Expression of miR-136 is associated with the primary cisplatin resistance of human epithelial ovarian cancer

Zhao, Henan; Li, Sha; Wang, Guang; Wu, Xian; Ding, Yanfang; Guo, Gordon; Jiang, Jiyong; Cui, Shiying

doi:10.3892/or.2014.3640

Cited by 54 publications

(46 citation statements)

References 21 publications

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“…served low expression of miR-136 in patients with chemoresistant epithelial ovarian cancer [34]. Generally, it has been demonstrated that miR-136 was down-regulated in TNBC [35], which is consistent with our study.…”

Section: Discussionsupporting

confidence: 82%

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%

Dysregulation of microRNAs in triple-negative breast cancer

et al. 2017

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“…In another study, overexpression of miR-136-5p negatively impacted proliferation of the LN229 glioblastoma cell line by downregulating matricellular cysteine rich angiogenic inducer 61 protein expression (23). miR-136-5p was also reported to be serve as an anti-oncogene in epithelial ovarian cancer (24). Gao et al (25) demonstrated that colorectal neoplasia differentially expressed is a target of miR-136-5p in colorectal cancer cells, and high levels of miR-136-5p may inhibit the migration and invasion of colorectal cancer cells.…”

Section: Discussionmentioning

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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“…Ectopic expression of miR-136 suppressed migration, invasion and epithelial-to-mesenchymal transition in breast cancer cells (19). A study by Zhao et al (31) identified that miR-136 expression level was decreased in patients with primary platinum-resistant ovarian cancer tissues compared with that in platinum-sensitive ovarian cancer tissues. Additionally, miR-136 was identified as a tumor suppressor and miR-136 under expression in ovarian cancer improved chemo resistance partly via the inhibition of apoptosis and promotion of the repair of cisplatin-induced DNA damage (31).…”

Section: Discussionmentioning

confidence: 99%

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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Expression of miR-136 is associated with the primary cisplatin resistance of human epithelial ovarian cancer

Cited by 54 publications

References 21 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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