Downregulation of microRNA‑301a inhibited proliferation, migration and invasion of non‑small cell lung cancer by directly targeting DLC1

Wu, Zhuyu; Li, Yaojun; Zhang, Guojun

doi:10.3892/ol.2017.6990

Cited by 9 publications

(6 citation statements)

References 38 publications

(47 reference statements)

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“…A research demonstrated miR-301b to stimulate cell invasion and facilitate drug resistance in pancreatic carcinoma [34]. Moreover, silencing of miR-301a could suppress cell proliferation, migration, and invasion in NSCLC, which implied to the functionality of miR-301a as a potential therapeutic strategy in NSCLC treatment [35]. Previous studies have proven that excised miR-301b could consequently inhibit bladder cancer cell proliferation, migration, and invasion [36].…”

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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“…The overexpression of PRDM13 upregulates DLC1 and then inhibits proliferation and invasion of U87 cells (Zhang et al, ). Downregulation of miR‑301a and miR‐483‐3p directly targets DLC1, which inhibits the proliferation of NSCLC and CRC (Wu, Li, & Zhang, ). Besides, two signaling pathways can mediate cancer cell proliferation by DLC1, one is the Wnt/β‐catenin signaling pathway.…”

Section: The Function and Signal Pathways Dlc1 Involvesmentioning

confidence: 99%

“…DLC1, interacting with CAV‐1 (B. Yang et al, ), FK506 binding protein 51 (FKBP51) (Takaoka, Ito, Miki, & Nakanishi, ), EF1A1 (Zhong et al, ) and S100A10 (Yang et al, ), promotes RhoA and ROCK activation and then controls cell migration and invasion (Yang et al, ). Besides, DLC1 is directly targeted by downregulation of exosomal miR‐141‐3p, miR‑301a and miR‐106b to inhibit cancer cell migration in prostate cancer, NSCLC and CRC (Wu et al, ; Ye et al, ; Zhang et al, ). Phosphorylation also modulates DLC1 activity, which conversely regulates the small GTPases, Rac1 and RhoA spatiotemporal activation, thus initiates the growth‐factor‐induced directed cell migration (Cao et al, ).…”

Section: The Function and Signal Pathways Dlc1 Involvesmentioning

confidence: 99%

A tumor suppressor DLC1: The functions and signal pathways

Zhang

2019

Journal Cellular Physiology

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Deleted in liver cancer‐1 (DLC1), a potential tumor suppressor, acts as a GTPase‐activating protein for Rho family members. In many human cancers, the DLC1 expression is frequently downregulated or inactivated, which allows cancer cells to proliferate and disseminate. In this review, we describe the characteristics and other members of the DLC1 family and delineate the signal pathways DLC1 involved in regulating cancer cell growth, colony formation, apoptosis, senescence, autophagy, migration and invasion. In addition, we explore the clinical data of DLC1 and the mechanisms that natural products upregulate the DLC1 expression to inhibit cancer. Despite these insights, many important unanswered questions remain about the exact mechanisms of DLC1‐mediated cancer suppression.

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“…miR-146 also plays regulatory roles in the NF-κB pathway, as it negatively regulates the protein levels of IL-1 receptor-associated kinase 1 (IRAK1) and TNF receptor-associated factor 6 (TRAF6) (29,30). miRNA-301a, which is located on chromosome 17q22, has been shown to be upregulated in a number of types of cancer, including hepatocellular carcinoma, pancreatic cancer, small cell lung cancer and breast cancer, which indicates a potential role for miRNA-301a in cancer development (31)(32)(33)(34). In GC, Wang et al (35) reported that the high expression of miRNA-301a was associated with GC cell proliferation and invasion by targeting Runt-related transcription factor 3 (RUNX3).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of miRNA‑301a‑3p promotes tumor progression in gastric cancer by suppressing NKRF and activating NF‑κB signaling

Xia

et al. 2020

Int J Oncol

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MicroRNA-301a (miRNA/miR-301a) and nuclear factor (NF)-κB signaling play important roles in tumor invasion, migration and progression. However, the role of miRNA-301a-3p in human gastric cancer (GC), and specifically in the activation of NF-κB signaling, remains unclear. The aim of the present study was to investigate miRNA-301a-3p expression in GC progression and the molecular mechanisms as regards the regulation of NF-κB signaling. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect miRNA-301a-3p expression in GC and paired normal tissues. The association between the expression of miRNA-301a-3p and patient pathological parameters and the prognosis of GC was statistically analyzed using an in situ hybridization (ISH) assay. An MTS assay and a Transwell assay were performed to evaluate the effects of miRNA-301a-3p on the proliferation, invasion and migration of GC cells. RT-qPCR and western blot analysis were used to analyze the association between miRNA-301a-3p and nuclear factor-κB repressing factor (NKRF) expression and the corresponding downstream NF-κB signaling molecules. A luciferase assay was used to verify the target effect of miRNA-301a-3p and NKRF. It was found that miRNA-301a-3p expression was significantly higher in 30 cases of primary GC compared with matched normal tissues. Additionally, the ISH assay indicated that the high expression of miRNA-301a-3p in GC was associated with tumor invasion depth, lymph node metastasis, lymph node invasion and tumor metastasis stage. Patients whose tumors had a higher miRNA-301a-3p expression level exhibited a poorer prognosis. The in vitro assay indicated that miRNA-301a-3p affected the proliferative and invasive ability of GC cells by targeting the expression of NKRF, which then affected NF-κB signaling. Therefore, it was hypothesize that miRNA-301a-3p promotes GC progression and affects the prognosis of patients with GC by targeting NKRF, which in turn, directly influences NF-κB activation.

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Downregulation of microRNA‑301a inhibited proliferation, migration and invasion of non‑small cell lung cancer by directly targeting DLC1

Cited by 9 publications

References 38 publications

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

A tumor suppressor DLC1: The functions and signal pathways

Upregulation of miRNA‑301a‑3p promotes tumor progression in gastric cancer by suppressing NKRF and activating NF‑κB signaling

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