MicroRNA‐498 promotes proliferation, migration, and invasion of prostate cancer cells and decreases radiation sensitivity by targeting PTEN

Duan, Xiumei; Liu, Xiaona; Li, Yuxin; Cao, Yuqing; Silayiding, Aidaeraili; Zhang, Rongkui; Wang, Jiping

doi:10.1002/kjm2.12108

Cited by 29 publications

(21 citation statements)

References 33 publications

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“…Proliferation, migration and invasion are important for tumorigenesis, and play a vital role in influencing tumor recurrence and metastasis ( 43 – 45 ). Radiation affects tumor cells in numerous aspects, including cell proliferation, colony formation, apoptosis rate, cell invasion, as well as other biological responses ( 46 , 47 ). The inhibition of tumor cell proliferation, migration and invasion by radiotherapy is of great value for controlling the progression of tumor cells ( 47 , 48 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑7/SP1/TP53BP1 axis may play a pivotal role in NSCLC radiosensitivity

et al. 2020

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MicroRNA-7 (miR-7) has been identified as a tumor suppressor in non-small cell lung cancer (NSCLC) and a radiosensitivity regulator. Numerous studies have revealed that specific protein 1 (SP1) plays a critical role in the tumorigenesis of various types of cancers and regulates radiosensitivity and tumor suppressor p53-binding protein 1 (TP53BP1), which plays an essential role in DNA repair. However, it is not clear whether miR-7 has a regulatory effect on SP1 and TP53BP1 in NSCLC. In the present study it was revealed that miR-7 directly binds to the 3′UTR of SP1, thereby suppressing SP1 expression to regulate radiosensitivity. Overexpression of miR-7 and SP1 and knockdown of miR-7 and SP1 were performed using lentiviral transfection. Protein and mRNA abundance of SP1 and TP53BP1 were determined using western blotting and RT-qPCR, respectively, while miR-7 binding to SP1 was validated using a luciferase reporter assay. Biological function analysis indicated that miR-7 negatively regulated SP1 and inhibited cell proliferation, migration, and invasion when combined with radiation. It was also revealed that the expression of TP53BP1 was positively regulated by SP1 or negatively regulated by miR-7. In conclusion, SP1 was a target of miR-7, and the decreased expression of SP1 resulting from miR-7 overexpression in NSCLC was vital for improving radiosensitivity in NSCLC cells. Moreover, SP1 expression was detected in 95 paired NSCLC and adjacent normal tissues, and it was determined that SP1 was significantly upregulated in NSCLC tissues and that its upregulation was correlated with the degree of tissue differentiation. Thus, SP1 and/or miR-7 may be potential molecular targets in NSCLC radiotherapy.

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Section: Discussionmentioning

confidence: 99%

miR‑7/SP1/TP53BP1 axis may play a pivotal role in NSCLC radiosensitivity

et al. 2020

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“…PTEN is regarded as a tumour suppressor gene in many diseases, and it was regulated by many kinds of miRNAs. In a murine glioma model, miR‐26a mediated PTEN repression enhances de novo tumour formation 33 ; Duan et.al proved that miR‐498 promotes proliferation, migration and invasion of prostate cancer cells and decreases radiation sensitivity by targeting PTEN 34 . Hao et al proved miR‐21 promotes proliferation and inhibits apoptosis of HSC through targeting PTEN/PI3K/Akt pathway 35 .…”

