RETRACTED ARTICLE: MicroRNA-422a functions as a tumor suppressor in non-small cell lung cancer through SULF2-mediated TGF-β/SMAD signaling pathway

Li, Weiqiang; Zhang, Jianpeng; Wang, Yanyu; Li, Xin-Zhen; Sun, Lin

doi:10.1080/15384101.2019.1632135

Cited by 19 publications

(24 citation statements)

References 41 publications

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“…In bladder cancer, Li et al draw a conclusion that miR-1298 serves a tumor suppressor by suppressing tumor cell proliferation, migration and invasion [32]. In the tumor progression of NSCLC, some aberrant miRNAs have important functional roles by regulating tumor cell processes, and have been determined as potential therapeutic targets [33][34][35]. Considering the dysregulation of miR-1298 in NSCLC, this study further explored its biological function in tumor progression.…”

Section: Discussionmentioning

confidence: 90%

MicroRNA-1298 is downregulated in non-small cell lung cancer and suppresses tumor progression in tumor cells

Wang

et al. 2019

Diagn Pathol

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Background: MicroRNAs (miRNAs) have been reported to serve pivotal roles in tumorigenesis. This study sough to assess the expression and clinical significance of microRNA-1298 (miR-1298) in patients with non-small cell lung cancer (NSCLC), and explore the functional role of miR-1298 in tumorigenesis. Methods: One hundred and twenty-one NSCLC patients were recruited in this study. The expression of miR-1298 was estimated using quantitative real-time PCR. Kaplan-Meier survival curves and Cox regression analysis were used to evaluate the prognostic value of miR-1298. Gain-and loss-of-function experiments were preformed to explore the biological function of miR-1298 in NSCLC cells. Results: Expression levels of miR-1298 were downregulated in NSCLC tissues and cells compared with the corresponding normal controls. The decreased expression of miR-1298 was associated with patients' lymph node metastasis and TNM stage. The low expression of miR-1298 predicted poor overall survival and served as an independent prognostic indicator in NSCLC patients. According to the cell experiments, NSCLC cell proliferation, migration and invasion were inhibited by the overexpression of miR-1298. Conclusion: All the data indicated that the downregulation of miR-1298 predicts poor prognosis of NSCLC, and the overexpression of miR-1298 in NSCLC cells leads to inhibited tumorigenesis. The aberrant miR-1298 may serve as a novel biomarker and therapeutic target in NSCLC.

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Section: Discussionmentioning

confidence: 90%

MicroRNA-1298 is downregulated in non-small cell lung cancer and suppresses tumor progression in tumor cells

Wang

et al. 2019

Diagn Pathol

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“…Some reports have also shown that oncomir miR-21 downregulates hMSH2 gene expression by targeting the 3 untranslated region of its mRNA [45], and that miR-155 can significantly downregulate hMSH2, hMSH6, and hMLH1 [46], while others have suggested that miRNAs play an important role in modulating cell cycle progression by targeting hMSH2 in lung cancer [42]. Although there are reports suggesting a relationship between the MMR mechanism and miRNA profiles [41,43,44,46], the underlying molecular mechanism by which tobacco smoke carcinogens induce miRNA deregulation and affect the expression profiles of mismatch repair genes, particularly in lung and head and neck cancer, is not yet known.Here, we attempt to explore whether NNK affects the expression of small regulatory molecules, such as known miRNA markers, previously associated with upper aerodigestive tract malignancies [47][48][49][50][51][52][53][54] that may directly or indirectly be involved in the regulation for MMR expression phenotypes. Understanding the molecular changes induced by various risk factors, such as tobacco smoke, which promote the development and progression of cancer, will help to develop new diagnostic and therapeutic approaches [55,56], leading to optimization of their management.…”

mentioning

confidence: 99%

“…Here, we attempt to explore whether NNK affects the expression of small regulatory molecules, such as known miRNA markers, previously associated with upper aerodigestive tract malignancies [47][48][49][50][51][52][53][54] that may directly or indirectly be involved in the regulation for MMR expression phenotypes. Understanding the molecular changes induced by various risk factors, such as tobacco smoke, which promote the development and progression of cancer, will help to develop new diagnostic and therapeutic approaches [55,56], leading to optimization of their management.…”

mentioning

confidence: 99%

The Effect of NNK, A Tobacco Smoke Carcinogen, on the miRNA and Mismatch DNA Repair Expression Profiles in Lung and Head and Neck Squamous Cancer Cells

