miR-101 Suppresses Vascular Endothelial Growth Factor C That Inhibits Migration and Invasion and Enhances Cisplatin Chemosensitivity of Bladder Cancer Cells

Ye, Lei; Li, Bin; Tong, Shiyu; Qi, Lin; Hu, Xiheng; Cui, Yunbo; Li, Zengbo; He, Wei; Zu, Xiongbing; Wang, Zhi; Chen, Minfeng

doi:10.1371/journal.pone.0117809

Cited by 29 publications

(21 citation statements)

References 47 publications

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“…Zhang et al (7) found that reduced miR-101 expression in bladder transitional cell carcinoma (BTCC) is associated with poor prognosis. Several targets of miR-101 have been identified in bladder cancer, including c-Met, cyclooxygenase (COX)-2 and vascular endothelial growth factor (VEGF)-C (8)(9)(10). However, the underlying mechanisms of the regulatory effects of miR-101 on bladder cancer cell proliferation and invasion have remained largely elusive.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-101 inhibits the proliferation and invasion of bladder cancer cells via targeting c-FOS

Long

Wu²,

Yang

et al. 2016

Molecular Medicine Reports

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MicroRNAs (miRs) have important roles in the parthenogenesis of malignancies. While it has been suggested that deregulation of miR‑101 is involved in bladder cancer, the underlying mechanisms have remained largely elusive. The present study aimed to investigate the roles of miR‑101 in the regulation of bladder cancer cell proliferation and invasion. Reverse‑transcription quantitative polymerase chain reaction analysis revealed that the expression of miR‑101 was significantly reduced in the HT‑1376, BIU87, T24 and 5637 several human bladder cancer cell lines compared to that in the SV‑HUC‑1 normal bladder epithelial cell line. Furthermore, a Targetscan search and a luciferase assay were used to identify c‑FOS as a novel target of miR‑101, and western blot analysis indicated that the protein expression of c‑FOS was shown to be negatively regulated by miR‑101 in bladder cancer T24 cells; however, c‑FOS mRNA expression was not affected. In addition, plasmid‑mediated overexpression of miR‑101 and small hairpin RNA‑mediated inhibition of c‑FOS significantly inhibited the proliferation and invasive capacity of T24 cells, as indicated by an MTT and a Transwell assay, respectively. However, plasmid‑mediated overexpression of c‑FOS reversed the inhibitory effects of miR‑101 overexpression on T24‑cell proliferation and invasion. In conclusion, the present study demonstrated that miR‑101 inhibits the proliferation and invasion of bladder cancer cells, at least partly via targeting c‑FOS, suggesting that miR-101/c‑FOS signaling may represent a potential therapeutic target for bladder cancer.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-101 inhibits the proliferation and invasion of bladder cancer cells via targeting c-FOS

Long

Wu²,

Yang

et al. 2016

Molecular Medicine Reports

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“…Reduced expression of miR-101 in patients with NSCLC has been shown to be related to reduced overall survival [25] through the promotion of cell proliferation, tumorigenesis, and invasion. Previous studies have indicated that low miR-101 expression contributes to chemotherapy-resistance in epithelial ovarian cancer [26], bladder cancer [27] and lung cancer [16]. However, whether miR-101 plays an important role in chemotherapy-induced EMT is unclear.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR-101 contributes to epithelial-mesenchymal transition in cisplatin resistance of NSCLC cells by targeting ROCK2

Yin

et al. 2016

Oncotarget

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Chemoresistance and epithelial-mesenchymal transition (EMT) in cancer are linked phenomena. EMT contributes to chemoresistance, however, little is known about whether chemotherapy can induce EMT in cancer cells. Here, we found that miR-101 expression was downregulated in cisplatin-resistant non-small cell lung cancer (NSCLC) cells. Restoration of miR-101 expression inhibited EMT and increased the sensitivity of cisplatin-resistant NSCLC cells to cisplatin in vitro by targeting ROCK2. Furthermore, ROCK2 protein level was inversely correlated with miR-101 level in NSCLC tissue samples. Kaplan-Meier analysis revealed that low miR-101 expression in NSCLC was correlated with poor survival time. In summary, our results provide novel mechanistic insights into the role of miR-101/ROCK2 signaling in the cisplatin resistance of NSCLC cells. Targeting of miR-101 is a potential therapeutic approach for NSCLC.

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“…Aberrant expression of miR-101 has previously been observed in various human cancers, such as gastric cancer (18), hepatocellular carcinoma (19), nasopharyngeal carcinoma (20), osteosarcoma (21), and breast cancer (22). Furthermore, miR-101 has been identified as a tumour suppressor in bladder cancer (23,24). Downregulation of miR-101 is associated with poor prognosis of patients with bladder transitional cell carcinoma (24).…”

Section: Introductionmentioning

confidence: 98%

“…Downregulation of miR-101 is associated with poor prognosis of patients with bladder transitional cell carcinoma (24). miR-101 directly targets vascular endothelial growth factor C, inhibits cell migration and invasion, and enhances cisplatin sensitivity by modulating the cyclooxygenase-2 pathway in bladder cancer cells (23,25). Our previous study illustrated that miR-101…”

Section: Introductionmentioning

confidence: 98%

MicroRNA‑101 inhibits cell migration and invasion in bladder cancer via targeting FZD4

et al. 2018

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Dysfunction of microRNAs (miRs) has been implicated in the development and progression of various human cancers. Our previous study demonstrated that miR-101 inhibited bladder cancer cell proliferation and invasion through inhibition of c-FOS expression. As an miR generally has many targets, other targets of miR-101 may also serve important roles in bladder cancer progression. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were used to examine mRNA and protein expression, respectively. Wound healing and Transwell assays were conducted to study cell migration and invasion, respectively. The luciferase reporter gene assay was performed to verify one of the targets of miR-101. The data in the present study indicate that the expression of miR-101 is significantly reduced in bladder cancer tissues compared with that in adjacent non-tumour tissues. In addition, miR-101 expression is also downregulated in bladder cancer cell lines compared with that in normal bladder epithelial cells. Furthermore, low expression of miR-101 was significantly associated with tumour metastasis, advanced clinical stage, and poor prognosis in bladder cancer. Frizzled class receptor 4 (FZD4) was identified as a novel target of miR-101 in bladder cancer cells. The expression of FZD4 was significantly upregulated in bladder cancer tissues and cell lines. Both miR-101 overexpression and FZD4 inhibition caused a significant reduction of the migration and invasion of bladder cancer cells, whereas overexpression of FZD4 reversed the suppressive effects of miR-101 on bladder cancer cell migration and invasion. In conclusion, it was demonstrated that miR-101 downregulation is associated with bladder cancer progression and that miR-101 can inhibit bladder cancer cell migration and invasion via directly targeting FZD4. The present study expands the understanding of the molecular mechanisms underlying bladder cancer progression.

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miR-101 Suppresses Vascular Endothelial Growth Factor C That Inhibits Migration and Invasion and Enhances Cisplatin Chemosensitivity of Bladder Cancer Cells

Cited by 29 publications

References 47 publications

MicroRNA-101 inhibits the proliferation and invasion of bladder cancer cells via targeting c-FOS

MicroRNA-101 inhibits the proliferation and invasion of bladder cancer cells via targeting c-FOS

Downregulation of miR-101 contributes to epithelial-mesenchymal transition in cisplatin resistance of NSCLC cells by targeting ROCK2

MicroRNA‑101 inhibits cell migration and invasion in bladder cancer via targeting FZD4

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