Section: Discussionmentioning

confidence: 99%

Identification lncRNA LOC102551149/miR‐23a‐5p pathway in hepatic fibrosis

Zhao

et al. 2020

Eur J Clin Investigation

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Background: Hepatic fibrosis is a worldwide incurable disease; due to the complex and unclear mechanism, there lack the effective therapeutic targets. However, the mechanism of miR-23a-5p underling this pathological process is largely not clear.The purpose of this study was to investigate the role of miR-23a-5p in hepatic fibrosis and HSC activation. Methods: The content of miR-23a-5p in hepatic fibrosis induced by Nnitrosodimethylamine (NDMA) and HSC activation induced by platelet-derived growth factor (PDGF) was detected by qRT-PCR. H&E staining, Masson staining and Shear wave electrography (SWE) were used to detect the degree of hepatic fibrosis. Immunohistochemistry staining, qRT-PCR and Western blot detect the related markers of liver fibrosis or HSC activation, as well as the related pathway genes and proteins. Dual-luciferase reporter system verifies the interaction between miR-23a-5p with PTEN or miR-23a-5p with lncRNA LOC102551149 in HSC-T6. siRNA and miRNA mimic transfer to HSC-T6 to detect the function of lncRNA LOC102551149 and miR-23a-5p on HSC activation. Results: After hepatic fibrosis and HSC activation happened, the expression of miR-23a-5p was up-regulated, whereas anti-miR-23a-5p can alleviate hepatic fibrosis and HSC activation. Further research shows miR-23a-5p can target PTEN and degrade it, causing activation of PI3K/Akt/mTOR/Snail pathway. lncRNA LOC102551149 can be used as a competition endogenous RNA (ceRNA) targeting miR-23a-5p through base pairing, and siRNA LOC102551149 or exogenous miR-23a-5p can induce HSC activation through PI3K/Akt/mTOR/Snail pathway. Conclusion: We demonstrate mechanism pathway of miR-23a-5p on hepatic fibrosis and HSC activation, which may develop a therapeutic target for hepatic fibrosis. K E Y W O R D S hepatic fibrosis, HSC activation, lncRNA LOC102551149, miR-23a-5p, PI3K/Akt, PTEN 2 of 14 | DONG et al.

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“…Finally, radiation response can also be regulated by miRNAs whose targets indirectly affect the cell cycle. In a recent publication, the phenotype of miR-498 was examined in DU145 and LNCaP cells after varying doses of ionizing radiation (1 to 8 Gy) [85]. miR-498 is implicated in proliferation progression of PCa cells and radioresistance by targeting Phosphatase and TENsin homolog (PTEN) ( Fig.…”

Section: Mirnas In Cell Cycle Progression After Radiationmentioning

confidence: 99%

microRNAs identified in prostate cancer: Correlative studies on response to ionizing radiation

et al. 2020

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As the most frequently diagnosed non-skin cancer in men and a leading cause of cancer-related death, understanding the molecular mechanisms that drive treatment resistance in prostate cancer poses a significant clinical need. Radiotherapy is one of the most widely used treatments for prostate cancer, along with surgery, hormone therapy, and chemotherapy. However, inherent radioresistance of tumor cells can reduce local control and ultimately lead to poor patient outcomes, such as recurrence, metastasis and death. The underlying mechanisms of radioresistance have not been fully elucidated, but it has been suggested that miRNAs play a critical role. miRNAs are small non-coding RNAs that regulate gene expression in every signaling pathway of the cell, with one miRNA often having multiple targets. By fine-tuning gene expression, miRNAs are important players in modulating DNA damage response, cell death, tumor aggression and the tumor microenvironment, and can ultimately affect a tumor's response to radiotherapy. Furthermore, much interest has focused on miRNAs found in biofluids and their potential utility in various clinical applications. In this review, we summarize the current knowledge on miRNA deregulation after irradiation and the associated functional outcomes, with a focus on prostate cancer. In addition, we discuss the utility of circulating miRNAs as non-invasive biomarkers to diagnose, predict response to treatment, and prognosticate patient outcomes.

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MicroRNA‐498 promotes proliferation, migration, and invasion of prostate cancer cells and decreases radiation sensitivity by targeting PTEN

Cited by 29 publications

References 33 publications

miR‑7/SP1/TP53BP1 axis may play a pivotal role in NSCLC radiosensitivity

miR‑7/SP1/TP53BP1 axis may play a pivotal role in NSCLC radiosensitivity

Identification lncRNA LOC102551149/miR‐23a‐5p pathway in hepatic fibrosis

microRNAs identified in prostate cancer: Correlative studies on response to ionizing radiation

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