Doukas

Vageli²,

Lazopoulos

et al. 2020

Cells

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Tobacco smoking is a common risk factor for lung cancer and head and neck cancer. Molecular changes such as deregulation of miRNA expression have been linked to tobacco smoking in both types of cancer. Dysfunction of the Mismatch DNA repair (MMR) mechanism has also been associated with a poor prognosis of these cancers, while a cross-talk between specific miRNAs and MMR genes has been previously proposed. We hypothesized that exposure of lung and head and neck squamous cancer cells (NCI and FaDu, respectively) to tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is capable of altering the expression of MSH2 and MLH1, key MMR components, by promoting specific miRNA deregulation. We found that either a low (1 µM) or high (2 µM) dose of NNK induced significant upregulation of "oncomirs" miR-21 and miR-155 and downregulation of "tumor suppressor" miR-422a, as well as the reduction of MMR protein and mRNA expression, in NCI and FaDu, compared to controls. Inhibition of miR-21 restored the NNK-induced reduced MSH2 phenotype in both NCI and FaDu, indicating that miR-21 might contribute to MSH2 regulation. Finally, NNK exposure increased NCI and FaDu survival, promoting cancer cell progression. We provide novel findings that deregulated miR-21, miR-155, and miR-422a and MMR gene expression patterns may be valuable biomarkers for lung and head and neck squamous cell cancer progression in smokers.Cells 2020, 9, 1031 2 of 22 and neck squamous cell carcinoma (HNSCC), represents one of the most aggressive malignancies with a high rate of mortality. [8,9]. Tobacco smoking has been one of the most well-established risk factors for both lung and head and neck cancers [1][2][3][4][5][6][7][8]. It is known that tobacco smoke contains a mixture of thousands of compounds, including a large number of known carcinogens [2]. It is believed that exposure of cells to tobacco smoke carcinogens can lead to DNA damage, which may cause chromosomal instability and increased cell proliferation [10][11][12][13]. In particular, tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which is one of the chemicals in tobacco smoke, has been linked to lung and head and neck cancer [14], and has also been shown to upregulate oncogenic pathways [15][16][17].The development and progression of lung and head and neck malignancies appear to be a complex process. Although multiple diagnostic and prognostic markers have been identified for both lung and head and neck cancers [18,19], the precise molecular mechanisms involved in the development and progression of these malignancies remain unclear.We understand that a functional DNA repair mechanism that includes the recognition and repair of mismatch DNA errors during DNA replication is essential in eliminating the harmful effect of several environmental risk factors, such as NNK, on the exposed cells [20][21][22][23]. A number of studies have shown that reduced expression of mismatch DNA repair (MMR) genes increases the incidence of microsatellite ...

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“…miR-422a negatively modulates the EGFR/MEK/ERK signaling pathway by targeting the mediator complex subunit (Med19) (44). Additionally, miR-422a serves as a tumor suppressor through the SULF2-mediated TGF-β/SMAD signaling pathway in non-small cell lung cancer (45). Furthermore, miR-422a inhibits the PI3K/AKT pathway by directly targeting PIK3CA and AKT1 in glioma and colorectal cancer, respectively (14,46).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑422a functions as a tumor suppressor in glioma by regulating the Wnt/β‑catenin signaling pathway via RPN2

et al. 2020

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MicroRNAs (miRs), which act as crucial regulators of oncogenes and tumor suppressors, have been confirmed to play a significant role in the initiation and progression of various malignancies, including glioma. The present study analyzed the expression and roles of miR-422a in glioma, and reverse transcription-quantitative PCR confirmed that miR-422a expression was significantly lower in glioblastoma multiforme (GBM) samples and cell lines compared with the low-grade glioma samples and the H4 cell line, respectively. miR-422a overexpression suppressed proliferation and invasion, and induced apoptosis in LN229 and U87 cell lines. Luciferase reporter assay, western blotting and RNA immunoprecipitation analysis revealed that ribophorin II (RPN2) is a direct functional target of miR-422a. Additionally, the overexpression of RPN2 partially reversed the miR-422a-mediated inhibitory effect on the malignant phenotype. Mechanistic investigation demonstrated that the upregulation of miR-422a inhibited β-catenin/transcription factor 4 transcriptional activity, at least partially through RPN2, as indicated by in vitro and in vivo experiments. Furthermore, RPN2 expression was inversely correlated with miR-422a expression in GBM specimens and predicted patient survival in the Chinese Glioma Genome Atlas, UALCAN, Gene Expression Profiling Interactive Analysis databases. In conclusion, the present data reveal a new miR-422a/RPN2/Wnt/β-catenin signaling axis that plays critical roles in glioma tumorigenesis, and it represents a potential therapeutic target for GBM.

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RETRACTED ARTICLE: MicroRNA-422a functions as a tumor suppressor in non-small cell lung cancer through SULF2-mediated TGF-β/SMAD signaling pathway

Cited by 19 publications

References 41 publications

MicroRNA-1298 is downregulated in non-small cell lung cancer and suppresses tumor progression in tumor cells

MicroRNA-1298 is downregulated in non-small cell lung cancer and suppresses tumor progression in tumor cells

The Effect of NNK, A Tobacco Smoke Carcinogen, on the miRNA and Mismatch DNA Repair Expression Profiles in Lung and Head and Neck Squamous Cancer Cells

MicroRNA‑422a functions as a tumor suppressor in glioma by regulating the Wnt/β‑catenin signaling pathway via RPN2

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