive regulation of C‐ets‐1 and negative regulation of miR‐128‐3p expression in basal‐like breast cancer cell lines and in triple‐negative breast cancer tissue.

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microRNA-128 plays a critical role in human non-small cell lung cancer tumourigenesis, angiogenesis and lymphangiogenesis by directly targeting vascular endothelial growth factor-C

Cited by 148 publications

References 43 publications

miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

miR-128 regulates the apoptosis and proliferation of glioma cells by targeting RhoE

The non-canonical role of vascular endothelial growth factor-C axis in cancer progression

TGFβ1 regulates HGF‐induced cell migration and hepatocyte growth factor receptor MET expression via C‐ets‐1 and miR‐128‐3p in basal‐like breast cancer

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