RETRACTED: Down-regulation of miR-373 increases the radiosensitivity of lung cancer cells by targeting TIMP2

Guo, Yinghua; Jiang, Yingxiao; Sang, Maozhong; Xu, Chunli

doi:10.1016/j.biocel.2018.04.014

Cited by 11 publications

(6 citation statements)

References 30 publications

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“…miRNAs can exert effective function in modulation of the radioinduced signaling pathways. Evidence suggests that miR373 and miR126 promote IR-induced apoptosis through the PI3K–Akt pathway in lung cancer 45,46. PTEN is an inhibitory modulator of Akt, and acts as a direct target of miR451.…”

Section: Regulatory Roles Of Tissue-specific Mirnas In Lung Cancer Ramentioning

confidence: 99%

<p>Tissue-specific and exosomal miRNAs in lung cancer radiotherapy: from regulatory mechanisms to clinical implications</p>

Long¹,

Zhang²,

Bai³

et al. 2019

CMAR

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Lung cancer is the most prevalent and deadly malignancy. Radiotherapy is a major treatment modality for lung cancer. Nevertheless, radioresistance poses a daunting challenge that largely limits the efficacy of radiotherapy. There is a pressing need for deciphering molecular mechanisms underlying radioresistance and elucidating novel therapeutic targets for individualized radiotherapy. MicroRNAs are categorized as small noncoding RNAs that modulate target-gene expression posttranscriptionally and are implicated in carcinogenesis and cancer resistance to treatment. Overwhelming evidence has unraveled that tissue-specific miRNAs are essential for regulation of the radiosensitivity in lung cancer cells through a complex interaction with multiple biological processes and radiation-induced pathways. Moreover, exosome-derived miRNAs are a novel horizon in lung cancer treatment in which exosomal miRNAs act as potential diagnostic and therapeutic biomarkers of radiotherapy. In the present review, we discuss the mediation of key biological processes and signaling pathways by tissue-specific miRNAs in lung cancer radiotherapy. Additionally, we provide new insight into the potential significance of exosomal miRNAs in radiation response. Lastly, we highlight miRNAs as promising predictors and therapeutic targets to tailor personalized lung cancer radiotherapy.

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Section: Regulatory Roles Of Tissue-specific Mirnas In Lung Cancer Ramentioning

confidence: 99%

<p>Tissue-specific and exosomal miRNAs in lung cancer radiotherapy: from regulatory mechanisms to clinical implications</p>

Long¹,

Zhang²,

Bai³

et al. 2019

CMAR

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“…[ 27 ] On the one hand, miR‐373 played oncogenic activities in gastric cancer, [ 28 ] renal cell carcinoma, [ 29 ] and lung cancer. [ 30 ] On the other hand, miR‐373 played as tumor‐suppressive role in glioma [ 31 ] and pancreatic cancer. [ 32 ] However, prior literatures have not been able to determine the effects of miR‐373 on medulloblastoma.…”

Section: Introductionmentioning

confidence: 99%

Retracted: Geniposide exhibits anticancer activity to medulloblastoma cells by downregulating microRNA‐373

2020

J Biochem & Molecular Tox

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Background: Medulloblastoma is a common tumor originates from central nervous system in children with metastatic potential. Geniposide is the major active ingredient separated from the fruit of Gardenia jasminoides Ellis. Herein, we tested the possible anticancer activity of geniposide on human medulloblastoma cells, as well as the potential underlying molecular mechanisms.Methods: Firstly, followed by geniposide incubation, cell viability, proliferation, apoptosis, migration, and invasion of medulloblastoma Daoy cells, along with microRNA-373 (miR-373) expression were tested, respectively. Then, the influences of miR-373 overexpression in the reduction of medulloblastoma cell proliferation, migration, and invasion and the elevation of apoptosis, triggered by geniposide treatment, were reinvestigated. Finally, the Ras/Raf/MEK/ERK pathway activity was analyzed. Results: Geniposide treatment inhibited medulloblastoma cell viability, proliferation, migration, and invasion, but promoted cell apoptosis. Surprisingly, miR-373 expression in medulloblastoma cells was obviously downregulated by geniposide treatment. miR-373 overexpression reversed the effects of geniposide on Daoy cells. Furthermore, geniposide hindered the Ras/Raf/MEK/ERK pathway by downregulating miR-373 expression. Conclusion: Geniposide exhibited anticancer activity on human medulloblastoma cells and blocked Ras/Raf/MEK/ERK pathway by downregulating miR-373 expression. K E Y W O R D S cell metastasis, cell proliferation, geniposide, medulloblastoma, microRNA-373, Ras/Raf/MEK/ ERK pathway

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“…The role of miRNAs is fulfilled by regulating the expression of target genes, which is regulated by complementary binding of the miRNA to the 3′-untranslated region (3′UTR) of the target gene mRNA (10,11). miRNAs may act as oncogenes or tumor suppressor genes in the development of cancer (12–15). Numerous studies have reported that the abnormal expression of miRNAs is closely associated with the development of various tumor types (13–18), and miRNAs are expected to be a novel molecular target for the diagnosis and treatment of cancer.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR‑214 attenuates the migration and invasion of triple‑negative breast cancer cells

Zhang

Zhao

et al. 2019

Mol Med Report

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Triple-negative breast cancer (TNBC) is a subtype of breast cancer. MicroRNA (miR)-214 is closely associated with controlling the development of tumor cells; therefore, in the present study, the target gene and effects of miR-214 on TNBC cells were explored. Luciferase activity was examined by luciferase reporter assay. The viability, invasion and migration of MDA-MB-231 TNBC cells were measured using Cell Counting kit-8, Transwell and wound-healing assays, respectively. The expression levels of various factors were determined using reverse transcription-quantitative polymerase chain reaction and western blotting. The results demonstrated that the expression levels of miR-214 were higher and the levels of α1-antitrypsin (α1-AT) were lower in TNBC tissues compared with in normal tissues. Subsequently, α1-AT was revealed to be a target of miR-214. Furthermore, inhibition of miR-214 decreased cell viability, invasion and migration, enhanced the expression of E-cadherin and tissue inhibitor of metalloproteinases-2, and reduced the expression of metastatic tumour antigen 1 and matrix metalloproteinase-2. Inhibition of miR-214 also significantly downregulated the phosphorylation of protein kinase B (Akt) and mammalian target of rapamycin (mTOR), and markedly downregulated that of phosphoinositide 3-kinase (PI3K); however, the expression levels of total PI3K, Akt and mTOR remained stable in all groups. Taken together, these findings indicated that α1-AT may be a target of miR-214. Downregulation of miR-214 markedly suppressed the viability, migration and invasion of MDA-MB-231 cells, and inhibited the PI3K/Akt/mTOR pathway. These findings suggested that miR-214 targeting α1-AT may be a potential mechanism underlying TNBC development.

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RETRACTED: Down-regulation of miR-373 increases the radiosensitivity of lung cancer cells by targeting TIMP2

Cited by 11 publications

References 30 publications

<p>Tissue-specific and exosomal miRNAs in lung cancer radiotherapy: from regulatory mechanisms to clinical implications</p>

<p>Tissue-specific and exosomal miRNAs in lung cancer radiotherapy: from regulatory mechanisms to clinical implications</p>

Retracted: Geniposide exhibits anticancer activity to medulloblastoma cells by downregulating microRNA‐373

Inhibition of miR‑214 attenuates the migration and invasion of triple‑negative breast cancer cells

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