Increased expression of microRNA-301a in nonsmall-cell lung cancer and its clinical significance

Shi, Yugen; Zang, Quan-Ling; Li, Guixin; Huang, Yan; Wang, Shizhong

doi:10.4103/0973-1482.146130

Cited by 14 publications

(4 citation statements)

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“…An aberrant expression of miRNAs has been observed in the pathogenesis of several diseases, including various human cancers [28]. Shi et al indicated an overexpression of miR-301a in NSCLC tissues [29]. Furthermore, a research observed an upregulated miR-301b expression in lung cancer tissues and cells [16].…”

Section: Discussionmentioning

confidence: 99%

microRNA-301b-3p downregulation underlies a novel inhibitory role of long non-coding RNA MBNL1-AS1 in non-small cell lung cancer

Xing

et al. 2019

Stem Cell Res Ther

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Background Non-small cell lung cancer (NSCLC) is the second most prevalent cause of cancer-related fatality. Long non-coding RNAs (lncRNAs) have been observed to exercise functions in NSCLC. Here, the current study aimed to explore the potential mechanism of lncRNA MBNL1-AS1 in NSCLC. Methods Microarray analysis was performed to screen the differentially expressed lncRNA associated with NSCLC and its potential mechanism. The lncRNA MBNL1-AS1 expression was quantified in 56 paired NSCLC and adjacent normal tissue samples. In an attempt to outline the function of lncRNA MBNL1-AS1 in NSCLC and to identify the interaction among lncRNA MBNL1-AS1, microRNA-301b-3p (miR-301b-3p) and TGFBR2, ectopic expression, depletion, and reporter assay experiments were conducted to detect CSC proliferation, migration, invasion, drug resistance, and sphere formation in NSCLC. Results Initially, the intersection among lncRNA MBNL1-AS1, miR-301b-3p, and TGFBR2 was observed in NSCLC. While a poor expression of lncRNA MBNL1-AS1 and TGFBR2, along with a high expression of miR-301b-3p was observed in NSCLC tissues. A demonstration of lncRNA MBNL1-AS1 restoration significantly decreased CSC proliferation, migration, invasion, drug resistance, and sphere formation in NSCLC. LncRNA MBNL1-AS1 functioned as a sponge of miR-301b-3p, which inverted the inhibitory role of lncRNA MBNL1-AS1 in CSC proliferation, migration, invasion, drug resistance, and sphere formation in NSCLC. LncRNA MBNL1-AS1 positively regulated TGFBR2 which was a target gene of miR-301b-3p. At last, upregulated lncRNA MBNL1-AS1 or depleted miR-301b-3p suppressed the xenograft tumor formation in vivo. Conclusion Collectively, the present study suggests an inhibitory role of lncRNA MBNL1-AS1 in CSC drug resistance of NSCLC by upregulating miR-301b-3p-targeted TGFBR2.

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Section: Discussionmentioning

confidence: 99%

microRNA-301b-3p downregulation underlies a novel inhibitory role of long non-coding RNA MBNL1-AS1 in non-small cell lung cancer

Xing

et al. 2019

Stem Cell Res Ther

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“…Intronic miR-301a, which is one of two mature forms of miR-301 (miR-301a and miR-301b), and its host gene, SKA2 (spindle and kinetochore-associated protein 2), are located on chromosome 17q22–23 in the human genome 25 . MiR-301a has been reported to be dysregulated not only in breast cancer 22 , 23 , 26 but also in a variety of malignant tumours, including prostate, gastric, pancreatic, lung, blood, colourectal, and melanoma 17 – 19 , 21 , 25 , 27 – 29 . As most studies have concluded, miRNA-301a was identified as an oncogenic miR, which played an important role in activating tumour cell invasion/migration, promoting cell proliferation, inhibiting apoptosis and enhancing chemosensitivity both in vitro and in vivo .…”

Section: Discussionmentioning

confidence: 99%

Elevated miR-301a expression indicates a poor prognosis for breast cancer patients

