miR-128 downregulation promotes growth and metastasis of bladder cancer cells and involves VEGF-C upregulation

Zhou, Xiaojing; Qi, Lin; Tong, Shiyu; Cui, Yulong; Chen, Jinbo; Huang, Tianxiang; Chen, Zhi; Zu, Xiongbing

doi:10.3892/ol.2015.3689

Cited by 45 publications

(38 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Padera et al (23) demonstrated that a high expression of VEGF-C facilitates lymphatic vessel hyperplasia surrounding tumors and lymphatic metastasis, but there are no functional lymphatic vessels within tumors, suggesting that functional lymphatic vessels that surround tumors are sufficient for lymphatic metastasis. In the present study, the expression of VEGF-C mRNA and protein in the bladder cancer tissues is significantly higher than normal tissues, being consistent with previous studies (24,25). Similar results were obtained from blood and urine samples from patients with bladder cancer, suggesting that changes in VEGF-C expression are associated with the occurrence and development of bladder cancer.…”

Section: Discussionsupporting

confidence: 81%

MicroRNA-186 regulates the invasion and metastasis of bladder cancer via vascular endothelial growth factor C

Ping

2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 81%

MicroRNA-186 regulates the invasion and metastasis of bladder cancer via vascular endothelial growth factor C

Ping

2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

show abstract

“…miR‐128 was reported as oncogene or tumour suppressor in various cancers. For example, miR‐128 was reported to be downregulated in cancer tissues and represses growth and metastasis of bladder cancer, lung cancer, and glioblastoma multiforme . However, different studies of the miR‐128 in carcinoma reported discordant conclusions.…”

Section: Discussionmentioning

confidence: 99%

NAIF1 suppresses osteosarcoma progression and is regulated by miR‐128

Kong

Zhang

2018

Cell Biochemistry & Function

View full text Add to dashboard Cite

Nuclear apoptosis‐inducing factor 1 (NAIF1) acts as an oncogene and involves in tumorigenesis in several cancers. However, the expression and mechanism of NAIF1 in osteosarcoma remains unclear. In this study, we demonstrated the downregulation of NAIF1 expression in both osteosarcoma tissues and cell lines. We next explored the potential role of NAIF1 in osteosarcoma cell proliferation and migration. The result showed that overexpression of NAIF1 evidently suppressed the cell proliferation and invasion of osteosarcoma. Furthermore, we investigated the potential mechanisms accounting for dysregulation of NAIF1 in osteosarcoma. The bioinformatic prediction and luciferase reporter assay revealed that miR‐128 is a direct upstream regulator of NAIF1 and regulates NAIF1 expression by binding the 3′‐UTR of NAIF1. Consistent with previous study, we found that miR‐128 was upregulated in both osteosarcoma tissues and cell lines. Moreover, miR‐128 expression levels were inversely correlated with that of NAIF1 in osteosarcoma tissues. Finally, functional assay showed that miR‐128 significantly suppressed osteosarcoma progression partially mediated by inhibiting NAIF1 expression. These data indicate that the miR‐128 and its target gene NAIF1 played important roles by regulating OS cell proliferation and migration phenotype. Significance of the study Osteosarcoma (OS) is the most common malignant bone tumour and the second leading cause of cancer‐related death affecting children and adolescents. Nuclear apoptosis‐inducing factor 1 (NAIF1) plays an inhibitory role in the initial steps of different carcinomas. However, the expression and mechanism of NAIF1 in osteosarcoma remains unclear. The data of this study indicated that the miR‐128 and its target gene NAIF1 played important roles by regulating OS cell proliferation and migration phenotype. It was demonstrated that NAIF1 would demonstrate important regulative effects and may be a promising therapeutic target of OS.

show abstract

“…First, we evaluated the cell toxicity exerted by EVOOE on two different BCa cell lines, T24 and 5637, which are characterized by two different grades and are widely used as in vitro models (31–33) as they cover the more frequent subtypes of BCa. 5637 cells well represent the E2F3/RB1 pathway due to amplification of 6p22.3, concomitant with loss of one copy of RB1 and mutation of the other copy.…”

Section: Discussionmentioning

confidence: 99%

Extra-virgin olive oil phenols block cell cycle progression and modulate chemotherapeutic toxicity in bladder cancer cells

et al. 2016

View full text Add to dashboard Cite

Epidemiological data indicate that the daily consumption of extra-virgin olive oil (EVOO), a common dietary habit of the Mediterranean area, lowers the incidence of certain types of cancer, in particular bladder neoplasm. The aim of the present study was to evaluate the antiproliferative activity of polyphenols extracted from EVOO on bladder cancer (BCa), and to clarify the biological mechanisms that trigger cell death. Furthermore, we also evaluated the ability of low doses of extra-virgin olive oil extract (EVOOE) to modulate the in vitro activity of paclitaxel or mitomycin, two antineoplastic drugs used in the management of different types of cancer. Our results showed that EVOOE significantly inhibited the proliferation and clonogenic ability of T24 and 5637 BCa cells in a dose-dependent manner. Furthermore, cell cycle analysis after EVOOE treatment showed a marked growth arrest prior to mitosis in the G2/M phase for both cell lines, with the subsequent induction of apoptosis only in the T24 cells. Notably, simultaneous treatment of mitomycin C and EVOOE reduced the drug cytotoxicity due to inhibition of ROS production. Conversely, the co-treatment of T24 cells with paclitaxel and the polyphenol extract strongly increased the apoptotic cell death at each tested concentration compared to paclitaxel alone. Our results support the epidemiological evidence indicating that olive oil consumption exerts health benefits and may represent a starting point for the development of new anticancer strategies.

show abstract

miR-128 downregulation promotes growth and metastasis of bladder cancer cells and involves VEGF-C upregulation

Abstract: Abstract. serves an important role in regulating growth, invasiveness, stem cell-like traits, differentiation and apoptosis of different types of tumor cells.

Cited by 45 publications

References 32 publications

MicroRNA-186 regulates the invasion and metastasis of bladder cancer via vascular endothelial growth factor C

MicroRNA-186 regulates the invasion and metastasis of bladder cancer via vascular endothelial growth factor C

NAIF1 suppresses osteosarcoma progression and is regulated by miR‐128

Extra-virgin olive oil phenols block cell cycle progression and modulate chemotherapeutic toxicity in bladder cancer cells

Contact Info

Product

Resources

About