miRNA-19 promotes non-small-cell lung cancer cell proliferation via inhibiting CBX7 expression

Peng, Xiaogang; Guan, Li; Gao, Baoan

doi:10.2147/ott.s181433

Cited by 33 publications

(25 citation statements)

References 33 publications

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“…Similar data were obtained, regarding miR-19, which inhibited CBX7 expression, which led to activation of proliferation, migration, and invasion of NSCLC cells [74].…”

Section: Epigenetic Factors In the Development Of Cancersupporting

confidence: 84%

Radon Biomonitoring and microRNA in Lung Cancer

Bersimbaev

Pulliero

Bulgakova

et al. 2020

IJMS

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Radon is the number one cause of lung cancer in non-smokers. microRNA expression in human bronchial epithelium cells is altered by radon, with particular reference to upregulation of miR-16, miR-15, miR-23, miR-19, miR-125, and downregulation of let-7, miR-194, miR-373, miR-124, miR-146, miR-369, and miR-652. These alterations alter cell cycle, oxidative stress, inflammation, oncogene suppression, and malignant transformation. Also DNA methylation is altered as a consequence of miR-29 modification induced by radon. Indeed miR-29 targets DNA methyltransferases causing inhibition of CpG sites methylation. Massive microRNA dysregulation occurs in the lung due to radon expose and is functionally related with the resulting lung damage. However, in humans this massive lung microRNA alterations only barely reflect onto blood microRNAs. Indeed, blood miR-19 was not found altered in radon-exposed subjects. Thus, microRNAs are massively dysregulated in experimental models of radon lung carcinogenesis. In humans these events are initially adaptive being aimed at inhibiting neoplastic transformation. Only in case of long-term exposure to radon, microRNA alterations lead towards cancer development. Accordingly, it is difficult in human to establish a microRNA signature reflecting radon exposure. Additional studies are required to understand the role of microRNAs in pathogenesis of radon-induced lung cancer.

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“…Similar data were obtained, regarding miR-19, which inhibited CBX7 expression, which led to activation of proliferation, migration, and invasion of NSCLC cells [74].…”

Section: Epigenetic Factors In the Development Of Cancersupporting

confidence: 84%

Radon Biomonitoring and microRNA in Lung Cancer

Bersimbaev

Pulliero

Bulgakova

et al. 2020

IJMS

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“…For example, miR-671-3p was shown to suppress NSCLC progression by directly binding to and inhibiting Cyclin D2 (CCND2) 27. Moreover, miR-19 was shown to promote NSCLC cell proliferation in vitro by binding to the 3ʹ-UTR of CBX7 mRNA and thereby inhibiting CBX7 expression 28. Our study is the first to explore the roles and mechanisms of miR-34c in the pathogenesis of NSCLC, and the results not only increase our understanding of NSCLC pathogenesis, but also suggest a new potential therapeutic target for NSCLC.…”

Section: Discussionmentioning

confidence: 99%

<p>MiR-34c acts as a tumor suppressor in non-small cell lung cancer by inducing endoplasmic reticulum stress through targeting HMGB1</p>

Long

Song

et al. 2019

OTT

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Objective To investigate the role of miR-34c in lung cancer. Methods The levels of microRNA-34c (miR-34c) expression in non-small cell lung cancer (NSCLC) tissue and cell lines were examined by the qRT-PCR assay. High mobility group box 1 (HMGB1) expression in NSCLC was assessed by immunohistochemical analysis (IHC), qRT-PCR, and Western blot assays. The effects of miR-34c overexpression or HMGB1 knockdown on cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry analysis, respectively. Cellular reactive oxygen species (ROS) production in NSCLC cells was detected using a ROS kit. The levels of Bax, p-ERK, eIF2α, GADD153, and IRE1α expression in treated NSCLC cells were measured by Western blot assays. In addition, the interaction between miR-34c and HMGB1 was verified by the dual-luciferase reporter assay. Results miR-34c was only slightly expressed, while HMGB1 was highly expressed in NSCLC tissues and cell lines. Overexpression of miR-34c or knockdown of HMGB1 inhibited cell proliferation, promoted cell apoptosis, and induced ER stress in NSCLC cells. In terms of mechanism, miR-34c negatively regulated HMGB1 expression by directly targeting the 3ʹ-untranslated region (UTR) of HMGB1 mRNA. In addition, we proved that HMGB1 overexpression could block the effects of miR-34c on NSCLC cell proliferation, apoptosis, and ER stress. Conclusion miR-34c may suppress NSCLC tumors by targeting HMGB1 mRNA, promoting endoplasmic reticulum stress, and increasing ROS levels. Our findings suggest that miR-34c has a role in NSCLC.

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“…Our GSEA analysis also indicated a "normal like", more differentiated phenotype of low PPS20 tumors with an enrichment of digestion and ion channel transport related gene sets. Among genes upregulated in this group, CBX7, MIA3 and KANK1 have been shown to have tumor suppressive activities including roles in inhibition of PLOS ONE cellular motility/migration and/or proliferation, and induction of cell cycle arrest in various malignancies [60][61][62][63][64][65][66][67]. PITPNA which we found as a good prognostic indicator, is suggested as favorable prognostic marker in pancreatic, endometrial and renal cancers in the Human Protein Atlas (www.proteinatlas.org) [68], and its overexpression was associated with longer survival in PDAC [69].…”

Section: Plos Onementioning

confidence: 99%

A novel 20-gene prognostic score in pancreatic adenocarcinoma

et al. 2020

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Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal cancers. Known risk factors for this disease are currently insufficient in predicting mortality. In order to better prognosticate patients with PDAC, we identified 20 genes by utilizing publically available high-throughput transcriptomic data from GEO, TCGA and ICGC which are associated with overall survival and event-free survival. A score generated based on the expression matrix of these genes was validated in two independent cohorts. We find that this "Pancreatic cancer prognostic score 20-PPS20" is independent of the confounding factors in multivariate analyses, is dramatically elevated in metastatic tissue compared to primary tumor, and is higher in primary tumors compared to normal pancreatic tissue. Transcriptomic analyses show that tumors with low PPS20 have overall more immune cell infiltration and a higher CD8 T cell/Treg ratio when compared to those with high PPS20. Analyses of proteomic data from TCGA PAAD indicated higher levels of Cyclin B1, RAD51, EGFR and a lower E-cadherin/Fibronectin ratio in tumors with high PPS20. The PPS20 score defines not only prognostic and biological subgroups but can predict response to targeted therapy as well. Overall, PPS20 is a stronger and more robust transcriptomic signature when compared to similar, previously published gene lists.

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miRNA-19 promotes non-small-cell lung cancer cell proliferation via inhibiting CBX7 expression

Cited by 33 publications

References 33 publications

Radon Biomonitoring and microRNA in Lung Cancer

Radon Biomonitoring and microRNA in Lung Cancer

<p>MiR-34c acts as a tumor suppressor in non-small cell lung cancer by inducing endoplasmic reticulum stress through targeting HMGB1</p>

A novel 20-gene prognostic score in pancreatic adenocarcinoma

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