miR-144-5p Enhances the Radiosensitivity of Non-Small-Cell Lung Cancer Cells via Targeting ATF2

Song, Lei; Peng, Liping; Hua, Shucheng; Li, Xiaoping; Ma, Lu‐Fang; Jie, Jing; Chen, Dong; Wang, Ying; Li, Dan

doi:10.1155/2018/5109497

Cited by 65 publications

(48 citation statements)

References 37 publications

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“…It has been reported that miR‐124 can enhance the radiation‐induced apoptosis of NSCLC cells via inhibition of STAT3 . Similarly, miR‐144‐5p can enhance the radiosensitivity of NSCLC cells by regulating ATF2 . In our present study, radiation therapy can increase the expression of miR‐155‐5p and miR‐760 in NSCLC cells.…”

Section: Introductionsupporting

confidence: 48%

“…We firstly investigated the roles of radiation on migration and invasion of NSCLC cells. It has been reported that radiation greater than 5 Gy can significantly inhibit the proliferation of NSCLC cells . Our data showed that the radiation of 2 Gy, which had no significant effect on cell proliferation , can significantly inhibit the wound healing of A549 (Fig.…”

Section: Resultsmentioning

confidence: 99%

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miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

et al. 2019

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MicroRNAs (miRNAs) play important roles in tumorigenesis of various cancers. Recent study suggested that miRNAs are involved in the therapeutic functions of radiation during cancer treatment. We found that radiation can decrease the migration and invasion of non-small cell lung cancer (NSCLC) cells. Mechanistically, radiation can significantly increase the expression of miR-155-5p and miR-760 in NSCLC cells. Knockdown of miR-155-5p and miR-760 can attenuate radiation suppressed proliferation of NSCLC cells. Among the various targets of miR-155-5p, radiation can decrease the expression of HIF-1α. Similarly, radiation can also suppress the expression of IL-6 via a miR-760 dependent pathway. Gain and loss of function studies confirmed that both HIF-1α and IL-6 were involved in the radiation suppressed proliferation of NSCLC cells. Collectively, our data showed that radiation can regulate the expression of miR-155-5p and miR-760 to suppress the malignancy of NSCLC cells. © 2019 BioFactors, 45(3):393-400, 2019

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Section: Introductionsupporting

confidence: 48%

Section: Resultsmentioning

confidence: 99%

miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

et al. 2019

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“…MiR-144 is detected in lung cancer cells with the expression of upregulated glucose transporter 1 (GLUT1) and enhanced glucose uptake [139]. Moreover, miR144-5p increases the radiosensitivity in NSCLC cells by targeting activating transcription factor 2 (ATF2) [140]. Chen Y et al evaluated the downregulation of miR-144-3p and its clinical value in NSCLC.…”

Section: Mir-144 In Lung Cancermentioning

confidence: 99%

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

Kooshkaki

Rezaei

Rahmati

et al. 2020

IJMS

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MicroRNAs (miRNAs) are small and non-coding RNAs that display aberrant expression in the tissue and plasma of cancer patients when tested in comparison to healthy individuals. In past decades, research data proposed that miRNAs could be diagnostic and prognostic biomarkers in cancer patients. It has been confirmed that miRNAs can act either as oncogenes by silencing tumor inhibitors or as tumor suppressors by targeting oncoproteins. MiR-144s are located in the chromosomal region 17q11.2, which is subject to significant damage in many types of cancers. In this review, we assess the involvement of miR-144s in several cancer types by illustrating the possible target genes that are related to each cancer, and we also briefly describe the clinical applications of miR-144s as a diagnostic and prognostic tool in cancers.Int. J. Mol. Sci. 2020, 21, 2578 2 of 23 of a mRNA molecule [3]. MiRNAs indicate a new perspective in the study of cancers. More than 50% of miRNA genes were discovered to be located within the genomic regions that are involved in cancers, suggesting their role in human cancer pathogenesis. In pathological conditions, MiRNAs can negatively regulate gene expression and they are associated with tumor growth, apoptosis, invasion, and metastasis. In the past, several studies have indicated the ability of miRNAs in the inhibition of tumors as a critical option for the improvement of cancer therapy [4,5]. Tumor activator miRNAs, called oncomiRs, are overexpressed in various cancers. On the contrary, suppressive tumor miRNAs are underexpressed [6][7][8]. Among several miRNAs assessed, miR-144s seem to have a role in several cancers. These miRNAs are located in the chromosomal region 17q11.2, being significantly destroyed in many types of cancers. The predicted stem-loop structure of miR-144s recognized by the miRBase (http://mirbase.org/) is shown in Figure 1A. The miR-144 hairpin gives rise to the "guide strand" miR-144-5p and the sister "passenger" strand miR-144-3p ( Figure 1B).

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“…4,5 Among those biomarkers, some act as protooncogenes, and some are considered as antioncogenes via controlling the survival and metastatic capacities of tumor cells. It has been well-established that miRNAs contribute to a wide range of physiological and pathological events, including the occurrence and development of various tumors.…”

Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‐105 promotes epithelial‐mesenchymal transition of nonsmall lung cancer cells through upregulating Mcl‐1

Jin

Qiang

et al. 2018

J of Cellular Biochemistry

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Background A growing number of microRNAs have been proved to play significant roles in limiting tumor growth and the epithelial‐mesenchymal transition (EMT) process of nonsmall cell lung cancer (NSCLC). Present work aims to study the function of microRNA (miR)‐105 in EMT of NSCLC cells, which is unrevealed yet. Methods Two NSCLC cell lines A549 and Calu‐3 were transfected with miR‐105 mimic, inhibitor, or scrambled control. And then the effects of miR‐105 were evaluated by performing trypan blue staining, transwell assay, ANNEXIN‐FITC/propidium iodide (PI) double staining and Western blot analysis. The expression levels of myeloid cell leukemia‐1 (Mcl‐1) after transfection were tested by real‐time quantitative polymerase chain reaction and Western blot analysis. Whether Mcl‐1 was a downstream effector of miR‐105, and the involvement of mammalian target of Rapamycin (mTOR) and p38 mitogen‐activated protein kinase (p38MAPK) signaling pathways were assessed. Results The overexpression of miR‐105 significantly increased the viability and migration of A549 and Calu‐3, but had no impacts on cell apoptosis. Meanwhile, E‐cadherin was remarkably downregulated, and N‐cadherin, Vimentin, ZEB1, and Snail were upregulated by miR‐105 overexpression. Mcl‐1 was positively regulated by miR‐105, and the effects of miR‐105 overexpression on A549 and Calu‐3 cells viability, migration and EMT were all flattened by Mcl‐1 silence. Both mTOR and p38MAPK pathways were activated in miR‐105‐overexpressing and Mcl‐1‐overexpressing cells. Besides, inhibition of mTOR and p38MAPK pathways by using Rapamycin and VX‐702 abolished the regulatory effects of Mcl‐1 on EMT. Conclusion Our study underlines the importance of miR‐105 in modulating NSCLC cells EMT. miR‐105 promoted the EMT of NSCLC cells possibly via upregulation of Mcl‐1 and thereby activation of mTOR and p38MAPK signaling.

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miR-144-5p Enhances the Radiosensitivity of Non-Small-Cell Lung Cancer Cells via Targeting ATF2

Cited by 65 publications

References 37 publications

miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

miR‐155‐5p and miR‐760 mediate radiation therapy suppressed malignancy of non‐small cell lung cancer cells

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

Retracted: MicroRNA‐105 promotes epithelial‐mesenchymal transition of nonsmall lung cancer cells through upregulating Mcl‐1

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