Identification of micro<scp>RNA</scp>s involved in the radioresistance of esophageal cancer cells

Su, Huafang; Jin, Xiance; Zhang, Xuebang; Xue, Shengliu; Deng, Xia; Shen, Lanxiao; Fang, Yun; Xie, Congying

doi:10.1002/cbin.10202

Cited by 42 publications

(34 citation statements)

References 28 publications

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“…Many miRNAs act as tumor suppressors; however, the evidence supporting those claims is barely correlative (Su et al, ). At present, there are a lack of substantial experimental data, and miRNA knockout mice with or predicted to have cancer have not been yet reported.…”

Section: Discussionmentioning

confidence: 99%

microRNA‐216b inhibits cell proliferation and migration in human melanoma by targeting FOXM1 in vitro and in vivo

Sun

Wang

et al. 2017

Cell Biology International

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MicroRNAs (miRNAs) play an increasingly important role in cancer growth by coordinately suppressing genes that control cell migration, proliferation, and invasion. The above results can be achieved through the regulation of gene expression by miRNAs by suppressing translation or the direct sequence-specific degradation of the targeted mRNA. In the present study, we indicate that the expression of miR-216b could be effectively repressed both in human melanoma tissues through a comparison with primary melanoma and in human melanoma cell lines through a comparison with a normal human keratinocyte line. Moreover, miR-216b induced a clear decrease in melanoma cell proliferation and migration in vitro. Forkhead box M1 (FOXM1) was confirmed as a target gene of miR-216b, and the overexpression of miR-216b markedly repressed the luciferase activity of reporter plasmids containing the FOXM1 3'-UTR (untranslated region). Furthermore, miR-216b suppressed melanoma cell growth in nude mice in vivo, with the effects of miR-216b overexpression on melanoma cell growth and proliferation reversed by FOXM1 overexpression. The results demonstrated that miR-216b is a tumor suppressor in melanoma, identified the FOXM1 signaling pathway as a target of miR-216b action, and suggested a potential therapeutic role for miR-216b in melanoma.

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Section: Discussionmentioning

confidence: 99%

microRNA‐216b inhibits cell proliferation and migration in human melanoma by targeting FOXM1 in vitro and in vivo

Sun

Wang

et al. 2017

Cell Biology International

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“…Numerous studies have reported that miRNAs are involved in the control of DNA damage or its repair mechanisms (19,20). In addition, miRNAs are involved in various malignant cell behaviors, including radioresistance (21)(22)(23)(24). miR-205, miR-7, miR-100 and miR-101 have been reported to be associated with tumor radioresistance (25)(26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-210 negatively regulates the radiosensitivity of nasopharyngeal carcinoma cells

Luo

Zhao

et al. 2017

Molecular Medicine Reports

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Radiotherapy is one of the primary methods of treatment of malignant tumors, however, resistance to radiation is a major problem. The reasons for the radioresistance are still poorly understood. However, it is generally accepted that microRNAs (miRNAs or miRs) can regulate the radiosensitivity of tumors. The present study therefore aimed to identify specific miRNAs and their effects on radioresistant cells. More specifically, the aim was to investigate specific miRNAs and their effects on radioresistant tumor cells. The radioresistant tumor cells (CNE‑2R) were established using a dose gradient method, and the miRNA expression profiles of CNE‑2R cells and the parental cells (CNE‑2) were determined. The expression of miR‑210 in CNE‑2R cells was significantly higher than in CNE‑2 cells. CNE‑2R cells were transfected with LV‑hsa‑miR‑210‑inhibitor, and CNE‑2 cells were transfected with LV‑hsa‑miR‑210. The expression of miR‑210 was confirmed by reverse transcription quantitative‑polymerase chain reaction. The percentages of CNE‑2R‑miR‑210‑inhibitor and CNE‑2 cells in the G2/M phase were higher than in the CNE‑2R and CNE‑2‑miR‑210 cells, and the percentages of cells in S phase were lower than in the CNE‑2R and CNE‑2‑miR‑210 cells. Following 4 Gy of radiation, CNE‑2R‑miR‑210‑inhibitor and CNE‑2 cells, which express low levels of miR‑210, had a higher apoptosis rate than CNE‑2R and CNE‑2‑miR‑210 cells. Following 4, 8 and 12 Gy of radiation, cell viability and survival fraction of CNE‑2R‑miR‑210‑inhibitor cells were lower than those of CNE‑2R and CNE‑2‑miR‑210 cells, and similar to those of CNE‑2 cells. Together, these findings strongly suggest that miR‑210 negatively regulates the radiosensitivity of tumor cells, and may therefore have therapeutic potential for the treatment of radiation resistance.

