miR-1236-3p suppresses the migration and invasion by targeting KLF8 in lung adenocarcinoma A549 cells

Bian, Tingting; Jiang, Daishan; Liu, Jian; Yuan, Xiaopeng; Feng, Jia; Li, Qian; Zhang, Qing; Li, Xiaoli; Liu, Yifei; Zhang, Jianguo

doi:10.1016/j.bbrc.2017.08.074

Cited by 34 publications

(29 citation statements)

References 36 publications

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“…Additionally, a quantity of researchers have validated that miRNAs are outstanding in mediating the biological behaviors like the cell proliferation, migration and invasion and so on through interacting with their downstream targets in quantities of cancers [ 36 , 37 ]. For example, miR-221/222 promotes the proliferation of breast cancer by regulating PTEN [ 38 ]; miR-155 represses the growth of lung cancer via targeting PDCD4 [ 39 ]; miR-1236-3p inhibits the metastasis and invasion of LAD cells by regulating KLF8 [ 40 ]. But how miR-193b-3p affects the progress of cervical cancer is not sure.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 enhances the radio-resistance of cervical cancer via miR-193b-3p/CCND1 axis

2017

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LncRNAs have become a hot topic in various cancer-related researches. Radio-resistance is a great threat for cancer therapy. However, how lncRNAs affect the radio-resistance in cervical cancer is masked. As for our paper, it was discovered that NEAT1 was highly expressed in cervical cancer tissues and non-sensitive tissues as well as radio-resistant cell lines. And the overexpression of NEAT1 accelerated proliferation, while the knockdown of NEAT1 had the opposite result. The effect of NEAT1 on cell proliferation was dependent on the dose of ionizing radiation. And the silence of NEAT1 also caused cell cycle arrest in G0/G1 phase, and triggered more apoptosis, indicating the oncogenic role of NEAT1 in cervical cancer. Next, mechanistic assays affirmed that NEAT1 could function as a ceRNA to regulate cyclin D1 through sponging miR-193b-3p in cervical cancer. Rescue assays were employed to validate that miR-193b-3p and cyclin D1 could inhibit NEAT1-mediated suppressive effect on proliferation, and its stimulative effect on cell cycle arrest and apoptosis. In general, this article disclosed that NEAT1 could facilitate the radio-resistance of cervical cancer via competitively binding miR-193b-3p to up-regulate the expression of cyclin D1.

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Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 enhances the radio-resistance of cervical cancer via miR-193b-3p/CCND1 axis

2017

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“…However, the prognosis is often poor in patients with metastasis or recurrence, and in patients aged >40 years ( 21 ). Low miR-1236-3p expression is associated with gastric cancer ( 8 ), ovarian carcinoma ( 11 ) and lung adenocarcinoma ( 22 ). However, the effect of miR-1236-3p on OS cell invasion and proliferation has not yet been studied.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑1236‑3p inhibits human osteosarcoma growth

Chen

et al. 2020

Oncol Lett

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Osteosarcoma (OS) is a common bone tumor with high mortality worldwide. The long-term survival rate of patients with metastatic or recurrent disease is <20%. The present study explored the biological role of microRNA (miRNA/miR)-1236-3p in OS. miRNA and mRNA expression levels were measured via reverse transcription-quantitative PCR. Fluorescence in situ hybridization was performed to determine miR-1236-3p expression levels in clinical specimens. Protein expression was measured via western blotting. Immunohistochemical analysis was used to detect Wnt target gene expression in tumor tissues. The interaction between the Wnt3a 3′untranslated region and miR-1236-3p was assessed via dual-luciferase reporter assays. Cell cycle, Transwell, Cell Counting Kit-8 and wound healing assays were conducted to evaluate the function of the miR-1236-3p/Wnt3a axis. Human OS (HOS) cells stably transfected with vector or miR-1236-3p sponge were injected subcutaneously into nude mice to assess the role of miR-1236-3p in vivo . miR-1236-3p expression was downregulated in OS tissues compared with chondroma tissues, and miR-1236-3p overexpression inhibited OS cell migration and proliferation compared with the negative control group. Furthermore, in vivo xenograft assays displayed enhanced tumour growth rates in the miR-1236-3p sponge group compared with the vector control group. In the present study, the results indicated that miR-1236-3p inhibited OS progression and Wnt3a was identified as a target of miR-1236-3p.

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“…EMT is a process that increases the metastasis and invasive potential of tumor cells, with losing epithelial cell characteristics and acquiring a mesenchymal pheno-type, including decreasing epithelial markers (cytokeratin or E-cadherin) and up-regulating mesenchymal indicators (VIM or N-cadherin) or transcription factors (Twist, Snail) [ 35 – 37 ]. Usually, inhibiting E-cadherin can induce invasiveness-related N-cadherin expression [ 38 , 39 ]. VIM may enhance migration and invasiveness and related to reduce E-cadherin and upregulating N-cadherin, while increased VIM is correlated with poor prognosis [ 20 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

Ang-2 promotes lung cancer metastasis by increasing epithelial-mesenchymal transition

et al. 2018

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Lung cancer is the most common malignant tumor with increasing angiopoietin-2 (Ang-2) and a high rate of metastasis. However, the mechanism of Ang-2 enhancing tumor proliferation and facilitating metastasis remains to be clarified. In this study, Ang-2 expression and its gene transcription on effects of biological behaviors and epithelial-mesenchymal transition (EMT) were investigated in lung cancers. Total incidence of Ang-2 expression in the cancerous tissues was up to 91.8 % (112 of 122) with significantly higher (χ2=103.753, P2=7.883, P=0.005), differentiation degree (χ2=4.554, P=0.033), tumor node metastasis (TNM) staging (χ2=5.039, P=0.025), and 5-year survival rate (χ2 =11.220, P2=18.881, P2=0.81, P=0.776) or III & IV (χ2=1.845, P=0.174). Over-expression of Ang-2 or Ang-2 mRNA in lung A549 and NCI-H1975 cells were identified among different cell lines. When silencing Ang-2 in A549 cells with specific shRNA-1 transfection, the cell proliferation was significantly inhibited in a time-dependent manner, with up-regulating E-cadherin, down-regulating Vimentin, Twist, and Snail expression, and decreasing invasion and metastasis of cancer cell abilities, suggesting that Ang-2 promote tumor metastasis through increasing EMT, and it could be a potential target for lung cancer therapy.

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miR-1236-3p suppresses the migration and invasion by targeting KLF8 in lung adenocarcinoma A549 cells

Cited by 34 publications

References 36 publications

LncRNA NEAT1 enhances the radio-resistance of cervical cancer via miR-193b-3p/CCND1 axis

LncRNA NEAT1 enhances the radio-resistance of cervical cancer via miR-193b-3p/CCND1 axis

MicroRNA‑1236‑3p inhibits human osteosarcoma growth

Ang-2 promotes lung cancer metastasis by increasing epithelial-mesenchymal transition

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