MicroRNA‐1275 induces radiosensitization in oesophageal cancer by regulating epithelial‐to‐mesenchymal transition via Wnt/β‐catenin pathway

Xie, Congying; You-yi, WU; Fei, Zhenghua; Fang, Yun; Xiao, Shenlan; Su, Huafang

doi:10.1111/jcmm.14784

Cited by 21 publications

(14 citation statements)

References 46 publications

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“…miR-221-3p and miR-222-3p reduce radiosensitivity in thyroid cancer cells. It was previously reported that EMT was associated with decreased cancer sensitivity to radiation therapy (22)(23)(24)(25). Therefore, a colony formation assay was used to determine the role of miR-221-3p and miR-222-3p in radiosensitivity.…”

Section: Mir-221-3p and Mir-222-3p Regulate The Expression Levels Of P-stat3 Emt-related Markers And Nis In Thyroid Cancer Cellsmentioning

confidence: 99%

miR‑221‑3p and miR‑222‑3p regulate the SOCS3/STAT3 signaling pathway to downregulate the expression of NIS and reduce radiosensitivity in thyroid cancer

Zhong

et al. 2021

Exp Ther Med

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The expression levels of microRNA (miR)-221-3p and miR-222-3p in thyroid cancer have been found to be upregulated compared with those in normal tissues. The present study aimed to determine the effects and potential underlying mechanisms of miR-221-3p and miR-222-3p on the regulation of radioactive iodine ( 131 I) uptake and radiosensitivity of thyroid cancer cells. The potential regulatory target genes of miR-221-3p and miR-222-3p were predicted by bioinformatics analysis, and reverse transcription-quantitative polymerase chain reaction was used to verify miR-221-3p, miR-222-3p and target gene expression levels in thyroid cancer tissues and cell lines. Overexpression of miR-221-3p or miR-222-3p in cell models was performed using lentivirus infection. Knockdown of miR-221-3p and miR-222-3p in cells was achieved using oligonucleotide inhibitor transfection.Western blotting was used to analyze the expression levels of target proteins. In addition, the effects of miR-221-3p and miR-222-3p on the radiosensitivity of thyroid cancer cells were verified using a colony formation assay. The results of the present study revealed that the expression levels of miR-221-3p and miR-222-3p were significantly upregulated, while the expression levels of suppressor of cytokine signaling 3 (SOCS3) were downregulated in thyroid cancer tissues. Furthermore, miR-221-3p and miR-222-3p overexpression downregulated the expression levels of SOCS3, E-cadherin and solute carrier family 5 member 5 (NIS), and upregulated the expression levels of phosphorylated STAT3 and vimentin. Following the overexpression of miR-221-3p or miR-222-3p in the FTC133 and TPC1 cell lines, their radiosensitivity was suppressed. In conclusion, the findings of the present study suggested that miR-221-3p and miR-222-3p may downregulate the expression levels of NIS and promote radioresistance. The potential mechanism was hypothesized to be associated with the miR-221-3p and miR-222-3p targeting of the SOCS3 gene, which may subsequently activate the STAT3 signaling pathway.

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Section: Mir-221-3p and Mir-222-3p Regulate The Expression Levels Of P-stat3 Emt-related Markers And Nis In Thyroid Cancer Cellsmentioning

confidence: 99%

miR‑221‑3p and miR‑222‑3p regulate the SOCS3/STAT3 signaling pathway to downregulate the expression of NIS and reduce radiosensitivity in thyroid cancer

Zhong

et al. 2021

Exp Ther Med

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“…For instance, the overexpression of miR-32-5p contributed to radioresistance by targeting Transducer of ERBB2, 1 in colorectal cancer (30). miR-1275 elevation diminished epithelialto-mesenchymal transition-induced radioresistance through Wnt/β-catenin signaling in esophageal cancer (31). Impediment of miR-365 suppressed the radiosensitivity of NSCLC via promoting cell division cycle 25A (32).…”

Section: Discussionmentioning

confidence: 99%

miR-335 Acts as a Tumor Suppressor and Enhances Ionizing Radiation-Induced Tumor Regression by Targeting ROCK1

Cheng

Shen

2020

Front. Oncol.

