MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

Zhao, Yaqi; Gu, Xiaoqing; Wang, Yanpeng

doi:10.1002/lary.28045

Cited by 8 publications

(8 citation statements)

References 32 publications

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“…Herein, our results illustrated that TIMP3 methylation levels were augmented and TIMP3 protein levels were suppressed in C666-1 and C666-1R cells, with C666-1R cells showing the more obvious alteration; meanwhile, after miR-613 overexpression, TIMP3 methylation levels were suppressed, and TIMP3 protein levels were facilitated in C666-1R cells, whereas further DNMT3B overexpression reversed the above trends in C666-1R cells. Consistent lowly expressed TIMP3 was previously reported in NPC tissues [42], while knockdown of TIMP3 methylation was associated with alleviation of breast cancer [34]. In short, these findings and data make it plausible to suggest that miR-613 reduces TIMP3 methylation levels by inhibiting DNMT3B.…”

Section: Disease Markerssupporting

confidence: 85%

“…Reduced TIMP3 Methylation by Inhibiting DNMT3B. TIMP3 was previously established to be lowly expressed in NPC tissues [42], and TIMP3 methylation is a common occurrence in many cancers [34,43,44]. DNMT3B further represents a major DNA methyltransferase regulated by miR-613.…”

Section: Mir-613mentioning

confidence: 99%

“…Tissue inhibitor of matrix metalloproteinases-3 (TIMP3) is a special member of the TIMP family, which possesses the ability to regulate tumor growth, metastasis, angiogenesis, and other physiological progress through matrix metalloproteinases [38]. Furthermore, as an independent and promising biomarker, TIMP3 plays a regulatory role in a plethora of cancers [39][40][41] and is lowly expressed in NPC tissues [42]. In addition, TIMP3 methylation has been documented in several malignancies [34,43,44].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-613 Enhances Nasopharyngeal Carcinoma Cell Radiosensitivity via the DNA Methyltransferase 3B/Tissue Inhibitor of Matrix Metalloproteinase-3/Signal Transducer and Activator of Transcription-1/Forkhead Box O-1 Axis

et al. 2022

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Nasopharyngeal carcinoma (NPC) is a common malignancy of the nasopharynx, and radioresistant represents the main obstacle in NPC treatment. Malignant transformation of normal cells is driven by genetic and epigenetic changes, which are primarily manifested as changes in miRNA levels and DNA methylation status. microRNA (miR)-613 plays an inhibitory role in several types of cancer. Herein, the current study sought to explore the roles of miR-613 in NPC cell radiosensitivity. miR-613 expression patterns in NPC tissues were detected, and its correlation with clinical indexes was analyzed. NP-69 and C666-1 cell lines were selected for cellular experimentation. Radioresistant cell line C666-1R was obtained by fractionated radiation. Cell viability, survival fraction, and apoptosis were detected by CCK-8, colony formation assay, and flow cytometry. The binding relation between miR-613 and DNMT3B was verified by dual-luciferase and RIP assays. miR-613 was lowly expressed in NPC tissues and cells, with lower expression levels in C666-1R than C666-1, and further correlated with lymph node metastasis, tumor size, and tumor metastasis. miR-613 overexpression reduced C666-1R cell viability and survival fraction and increased apoptosis, while C666-1 cells with silencing miR-613 presented the opposite trends. miR-613 targeted DNMT3B. miR-613 and DNMT3B overexpression led to enhanced C666-1R cell viability and survival fraction and decreased apoptosis. miR-613 reduced TIMP3 methylation and elevated TIMP3 protein level by inhibiting DNMT3B. miR-613 enhanced NPC radiosensitivity by inhibiting the DNMT3B/TIMP3/STAT1/FOXO1 pathway. Collectively, miR-613 inhibited DNMT3B, reduced TIMP3 methylation, and increased TIMP3 protein level, thus inhibiting the STAT1/FOXO1 pathway and enhancing the radiosensitivity of NPC cells.

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Section: Disease Markerssupporting

confidence: 85%

Section: Mir-613mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA-613 Enhances Nasopharyngeal Carcinoma Cell Radiosensitivity via the DNA Methyltransferase 3B/Tissue Inhibitor of Matrix Metalloproteinase-3/Signal Transducer and Activator of Transcription-1/Forkhead Box O-1 Axis

et al. 2022

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“…In vitro experiments revealed that miR‐103 regulates the late stages of autophagy in human keratinocytes 19 . Additionally, an increasing number of reports outlined the involvement of miR‐103 in the proliferation, migration, invasion, and apoptosis of tumour cells 20,21 . It was believed that wound healing and tumours were similar in molecular and functional mechanisms 22 .…”

Section: Introductionmentioning

confidence: 99%

Changes in miroRNA‐103 expression in wound margin tissue are related to wound healing of diabetes foot ulcers

