Upregulation of miR-489-3p and miR-630 inhibits oxaliplatin uptake in renal cell carcinoma by targeting OCT2

Chen, Lu; Chen, Le; Qin, Zhiyuan; Lei, Jinxiu; Ye, Sheng; Zeng, Kui; Wang, Hua; Ying, Meidan; J, Gao; Zeng, Su; Yu, Lushan

doi:10.1016/j.apsb.2019.01.002

Cited by 58 publications

(32 citation statements)

References 43 publications

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“…These results provided direct evidence that human urinary EVs could be classified as exosomes [12]. In addition, characterization of EVs derived from the culture medium of RCC cell lines was described in our previous study [13]. To investigate the integrity of EVs and exclude contamination of cell-free RNA, human urinary EVs were incubated with or without RNase A for 1 h at 37 • C. RNA was then extracted and assessed using the Agilent 2100 Bioanalyzer 3 of system.…”

Section: Isolation and Characterization Of Evs From Human Urinementioning

confidence: 65%

miR-224-5p Contained in Urinary Extracellular Vesicles Regulates PD-L1 Expression by Inhibiting Cyclin D1 in Renal Cell Carcinoma Cells

Qin

Sun

Chen

et al. 2021

Cancers

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The abundant miRNAs in urinary extracellular vesicles (EVs) represent ideal reservoirs for biomarker discovery, especially in renal cell carcinoma (RCC). However, the content and biological functions of microRNAs contained in urinary EVs in RCC remain ambiguous. In this study, urinary EVs were isolated and characterized from RCC patients and healthy volunteers. Differentially expressed microRNAs in urinary EVs were screened by small RNA sequencing. The target gene and biological functions of selected microRNAs were investigated through multifaceted methods. Results indicated that miR-224-5p was significantly upregulated in urinary EVs of RCC patients compared to healthy volunteers. The overexpression of miR-224-5p inhibited RCC cell proliferation and induced cell cycle arrest. The gene CCND1 encoding cyclin D1 was identified as a direct target of miR-224-5p via prediction and validation. Moreover, the invasive and metastatic abilities of RCC cells were enhanced by miR-224-5p. Interestingly, miR-224-5p also increased the stability of PD-L1 protein by inhibiting CCND1. This effect could be transmitted via EVs and further promoted the resistance of RCC cells to T cell-dependent toxicity. In summary, urinary EVs containing miR-224-5p were identified as a potential biomarker in RCC. Regulation of PD-L1 protein expression by miR-224-5p through suppressing CCND1 elucidates new roles of miR-224-5p in RCC progression.

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Section: Isolation and Characterization Of Evs From Human Urinementioning

confidence: 65%

miR-224-5p Contained in Urinary Extracellular Vesicles Regulates PD-L1 Expression by Inhibiting Cyclin D1 in Renal Cell Carcinoma Cells

Qin

Sun

Chen

et al. 2021

Cancers

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“…The role of MiRNAs in tumors is extensive. The miR-489-3p found in this study is known to inhibit the growth of a variety of tumors, such as bladder cancer [28], renal cell carcinoma [29], and osteosarcoma [17]. However, its relationship with pancreatic cancer is unclear.…”

Section: Discussionmentioning

confidence: 77%

MiR-489-3p reduced pancreatic cancer proliferation and metastasis by targeting PKM2 and LDHA involving glycolysis

