miR-339-5p Increases Radiosensitivity of Lung Cancer Cells by Targeting Phosphatases of Regenerating Liver-1 (PRL-1)

Wang, Jia; Jiang, Mawei; Xia, Shi’an

doi:10.12659/msm.910808

Cited by 16 publications

(13 citation statements)

References 23 publications

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“…Similar to lncRNA, miRNA is involved in multiple cancers and functions as the regulator of radiosensitivity. 52 , 53 For instance, miR-99a enhances the radiosensitivity of NSCLC cells by targeting the expression of mammalian target of rapamycin. 54 Upregulated miR-328-3p makes NSCLC cells more sensitive to radiotherapy.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

Niu

Huang

et al. 2020

Technol Cancer Res Treat

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Background: PTPRG antisense RNA 1 has been well-documented to exert an oncogenic role in diverse neoplasms. However, the precise role of PTPRG antisense RNA 1 in regulating radiosensitivity of nonsmall cell lung cancer cells remains largely elusive. Methods: Expression levels of PTPRG antisense RNA 1 and miR-200c-3p in nonsmall cell lung cancer tissues and cells were detected by quantitative real-time polymerase chain reaction, while transcription factor 4 expression was examined by immunohistochemistry and Western blot. After nonsmall cell lung cancer cells were exposed to X-ray with different doses in vitro, Cell Counting Kit -8 assay and colony formation assay were conducted to determine the influence of PTPRG antisense RNA 1 on cell viability. Interaction between miR-200c-3p and PTPRG antisense RNA 1 as well as transcription factor 4 was investigated by dual luciferase reporter assay. Result: In nonsmall cell lung cancer tissues, the expressions of PTPRG antisense RNA 1 and transcription factor 4 were significantly upregulated, whereas the expression of miR-200c-3p was downregulated. It was also proved that PTPRG antisense RNA 1 and 3′-untranslated region of transcription factor 4 can bind to miR-200c-3p. Under X-ray irradiation, overexpressed PTPRG antisense RNA 1 could promote the viability and enhance the radioresistance of nonsmall cell lung cancer cells, and this effect was partially weakened by miR-200c-3p mimics. Transcription factor 4 was identified as a target gene of miR-200c-3p, which could be positively regulated by PTPRG antisense RNA 1. Conclusion: PTPRG antisense RNA 1 reduces the radiosensitivity of nonsmall cell lung cancer cells via modulating miR-200c-3p/TCF4 axis.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

Niu

Huang

et al. 2020

Technol Cancer Res Treat

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“…Haijun Li et al reported that reduced miR‐339 expression predicts the poor prognosis of GC. In ovarian cancer, miR‐339 inhibited the tumor progress by directly regulating NACC1 and Bcl6 while miR‐339 regulated the metastasis of colorectal cancer via targeting PRL‐1 . LncRNA RP11‐81H3.2 might function as a ceRNA and sponge the miR‐339.…”

Section: Discussionmentioning

confidence: 99%

RP11‐81H3.2 promotes gastric cancer progression through miR‐339‐HNRNPA1 interaction network

et al. 2020

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Recent studies have demonstrated that various long non‐coding RNAs (lncRNAs) participate in the gastric cancer (GC) development and metastasis. Some lncRNAs exert their regulatory function by interacting with microRNAs. Here we identified a novel lncRNA RP11‐81H3.2 that was highly expressed in the GC tissue and cell lines. RP11‐81H3.2 knockdown significantly inhibited the proliferation, migration, and invasion of GC cells. Mechanistically, we demonstrated that RP11‐81H3.2 directly interacted with miR‐339 while miR‐339 regulated the HNRNPA1 expression by targeting HRRNPA1 3’‐UTR. RP11‐81H3.2‐miR‐339‐HNRNPA1 interaction network regulated the GC cell proliferation, migration, and invasion. Moreover, our results confirmed that RP11‐81H3.2 knockdown suppressed the tumor growth of GC in a xenograft model in vivo. In summary, the results suggest that RP11‐81H3.2 functions as an oncogene in GC and could be utilized as a promising diagnosis and therapeutic marker for GC treatment.

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“…Expression of miRNAs is essential for multiple biological processes, such as cell proliferation and differentiation (12,13). However, the aberrant expression of certain miRNAs and the subsequent dysregulation of target gene expression have been associated with the genesis and progression of multiple types of cancer (14,15). Downregulation of miRNA (miR)-124-5p is associated with lymphangiogenesis in human gastric cancer (16); additionally, low expression levels of miR-124-5p have been detected in glioma and colorectal cancer cells (17,18).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of microRNA‑124‑5p sensitizes non‑small cell lung cancer cells to treatment with 5‑fluorouracil via AEG‑1 regulation

et al. 2020

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Chemotherapeutic resistance represents a major obstacle for the treatment of patients with non-small cell lung cancer (NSCLC); however, the associated molecular mechanisms underpinning the development of resistance remain poorly characterized. In the current study, 5-fluorouracil (5-FU)-resistant A549 cells (A549/5-FU) were generated from A549 cells. Reverse transcription-quantitative PCR and western blotting were used to detect microRNA(miR)-124-5p and astrocyte elevated gene 1 (AEG-1) expression levels in cells and tumor tissues. In addition, the cytotoxic effect of 5-FU on the cells was determined using the Cell Counting Kit-8 assay, and the Dual-luciferase reporter assay was used to validate AEG-1 as a target gene of miR-124-5p. Transfection with a miR-124-5p mimic enhanced inhibition of cell viability induced by 5-FU in A549/5-FU cells, whereas miR-124-5p inhibitor transfection partially reversed 5-FU-induced cell viability inhibition in A549 and H1299 cells. A decrease in miR-124-5p expression level was observed in A549/5-FU cells compared with the parental A549 cells. Furthermore, AEG-1 was predicted as a target gene of miR-124-5p, and its expression was increased in A549/5-FU cells compared with A549 cells. Additionally, the upregulation of miR-124-5p was associated with lower expression levels of AEG-1 in A549/5-FU cells, compared with parental A549 cells. Moreover, the Dual-luciferase reporter assay confirmed the ability of miR-124-5p to bind directly to the 3'-untranslated region of AEG-1 mRNA. Notably, the overexpression of AEG-1 reversed the ability of the miR-124-5p mimic to increase the sensitivity of A549/5-FU cells to 5-FU treatment. Additionally, a significant negative correlation between miR-124-5p expression and AEG-1 mRNA levels was detected in 40 pairs of NSCLC tissues and their corresponding adjacent paracancerous tissues. The results of the present study indicated that miR-124-5p may regulate the chemotherapeutic sensitivity of NSCLC cells, and may therefore represent a promising biomarker or therapeutic target for patients with NSCLC.

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miR-339-5p Increases Radiosensitivity of Lung Cancer Cells by Targeting Phosphatases of Regenerating Liver-1 (PRL-1)

Cited by 16 publications

References 23 publications

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

RP11‐81H3.2 promotes gastric cancer progression through miR‐339‐HNRNPA1 interaction network

Overexpression of microRNA‑124‑5p sensitizes non‑small cell lung cancer cells to treatment with 5‑fluorouracil via AEG‑1 regulation

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