Zhao

Tang

et al. 2022

International Wound Journal

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To investigate the relationship between small noncoding microRNA-103 (miR-103) and wound healing of diabetic foot ulcers (DFU) and the underlying molecular mechanism, forty type 2 diabetes mellitus with DFU (DFU group), and 20 patients with a chronic skin ulcer of lower limbs and normal glucose tolerance (SUC group) were included. Quantitative real-time PCR method was used to determine miR-103 expression levels in the wound margin tissue of subjects, and to analyse the relationship between the expression of miR-103 and DFU wound healing. In vitro experiments were also performed to understand the effect of miR-103 on the high glucose-induced injury of normal human dermal fibroblasts (NHDFs) cells. The results showed that the miR-103 expression level in the DFU group was significantly higher than that in the SUC group [5.81 (2.25-9.36) vs 2.08 (1.15-5.72)] (P < 0.05). The expression level of miR-103 in the wound margin tissue of DFU was negatively correlated with the healing rate of foot ulcers after four weeks (P = 0.037). In vitro experiments revealed that miR-103 could inhibit the proliferation and migration of NHDF cells and promote the apoptosis of NHDF cells by targeted regulation of regulator of calcineurin 1 (RCAN1) gene expression in a high glucose environment. Downregulation of miR-103 could alleviate high glucose-induced NHDF cell injury by promoting RCAN1 expression. Therefore, the increased expression of miR-103 is involved in the functional damage of NHDF cells induced by high-glucose conditions, which is related to poor wound healing of DFU.These research findings will provide potential targets for the diagnosis and treatment of chronic skin wounds in diabetes. K E Y W O R D S foot ulcer, human dermal fibroblasts, miR-103, RCAN1, type 2 diabetets Xiaotong Zhao and Murong Xu contributed equally to this study.

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“…29,30 Tissue inhibitor of metalloproteinase-3 (TIMP3), located on chromosome 22q12, is an endogenous inhibitor of protease activity. 31 Interestingly, TIMP3 can be regulated by many miRNAs in cancers, including miR-103 in nasopharyngeal carcinoma (NPC), 32 miR-21 in HCC 33 and miR-17-5p in bladder cancer. 34 More importantly, accumulating evidence has indicated that TIMP3 also affects the tumorigenesis of HCC.…”

Section: Introductionmentioning

confidence: 99%

Remifentanil reduces the proliferation, migration and invasion of HCC cells via lncRNA NBR2/miR‐650/TIMP3 axis

Liang

2022

Int J Experimental Path

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Cancer cell hyperproliferation and metastasis are major causes of cancer‐associated mortality. Although the use of anaesthetics and analgesics may affect cancer cell metastasis, the underlying molecular mechanism remains unclear. This study aimed to explore the mechanisms of action of remifentanil on hepatocellular carcinoma (HCC) progression. Cell viability was measured by the 3‐(4, 5‐dimethyl‐2‐thiazolyl)‐2, 5‐diphenyl‐2‐h‐tetrazolium bromide assay. Quantitative real‐time polymerase chain reaction and Western blotting were performed to assess the expression levels of long non‐coding RNA (lncRNA) neighbour of BRCA1 gene 2 (NBR2), microRNA (miR)‐650 and tissue inhibitor of metalloproteinase‐3 (TIMP3) in HCC cells. Wound healing and transwell assays were employed to evaluate the migration and invasion of HCC cells respectively. The target relationships between miR‐650 and NBR2/TIMP3 were confirmed by dual luciferase reporter assay. Remifentanil reduced the viability of HCC cells in a dose‐dependent manner. Remifentanil treatment significantly increased the expression of lncRNA NBR2 and TIMP3, and repressed miR‐650 expression in HCC cells. Decreased lncRNA NBR2 or increased miR‐650 promoted the proliferation, migration and invasion of remifentanil‐treated HCC cells. LncRNA NBR2 targeted miR‐650, and miR‐650 further targeted TIMP3. Moreover, miR‐650 down‐regulation or TIMP3 up‐regulation reversed the effects of lncRNA NBR2 knockdown that caused an enhancement of cell viability, migration and invasiveness in remifentanil‐treated HCC cells. Thus remifentanil reduces the proliferation, migration and invasion of HCC cells via the lncRNA NBR2/miR‐650/TIMP3 axis in vitro.

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MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

Cited by 8 publications

References 32 publications

MicroRNA-613 Enhances Nasopharyngeal Carcinoma Cell Radiosensitivity via the DNA Methyltransferase 3B/Tissue Inhibitor of Matrix Metalloproteinase-3/Signal Transducer and Activator of Transcription-1/Forkhead Box O-1 Axis

MicroRNA-613 Enhances Nasopharyngeal Carcinoma Cell Radiosensitivity via the DNA Methyltransferase 3B/Tissue Inhibitor of Matrix Metalloproteinase-3/Signal Transducer and Activator of Transcription-1/Forkhead Box O-1 Axis

Changes in miroRNA‐103 expression in wound margin tissue are related to wound healing of diabetes foot ulcers

Remifentanil reduces the proliferation, migration and invasion of HCC cells via lncRNA NBR2/miR‐650/TIMP3 axis

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