Exosome–transmitted long non-coding RNA PTENP1 suppresses bladder cancer progression

Zheng, Rui; Du, Mulong; Wang, Xiaowei; Xu, Weidong; Liang, Jiayuan; Wang, Wenying; Lv, Qiang; Qin, Chao; Chu, Haiyan; Wang, Meilin; Lin, Yuan; Qian, Ji; Zhang, Zhengdong

doi:10.1186/s12943-018-0880-3

Cited by 230 publications

(172 citation statements)

References 49 publications

Supporting

Mentioning

169

Contrasting

Order By: Relevance

“…Cancer-related reports involve a large quantity of data on the effects of EVs circRNAs. 29 With efforts made in this study, it was QRT-PCR results showed that circ-0000190 was primarily distributed in the cytoplasmic fraction of osteosarcoma cells. 28 For instance, EVs from normal cells transferred PTENP1 to bladder cells, which suppresses bladder cancer progression.…”

Section: Discussionmentioning

confidence: 78%

Extracellular nanovesicles‐transmitted circular RNA has_circ_0000190 suppresses osteosarcoma progression

Pei

Wang

et al. 2020

J Cellular Molecular Medi

View full text Add to dashboard Cite

Under the microenvironment, tumour progression is substantially affected by cellcell communication. In spite of the mediating effect of extracellular nanovesicles (EVs) on cell-cell communication by packaging into circRNAs, the effect of EVs circRNA hsa_circ_0000190 (circ-0000190) in osteosarcoma is still not clear. Circ-0000190 expressions in tissues and EVs from plasma were compared between osteosarcoma patients and controls. Thereafter, receiver operating characteristic (ROC) curve was drawn and area under the curve was calculated to examine whether the diagnostic results were accurate, and the effect of EVs circ-0000190 was dug out via the determination of cell phenotypes and animal assays. Results showed circ-0000190 exhibited an obvious reduction in EVs and tissues of osteosarcoma patients (P < .05). It was also discovered that EVs encapsulated the majority of circ-0000190, and EVs-encapsulated circ-0000190 could be applied to make a distinction between osteosarcoma patients and controls. Besides, EVs circ-0000190 in osteosarcoma cells transported from normal cells weakened the capacities of osteosarcoma cells to migrate, proliferate and invade, so as to block their biological malignant behaviours (P < .05). In addition, under the action of EVs circ-0000190, tumour growth was impeded and the expression of TET1 was inhibited via the competitive binding to miR-767-5p. In all, EVs circ-0000190 has a good prospect as it can be regarded as a new biomarker for detecting osteosarcoma. EVs circ-0000190 transported from normal cells to osteosarcoma cells impeded the in vitro and in vivo development of osteosarcoma, implying that EVs circ-0000190 exerts an effect on communication between normal cells and osteosarcoma cells in the carcinogenesis process of osteosarcoma.

show abstract

Section: Discussionmentioning

confidence: 78%

Extracellular nanovesicles‐transmitted circular RNA has_circ_0000190 suppresses osteosarcoma progression

Pei

Wang

et al. 2020

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Exosomes secreted by human colon cancer cells can transmit miR-210 to neighboring metastatic cells to influence their adhesion (Bigagli, Luceri, Guasti, & Cinci, 2016). Similarly, exosome-transmitted long ncRNA PTENP1 participates in normal-cell-to-bladder-cell communication during the carcinogenesis of bladder cancer (Zheng et al, 2018). Our study revealed that exosomes act as intercellular communicators to transmit miR-221 to normal recipient cells to increase cell viability, but the mechanism needs further investigation.…”

Section: Discussionmentioning

confidence: 71%

Exosomal miR‐221 derived from hydroquinone‐transformed malignant human bronchial epithelial cells is involved in cell viability of recipient cells