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Recent development of integrative therapy against melanoma combines surgery, radiotherapy, targeted therapy, and immunotherapy; however, the clinical outcomes of advanced stage and recurrent melanoma are poor. As a skin cancer, melanoma is generally resistant to radiotherapy. Hence, there is an urgent need for evaluation of the mechanisms of radioresistance. The present study identified miR-335 as one of the differential expression of miRNAs in recurrent melanoma biopsies post-radiotherapy. The expression of miR-335 declined in melanoma tissues compared to the adjacent tissues. Moreover, miR-335 expression correlated with advanced stages of melanoma negatively. Consistent with the prediction of STARBASE and miRDB database, miR-335 targeted ROCK1 via binding with 3 ′ -UTR of ROCK1 directly, resulting in attenuation of proliferation, migration, and radioresistance of melanoma cells. The authors validated that overexpression of miR-335 enhanced X-ray-induced tumor regression by B16 mouse models. Briefly, the present findings gained insights into miR-335/ROCK1-mediated radiosensitivity and provided a promising therapeutic strategy for improving radiotherapy against melanoma.

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“…Several studies have identi ed that miR-1275 participate in and regulates the genesis and progression of tumors [25][26][27][28][29]. Xie et.al reported that in glioblastoma miR-1275 was involved in the modulation of a series of genes related to tumor progression, CSCs maintenance, cell maturation and differentiation, which provided a new therapeutic target for differentiation induction therapy [25].…”

Section: Discussionmentioning

confidence: 99%

miR-1275 Targets MDK/AKT Signaling to Inhibit Breast Cancer Chemoresistance by Lessening the Properties of Cancer Stem Cells

Han

Wang

et al. 2021

Preprint

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Background: Chemoresistance is a major obstacle in the neoadjuvant chemotherapy (NCT) of locally advanced breast cancer (LABC). Identification of miRNAs as prognostic biomarkers may help overcome chemoresistance of breast cancer (BC). The aim of this study was to evaluate the expression level of miR-1275 in plasma samples and the biological functions in the chemoresistance of BC.Methods: The expression levels of miR-1275 in plasma samples and cells were measured by RT-qPCR. The associations between the expression levels of miR-1275 and clinicopathological features were studied. CRISPR/Cas9-mediated gene editing was used to construct miR-1275 knock-out cells. CCK-8, colony formation assays, epirubicin accumulation assay and xenograft tumor models were used to detect the sensitivity of breast cancer cells to epirubicin in vitro and in vivo. Mammosphere formation assay, flow cytometry analysis and western blot analyses were used to evaluate the effects of miR-1275 on cancer stem cells (CSCs) characteristics in BC cells. Dual-luciferase reporter, RNA pulldown, ELISA and IHC were used to verify the relationship between the expression of miR-1275 and Midkine (MDK). Results: We found that miR-1275 was significantly downregulated in plasma from patients resistant to chemotherapy with LABC and in chemoresistant breast cancer cell lines, while patients with low levels of miR-1275 show poor overall survival. Mir-1275 knock-out promoted chemoresistance in breast cancer cells by increasing the properties of cancer stem cells in vitro and in vivo. Mechanistically, we identified that Midkine was determined to be direct downstream protein of miR-1275 which initiated PI3K/Akt signaling in breast cancer cells.Conclusions: We demonstrated that the high expression level of miR-1275 in plasma predicted better response to NCT. The reduction of miR-1275 promoted BC cells chemoresistance by increasing CSC properties via targeting MDK/AKT axis. The potential of miR-1275 as a new prognostic biomarker and therapeutic target of breast cancer patients was identified.

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MicroRNA‐1275 induces radiosensitization in oesophageal cancer by regulating epithelial‐to‐mesenchymal transition via Wnt/β‐catenin pathway

Cited by 21 publications

References 46 publications

miR‑221‑3p and miR‑222‑3p regulate the SOCS3/STAT3 signaling pathway to downregulate the expression of NIS and reduce radiosensitivity in thyroid cancer

miR‑221‑3p and miR‑222‑3p regulate the SOCS3/STAT3 signaling pathway to downregulate the expression of NIS and reduce radiosensitivity in thyroid cancer

miR-335 Acts as a Tumor Suppressor and Enhances Ionizing Radiation-Induced Tumor Regression by Targeting ROCK1

miR-1275 Targets MDK/AKT Signaling to Inhibit Breast Cancer Chemoresistance by Lessening the Properties of Cancer Stem Cells

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