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“…miR-301a has also been shown to have a cancerous function in several human tumors, such as pancreatic, prostate, colorectal, and breast cancers (Ma et al, 2014;Zhang et al, 2014;Xia et al, 2015;Xie et al, 2015). Furthermore, miR-301a expression is associated with radiotherapy resistance (Su et al, 2014). However, the role of miR-301a in OS tumor development and metastasis has only recently been investigated and remains largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Upregulated microRNA-301a in osteosarcoma promotes tumor progression by targeting CDC14A

Wang

et al. 2016

Genet. Mol. Res.

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ABSTRACT. MicroRNAs (miRs) are associated with tumor progression in various cancers, such as gastric and hepatic carcinomas, and lung cancer. miR-301a is overexpressed and displays oncogenic activity in cancers. We investigated the biological involvement of miR301a in osteosarcoma (OS). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyze expression levels of miR-301a in 24 OS and matched adjacent non-tumor tissues. A miR-301a mimic was transferred into OS cell lines U-2 OS and MG-63 to upregulate miR-301a. The effects of miR-301a were investigated by examining cell proliferation, migration, and the cell cycle. The miR-301 target was predicted by TargetScan and confirmed by western blotting and qRT-PCR. The expression of miR-301a was significantly higher in OS tissues compared with the matched adjacent non-tumor tissues (0.959 ± 0.39 vs 3.9516 ± 1.18). Upregulated miR-301a significantly increased proliferation at 48 and 72 h compared to the negative control (U-2 OS: 2.11 ± 0.21 vs 2.88 ± 0.24; 2.70 ± 0.26 vs 3.71 ± 0.24; MG-63: 2.19 ± 0.20 vs 3.19 ± 0.22; 3.1 ± 0.25 vs 4.01 ± 0.27) and migration capability (U-2 OS: 100 ± 20.19 vs 150.68 ± 32.83; MG-63: 100 ± 17.20 vs 133.35 ± 26.26), and decreased apoptosis in both U-2 OS (10.87 ± 2.53 vs 4.01 ± 2.23) and MG-63 (15.26 ± 2.15 vs 8.25 ± 3.07). The cell cycle studies revealed that miR-301a caused an increase of the G2 population in U-2 OS (38.6 ± 6.58 vs 47.2 ± 7.27) and . Additional experiments indicated that CDC14A was upregulated by miR-301a (0.63 ± 0.06 vs 0.98 ± 0.06; 1.49 ± 0.25 vs 2.99 ± 0.14). Overexpressed miR-301a may increase CDC14A expression and promote cell proliferation and migration in OS cells. Therefore, miR301a may be useful for osteosarcoma diagnosis and therapy.

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Identification of microRNAs involved in the radioresistance of esophageal cancer cells

Cited by 42 publications

References 28 publications

microRNA‐216b inhibits cell proliferation and migration in human melanoma by targeting FOXM1 in vitro and in vivo

microRNA‐216b inhibits cell proliferation and migration in human melanoma by targeting FOXM1 in vitro and in vivo

MicroRNA-210 negatively regulates the radiosensitivity of nasopharyngeal carcinoma cells

Upregulated microRNA-301a in osteosarcoma promotes tumor progression by targeting CDC14A

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