miR-136 suppresses tumor invasion and metastasis by targeting RASAL2 in triple-negative breast cancer

Yan, Meisi; Li, Xiaobo; Tong, Dandan; Han, Changsong; Zhao, Ruihua; He, Yan; Jin, Xiaoming

doi:10.3892/or.2016.4767

Cited by 72 publications

(73 citation statements)

References 32 publications

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“…Generally, it has been demonstrated that miR-136 was down-regulated in TNBC [35], which is consistent with our study. Yan et al showed that suppression of tumor invasion and metastasis by miR-136 was mediated through targeting RASAL2, which plays oncogenic role in TNBC.…”

Section: Discussionsupporting

confidence: 82%

“…Yan et al showed that suppression of tumor invasion and metastasis by miR-136 was mediated through targeting RASAL2, which plays oncogenic role in TNBC. Moreover, expression of miR-136 was negatively correlated with WHO grades in TNBC [35]. In summary, the present study confirms the aberrant expression of miRNAs in TNBC patients when compared to healthy tissues.…”

Section: Discussionsupporting

confidence: 74%

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Dysregulation of microRNAs in triple-negative breast cancer

et al. 2017

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Objectives: Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited treatment options and poor prognosis. TNBC is usually diagnosed at a relatively young age and is characterized by high risk of developing metastases. Some epigenetic regulation of gene expression is associated with TNBC. Expression of microRNAs (miRNAs) can serve as a potential tool for identifying critical biomarkers in TNBC.The aim of our study is to examine expression of selected miRNAs in TNBC and to assess the relationship between miRNA expression and clinicopathological factors. Material and methods:Expression levels of 19 selected miRNAs were compared between cancerous and normal breast tissues by use of qPCR method. We have evaluated the relationship between the expression level of miRNAs and clinicopathological factors such as: age, tumor size and lymph node status. Results:We found that in TNBC tissues, when compared with normal breast tissues, the expression of miR-190a, miR-136-5p and miR-126-5p was significantly reduced (p = 0.0041, p = 0.0007, p = 0.0007, respectively) whereas expression of miR-135b-5p and miR-182-5p was significantly increased (p = 0.0194, p = 0.0041, respectively). We found a linear trend for tumor size and expression of miR-126-5p (p = 0.0296) and miR-135b-5p (p = 0.0241). Conclusions:Our study confirms that miRNA expression profile is dysregulated in TNBC patients compared to healthy controls. and miR-182-5p may be associated with development and progression of TNBC.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 74%

Dysregulation of microRNAs in triple-negative breast cancer

et al. 2017

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“…miR-136-5p was also reported to be downregulated in triple-negative breast cancer by targeting RAS protein activator like 2, and act as a tumor suppressor (12). Yang et al (20) also described miR-136-5p as a tumor suppressor in lung adenocarcinoma, and revealed that this occurred through the targeting of SMAD family member (Smad)2 and Smad3.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have demonstrated that miR-136-5p is involved in a number of types of carcinoma, including (12) and non-small cell lung cancer (NSCLC) (13). However, the function of miR-136-5p in RCC remains to be explored.…”

Section: Introductionmentioning

confidence: 99%

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

et al. 2018

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Abstract. MicroRNAs (miRs) are involved in diverse physiological and developmental processes at the post-transcriptional level in cells. Previous studies have demonstrated that miR-136-5p is involved in certain types of cancer. However, the function of miR-136-5p in renal cell carcinoma (RCC) remains to be fully elucidated. In present study, miR-136-5p expression levels were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and MTT assays, CCK-8 assays, Transwell assays, wound healing assays and flow cytometry were performed to investigate the function of miR-136-5p in RCC. RT-qPCR revealed that the expression of miR-136 was significantly lower in RCC tissues and cells compared with adjacent non-tumor tissues and cells in vitro. miR-136-5pwas also demonstrated to be associated with RCC cell proliferation, viability, migration, invasion and apoptosis. miR-136-5p may therefore function as a tumor suppressor in RCC. Further studies are required to elucidate the molecular mechanisms and signaling pathways underlying these functions of miR-136-5p, to investigate the potential function of miR-136-5p as a biomarker for the early detection and prognosis of RCC, and its potential as a therapeutic target for the treatment of RCC.

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“…Previous studies have reported that the abnormal expression of miR-136 has important roles in the progression of several types of human cancer (19)(20)(21)(22). To the best of our knowledge, the expression pattern, precise function and underlying molecular mechanisms of miR-136 have not been resolved in gastric cancer thus far.…”

Section: Introductionmentioning

confidence: 93%

Microrna-136 promotes proliferation and invasion ingastric cancer cells through Pten/Akt/P-Akt signaling pathway

2018

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Abstract. Gastric cancer is the fourth most common cancer and the second most frequent cause of cancer-associated mortality in the world. Previous studies have revealed that expression levels of microRNAs (miRNAs) are associated with the initiation and progression of several types of cancer, including gastric cancer. Previous studies have demonstrated that the abnormal expression of miRNA-136 may serve a function in the progression of several types of human cancer. However, the expression pattern of miR-136, its functions and underlying molecular mechanisms in gastric cancer remain unresolved. In the present study, it was revealed that the expression of miR-136 was aberrantly up regulated in gastric cancer tissues and cell lines. The suppression of miR-136 was able to inhibit proliferation and invasion in gastric cancer cell lines. Furthermore, phosphatase and tensin homolog (PTEN) was identified as a direct target gene of miR-136 in gastric cancer. PTEN was under expressed in gastric cancer tissues compared with non-tumor gastric tissues, and PTEN expression was negatively correlated with miR-136 expression. Furthermore, PTEN overexpression mimics the effects of miR-136 knockdown on gastric cancer cells. Additionally, miR-136 under expression decreased phospho-(p) AKT expression, but did not affect AKT expression in gastric cancer cells. In conclusion, the data of the present study suggest that miR-136 acts as an oncogene in gastric cancer via regulation of the PTEN/AKT/p-AKT signaling pathway and may potentially serve as a novel therapeutic target for the treatment of gastric cancer.

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miR-136 suppresses tumor invasion and metastasis by targeting RASAL2 in triple-negative breast cancer

Cited by 72 publications

References 32 publications

Dysregulation of microRNAs in triple-negative breast cancer

Dysregulation of microRNAs in triple-negative breast cancer

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

Microrna-136 promotes proliferation and invasion ingastric cancer cells through Pten/Akt/P-Akt signaling pathway

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