MicroRNA‑138 inhibits SOX12 expression and the proliferation, invasion and migration of ovarian cancer cells

Qu, Miaomiao; Zhu, Yongning; Jin, Meng

doi:10.3892/etm.2018.6375

Cited by 19 publications

(24 citation statements)

References 37 publications

(39 reference statements)

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“…MiR-138, a significant tumor-related miRNA, is known to play opposite and different functions according to the types of malignancies. MiR-138 has been reported as a tumor suppressor in multiple human solid cancers such as colorectal cancer, non-small-cell lung cancer, hepatocellular carcinoma, glioma carcinoma, and ovarian cancer, in which its reduced expression was shown to promote cell proliferation of cancer cells [63,64,65,66,67]. While the majority of studies have mentioned that miR-138 was downregulated, possibly playing a tumor-suppressive role, opposite results have been found in gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

Deregulation of miRNA in Helicobacter pylori-Induced Gastric MALT Lymphoma: From Mice to Human

Blosse

Lévy

Robe

et al. 2019

JCM

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Gastric MALT lymphoma (GML) is directly caused by Helicobacter pylori infection but occurs only in a small number of infected subjects. Mechanisms underlying the initiation and progression of GML remain unclear. MicroRNAs (miRNAs) are small non-coding RNAs that are now considered as major players in inflammation and carcinogenesis, acting as oncogenes or tumor suppressors. Previous laboratory studies have shown in a GML mouse model that overexpression of a distinct set of five miRNAs (miR-21a, miR-135b, miR-142a, miR-150, miR-155) could play a critical role in the pathogenesis of GML. Our goal was to compare the miRNA expression profile obtained in the GML mouse model to that in human GML (11 cases of GML compared to 17 cases of gastritis control population). RTqPCR on the five dysregulated miRNAs in the GML mouse model and PCR array followed by RTqPCR confirmation showed that four miRNAs were up-regulated (miR-150, miR-155, miR-196a, miR-138) and two miRNAs down-regulated (miR-153, miR-7) in the stomachs of GML patients vs. gastritis control population. The analysis of their validated targets allowed us to postulate that these miRNAs (except miR-138) could act synergistically in a common signaling cascade promoting lymphomagenesis and could be involved in the pathogenesis of GML.

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Section: Discussionmentioning

confidence: 99%

Deregulation of miRNA in Helicobacter pylori-Induced Gastric MALT Lymphoma: From Mice to Human

Blosse

Lévy

Robe

et al. 2019

JCM

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“…23 MiR-138 targeted SOX12 to inhibit proliferation, invasion, and migration in ovarian cancer. 24 Silencing SOX12 repressed proliferation and metastasis of lung cancer cells. 25 However, never has SOX12 been associated with PTC, and its relation with miR-423-5p and NR2F1-AS1 remains unknown.…”

Section: Introductionmentioning

confidence: 99%

“…For instance, SOX12 promoted metastasis of gastric cancer through inducing MMP7 and IGF1 . MiR‐138 targeted SOX12 to inhibit proliferation, invasion, and migration in ovarian cancer . Silencing SOX12 repressed proliferation and metastasis of lung cancer cells .…”

Section: Introductionmentioning

confidence: 99%

NR2F1‐AS1 regulated miR‐423‐5p/SOX12 to promote proliferation and invasion of papillary thyroid carcinoma

Yang

Liu

Chang

et al. 2019

J of Cellular Biochemistry

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Papillary thyroid carcinoma (PTC) is an aggressive histological subtype of thyroid carcinoma (THCA), whose occurrence rate is high. The participation of long noncoding RNAs in the pathologies of cancers has attracted significant attention during the past decades. The purpose of the current study is to investigate the role of NR2F1 antisense RNA 1 (NR2F1‐AS1) in PTC. The expression of NR2F1 in THCA samples was analyzed by bioinformatics tool gene expression profiling interactive analysis. Levels of NR2F1‐AS1, microRNA‐423‐5p (miR‐423‐5p), and SRY‐box 12 (SOX12) were evaluated by a quantitative reverse transcription‐polymerase chain reaction and Western blot. The impact of NR2F1‐AS1 on PTC cell proliferation and invasion was assessed by Cell Counting Kit‐8, EdU, and Transwell invasion assays. The interactions among NR2F1‐AS1, miR‐423‐5p, and SOX12 were determined by RNA immunoprecipitation and luciferase reporter assays. Consequently, we found that NR2F1‐AS1 and SOX12 levels were elevated in PTC, whereas miR‐423‐5p was downregulated in PTC cells. Functionally, NR2F1‐AS1 silence led to reduced proliferation and invasion of PTC cells. Mechanistically, NR2F1‐AS1 interacted with miR‐423‐5p to induce SOX12 expression in PTC cells. In conclusion, the present study firstly stated that NR2F1‐AS1 regulated miR‐423‐5p/SOX12 to promote proliferation and invasion of PTC, indicating NR2F1‐AS1 as a potential novel target for the molecular‐targeted therapy of PTC.

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“…27 MiR-138 inhibits the proliferation, invasion, and migration of ovarian cancer cells. 28 MiR-138 suppresses the proliferation, metastasis, and autophagy of non-small cell lung cancer. 29 Our results supported the above function of miR- 138: miR-138 suppressed cell proliferation and invasion.…”

Section: Discussionmentioning

confidence: 99%

miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancer

Xun

et al. 2020

Thoracic Cancer

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Background Long non‐coding RNA‐urothelial carcinoma associated 1 (LncRNA‐UCA1) is a crucial oncogene that is deregulated in many types of cancers. However, the mechanism of UCA1 function, especially for its posttranscriptional regulation in lung cancer, remains unclear. Methods miRCode was used to predict potential miRNA candidates that might target UCA1. The targets of miR‐138 and miR‐193 on UCA1 and CDK6 were verified by luciferase reporter analysis. Western blotting was used to detect protein levels. The RNA level was evaluated using quantitative real‐time polymerase chain reaction (PCR). Proliferation, wound healing, and transwell invasion assays were performed to assess cell proliferation and invasion abilities. Correlations between miR‐138 or miR‐193 and UCA1 in lung cancer tissues was assessed using quantitative real‐time PCR. Results miR‐138 and miR‐193 specifically targeted and regulated lncRNA‐UCA1. MiR‐138 and miR‐193 both suppressed cell proliferation and cell cycle progression. Moreover, miR‐138 and miR‐193 inhibited cell migration and invasion. Overexpression of UCA1 reversed the proliferation, migration, and invasion suppression effects of miR‐138 or miR‐193. Furthermore, miR‐138/193 affected the expression of UCA1 downstream genes. UCA1 regulated the expression of CDK6 as a miR‐138 and miR‐193 common target. In human lung cancer tissues, our study showed a significant negative correlation between miR‐138 or miR‐193 and UCA1 in lung cancer tissues. Conclusions Our results demonstrated that miR‐138 and miR‐193 affect cell function by directly targeting and regulating UCA1 in lung cancer.

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MicroRNA‑138 inhibits SOX12 expression and the proliferation, invasion and migration of ovarian cancer cells

Cited by 19 publications

References 37 publications

Deregulation of miRNA in Helicobacter pylori-Induced Gastric MALT Lymphoma: From Mice to Human

Deregulation of miRNA in Helicobacter pylori-Induced Gastric MALT Lymphoma: From Mice to Human

NR2F1‐AS1 regulated miR‐423‐5p/SOX12 to promote proliferation and invasion of papillary thyroid carcinoma

miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancer

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