Zheng

Huang

Yao

et al. 2018

Sci Rep

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Although microRNA-301a (miR-301a) has been reported to function as an oncogene in many human cancers, there are limited data regarding miR-301a and breast tumours. In this study, we first detected the expression of miR-301a using an in situ hybridization (ISH) -based classification system in 380 samples of BC tissue, including both non-TNBC (triple-negative breast cancer) and TNBC specimens. Our results suggest that analysing miR-301a expression in breast tissue biopsy specimens at the time of diagnosis could have the potential to identify patients who might be candidates for active surveillance. We validated our results that higher expression of miR-301a is associated with a decreased OS in independent public breast cancer databases, such as TCGA and METABRIC, using the online webtool Kaplan-Meier Plotter, which provided additional powerful evidence to confirm the prognostic value of miR-301a. MiR-301a may serve as a potential therapeutic target for patients with breast cancer. According to our results, miR-301a should be considered, and novel therapeutic options are needed to target this aggressive miR-301a-positive type of breast cancer to reduce recurrence and the mortality rate.

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“…Furthermore, deletion of miR-301a in hematopoietic cells leads to reduced development of colitis-associated colon cancer [15]. In patients with NSCLC, miR-301a is most highly expressed in tumor tissues and is associated with poor differentiation and lymph node metastasis [16]. Collectively, these in vitro and in vivo data indicate that miR-301a has an important role in the tumor microenvironment and tumor metastasis.…”

Section: Introductionmentioning

confidence: 99%

miR-301a promotes lung tumorigenesis by suppressing Runx3

Zhong

Wang

et al. 2019

Mol Cancer

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Background Our previous report demonstrated that genetic ablation of miR-301a reduces Kras -driven lung tumorigenesis in mice. However, the impact of miR-301a on host anti-tumor immunity remains unexplored. Here we assessed the underlying molecular mechanisms of miR-301a in the tumor microenvironment. Methods The differentially expressed genes were identified by using deep sequencing. The immune cell counts, and cytokines expression were analyzed by realtime PCR, immunohistochemistry and flow cytometry. The role of miR-301a/Runx3 in lung tumor was evaluated on cell growth, migration and invasion. The function of miR-301a/Runx3 in regulating tumor microenvironment and tumor metastasis were evaluated in Kras transgenic mice and B16/LLC1 syngeneic xenografts tumor models. Results In this work, we identified 1166 up-regulated and 475 down-regulated differentially expressed genes in lung tumor tissues between Kras LA2 and miR-301a −/− ; Kras LA2 mice. Immune response and cell cycle were major pathways involved in the protective role of miR-301a deletion in lung tumorigenesis. Overexpression of the miR-301a target, Runx3, was an early event identified in miR-301a −/− ; Kras LA2 mice compared to WT-Kras LA2 mice. We found that miR-301a deletion enhanced CD8 + T cell accumulation and IFN-γ production in the tumor microenvironment and mediated antitumor immunity. Further studies revealed that miR-301a deficiency in the tumor microenvironment effectively reduced tumor metastasis by elevating Runx3 and recruiting CD8 + T cells, whereas miR-301a knockdown in tumor cells themselves restrained cell migration by elevating Runx3 expression. Conclusions Our findings further underscore that miR-301a facilitates tumor microenvironment antitumor immunity by Runx3 suppression in lung tumorigenesis. Electronic supplementary material The online version of this article (10.1186/s12943-019-1024-0) contains supplementary material, which is available to authorized users.

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Increased expression of microRNA-301a in nonsmall-cell lung cancer and its clinical significance

Abstract: miR-301a may represent a novel prognostic indicator, a biomarker for the early detection of lymph node metastasis and a therapeutic target in NSCLC.

Cited by 14 publications

References 1 publication

microRNA-301b-3p downregulation underlies a novel inhibitory role of long non-coding RNA MBNL1-AS1 in non-small cell lung cancer

microRNA-301b-3p downregulation underlies a novel inhibitory role of long non-coding RNA MBNL1-AS1 in non-small cell lung cancer

Elevated miR-301a expression indicates a poor prognosis for breast cancer patients

miR-301a promotes lung tumorigenesis by suppressing Runx3

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