Jiang

Huang

Lian

et al. 2019

J of Applied Toxicology

View full text Add to dashboard Cite

miR‐221, an oncogenic microRNA, can promote cell proliferation and is highly expressed in various types of tumors. However, the role of exosomal miR‐221 in benzene‐caused carcinogenesis remains elusive. Our study was designed to investigate whether exosomes secreted by the hydroquinone (HQ; an active metabolite of benzene)‐transformed malignant cells can transmit miR‐221 to normal recipient cells and its possible effects on cell viability. Our investigation revealed that expression levels of miR‐221 were significantly increased in HQ‐transformed malignant cells relative to normal controls. Furthermore, exposure of control cells to exosomes that were derived from HQ‐transformed malignant cells increased miR‐221 levels and promoted their proliferation. Analyses of the biological potency of exosomes derived from HQ‐transformed malignant cells in which miR‐221 levels were decreased using an inhibitor, showed that both miR‐221 levels and proliferation of recipient cells were decreased, but still were higher than those of normal 16HBE cells. Our study indicates that exosomal miR‐221 derived from HQ‐transformed malignant human bronchial epithelial cells is involved in the proliferation of recipient cells.

show abstract

“…Cell cycle was analyzed as described previously (Zheng et al ). After treatment with PNP, T24 cells were harvested and suspended in 70% cold ethanol and then incubated overnight at 4°C.…”

Section: Methodsmentioning

confidence: 99%

“…Cell cycle was analyzed as described previously (Zheng et al 2018). After treatment with PNP, T24 cells were harvested and suspended in 70% cold ethanol and then incubated overnight at 4 C. After centrifugation, the cells were washed with cold PBS, then suspended in 500 μL PBS, and incubated with 50 μL RNase A (20 μg/mL terminal concentration) for 30 min.…”

Section: Cell Cycle Analysismentioning

confidence: 99%

4‐nitrophenol exposure in T24 human bladder cancer cells promotes proliferation, motilities, and epithelial‐to‐mesenchymal transition

Dong

Chen

Wang

et al. 2019

Environ and Mol Mutagen

View full text Add to dashboard Cite

Although health hazards of 4‐nitrophenol (PNP) exposure have been reported, the adverse effects of PNP exposure on cancer biological features are still unknown. We investigated the effects of administration of PNP in T24 human bladder cancer cells. The results showed that PNP exposure promoted cellular proliferation, migration and invasion, inhibited adhesion and apoptosis in vitro. Using quantitative real‐time PCR, we found that (1) the mRNA expression levels of cell‐cycle regulators PCNA, cyclin D1 and COX‐2 were increased in PNP‐treated cells compared to controls, however, that of pro‐apoptotic gene Bax was decreased; (2) the expression level of EMT‐associated gene E‐cadherin was decreased in PNP‐treated cells, whereas those of N‐cadherin, vimentin, snail, and slug were increased; (3) the expression levels of cancer‐promoting genes HIF‐1, IL‐1β, VEGFα and K‐Ras were enhanced, but those of tumor suppressors p53, PTEN and BRCA were decreased. There was a positive association between PNP exposure times and the promotion effects. Finally, we found that the expression level of PPARγ (γ1 isoform) was increased in PNP‐treated T24 cells. GW9662, a specific PPARγ antagonist, attenuated PNP‐induced cell migration and invasion. These findings indicate that PNP exposure may promote bladder cancer growth and progression involving PPARγ signaling. PPARγ is a potential target for development of novel intervention study on environment pollution. Environ. Mol. Mutagen. 61:316–328, 2020. © 2019 Wiley Periodicals, Inc.

show abstract

Exosome–transmitted long non-coding RNA PTENP1 suppresses bladder cancer progression

Cited by 230 publications

References 49 publications

Extracellular nanovesicles‐transmitted circular RNA has_circ_0000190 suppresses osteosarcoma progression

Extracellular nanovesicles‐transmitted circular RNA has_circ_0000190 suppresses osteosarcoma progression

Exosomal miR‐221 derived from hydroquinone‐transformed malignant human bronchial epithelial cells is involved in cell viability of recipient cells

4‐nitrophenol exposure in T24 human bladder cancer cells promotes proliferation, motilities, and epithelial‐to‐mesenchymal transition

Contact Info

Product

Resources

About