Zhang

Shen

et al. 2020

Preprint

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Background: Malignant proliferation and chemotherapy resistance are some of the causes of high mortality in pancreatic cancer. MicroRNAs have long been a hot spot in cancer research and are involved in tumor formation and metabolic stress responses. miR-489-3p is involved in inhibiting the growth of many tumors, but its relationship with the growth and metabolism of pancreatic cancer is not clear. Methods：We used RNA in situ hybridization to analyze the differential expression of miR-489-3p in pancreatic cancer tissues and adjacent tissues. The qRT-PCR experiment detected the content of miR-489-3p in pancreatic cancer cell lines and ordinary pancreatic ductal epithelial cells. Then we did experiments in vivo (subcutaneous tumor formation in nude mice) and in vitro (plate cloning, transwell, glycolysis related experiments) experiments to verify that miR-489-3p can continue the invasion and metastasis of pancreatic cancer and glucose metabolism. Furthermore, we confirmed that LDHA and PKM2 are the two targets of miR-489-3p through dual luciferase reporter gene experiments. Finally, several reply experiments were done to verify the regulation mechanism of miR-489-3p.Results: We determined that miR-489-3p is under-expressed in pancreatic cancer tissues by RNA in situ hybridization, and the function acquisition and deletion experiments and glycolysis experiments confirmed that miR-489-3p can inhibit the proliferation and invasion of Glycolysis. We then analyzed the website to find that miR-489-3p can target LDHA and PKM, and then we verified this finding with a luciferase report experiment. Therefore, we proceeded with recovery experiments on LDHA and PKM2, and concluded that miR-489-3p performs its function by targeting LDHA and PKM2. Finally, in vivo experiments confirmed that highly expressed miR-489-3p inhibited the growth of pancreatic cancer. Conclusion: In short, we identified miR-489-3p as a novel chemotherapy target for pancreatic cancer, and its diagnostic value deserves further study.

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“…Furthermore, it was found that miR-489-3p depletion could restore the influences of LEF1-AS1 silence on glioma cell proliferation and apoptosis. Besides, miR-489-3p was identified as a tumor suppressor in renal cell carcinoma 25 , 26 and bladder cancer 27 . Taken together, our study first shed new light on the relationship between LEF1-AS1 and miR-489-3p in glioma.…”

Section: Discussionmentioning

confidence: 99%

LEF1-AS1 accelerates tumorigenesis in glioma by sponging miR-489-3p to enhance HIGD1A

Cheng

Wang

et al. 2020

Cell Death Dis

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Long non-coding (lncRNA) lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1) has been validated to be implicated in manifold cancers, whereas its function in glioma has not been understood thoroughly. Hence, in this study, we tested that LEF1-AS1 expression was significantly upregulated in glioma tissues and cell lines. Besides, knockdown of LEF1-AS1 repressed cell proliferation while activated apoptosis in glioma cells in vitro, and also suppressed tumor growth in vivo. RNA pull-down and luciferase reporter assays affirmed that LEF1-AS1 could bind with miR-489-3p. In addition, miR-489-3p expression was downregulated in glioma cells. Moreover, miR-489-3p depletion partly offset LEF1-AS1 knockdown-mediated function on proliferation and apoptosis. Further, HIGD1A identified as the target gene of miR-489-3p was upregulated in glioma cells. HIGD1A silence could restrict the process of glioma. In rescue assays, upregulation of HIGD1A remedied the inhibitory impacts of LEF1-AS1 silence on glioma cell growth. In summary, our studies corroborated the regulatory mechanism of LEF1-AS1/miR-489-3p/HIGD1A axis in glioma, suggesting that targeting LEF1-AS1 might be a promising method for glioma therapy in the future.

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Upregulation of miR-489-3p and miR-630 inhibits oxaliplatin uptake in renal cell carcinoma by targeting OCT2

Cited by 58 publications

References 43 publications

miR-224-5p Contained in Urinary Extracellular Vesicles Regulates PD-L1 Expression by Inhibiting Cyclin D1 in Renal Cell Carcinoma Cells

miR-224-5p Contained in Urinary Extracellular Vesicles Regulates PD-L1 Expression by Inhibiting Cyclin D1 in Renal Cell Carcinoma Cells

MiR-489-3p reduced pancreatic cancer proliferation and metastasis by targeting PKM2 and LDHA involving glycolysis

LEF1-AS1 accelerates tumorigenesis in glioma by sponging miR-489-3p to enhance HIGD1A

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