Decreased miR-134 expression and its tumor-suppressive function in human osteosarcoma

Bao, Yong-Rui; Peng, Lifen; Ji, Ma; K, Liu; Li, Wei

doi:10.4238/2015.december.14.4

Cited by 6 publications

(12 citation statements)

References 24 publications

(25 reference statements)

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“…Previous research has identified consistently decreased miR-134 expression in many types of cancers (11)(12)(13). To investigate miR-134 expression in GC, we collected 26 human GC specimens and pair-matched gastric adjacent non-neoplastic mucosa.…”

Section: Mir-134 Is Downregulated In Gcmentioning

confidence: 89%

“…Previous studies identified a close relationship between miR-134 and the progression of various types of cancers. In patients with colorectal cancer, osteosarcoma and breast cancer, miR-134 was found to be decreased and to act as a tumor-suppressor (11)(12)(13). In the present study, we provide evidence that miR-134 is downregulated in GC tissues and cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…Reciprocally, tumor-suppressor miRNAs, such as miR-101 and miR-375, were found to be downregulated in GC and led to overexpression of the oncogenic genes EZH2 and PDK1 (9,10). Apart from these miRNAs, miR-134 has been revealed to be downregulated in many solid cancers (11)(12)(13). In gastrointestinal stromal tumors, miR-134 was confirmed to be downregulated (14), suggesting a conceivable role of miR-134 in the pathogenesis of GC.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-134 suppresses cell proliferation in gastric cancer cells via targeting of GOLPH3

2017

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Emerging evidence has shown that microRNAs (miRNAs) play critical roles in tumor development and progression. miR-134 has been found to act as a tumor-suppressor in numerous types of cancers. However, little is known concerning the potential role of miR-134 in gastric carcinogenesis. In the present study, we found that miR-134 was highly downregulated in gastric cancer tissues and cell lines when compared with levels in their adjacent non-tumor tissues and the normal human gastric epithelial cell line GES-1. Additionally, overexpression of miR-134 was accompanied by reduced cell proliferation in vitro and decreased tumor size in vivo. Further investigation by luciferase reporter assay indicated that Golgi phosphoprotein 3 (GOLPH3), a potent oncogene, was a direct target of miR-134. The activity of a luciferase reporter carrying the miR-134 binding site in the 3'-untranslated region (3'-UTR) of GOLPH3 was repressed by overexpression of miR-134, while a mutation in the 3'-UTR of GOLPH3 abrogated this effect, indicating that GOLPH3 is a target gene of miR-134. Overexpression of GOLPH3 blocked the antiproliferative effect of pre-miR-134 in gastric carcinoma cells. Furthermore, overexpression of miR-134 was associated with decreased phosphorylation of AKT, mTOR and S6K. Taken together, these data suggest that miR-134 regulates gastric cancer cell proliferation, at least potentially, through downregulation of the GOLPH3 gene, implicating a candidate tumor-suppressor miRNA in the pathogenesis of gastric cancer.

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Section: Mir-134 Is Downregulated In Gcmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA-134 suppresses cell proliferation in gastric cancer cells via targeting of GOLPH3

2017

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“…High expression of miR-134 presented bulky carcinoma size and terminal clinicopathological period, while the lower was inverse. Moreover, decreased miR-134 expression contributed to lower total survival, which uncovered it might be a promising biomarker and approach in osteosarcoma therapy and prognosis 92 . Gunawan and colleagues 93 found that deletions of chromosomal regions 14q were apt to happen in gastric carcinoma and that they were tightly related to cytogenetical evolution, while they did not apparently correlate with lesser disease-free survival.…”

Section: Main Textmentioning

confidence: 99%

miR-134: A Human Cancer Suppressor?

Pan

Zhang

Sun

et al. 2017

Molecular Therapy - Nucleic Acids

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MicroRNAs (miRNAs) are small noncoding RNAs approximately 20–25 nt in length, which play crucial roles through directly binding to corresponding 3′ UTR of targeted mRNAs. It has been reported that miRNAs are involved in numerous of diseases, including cancers. Recently, miR-134 has been identified to dysregulate in handles of human cancers, such as lung cancer, glioma, breast cancer, colorectal cancer, and so on. Increasing evidence indicates that miR-134 is essential for human carcinoma and participates in tumor cell proliferation, apoptosis, invasion and metastasis, drug resistance, as well as cancer diagnosis, treatment, and prognosis. Nevertheless, its roles in human cancer are still ambiguous, and its mechanisms are sophisticated as well, referring to a variety of targets and signal pathways, such as STAT5B, KRAS, MAPK/ERK signal pathway, Notch pathway, etc. Herein, we review the crucial roles of miR-134 in scores of human cancers via analyzing latest investigations, which might provide evidence for cancer diagnose, treatment, prognosis, or further investigations.

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“…It exhibits oncogenic activity in head and neck carcinoma and lung adenocarcinoma 9 , 10 , 11 as well as tumor suppressive activity in breast cancer, glioma, hepatocellular carcinoma, osteosarcoma and renal cell carcinoma. 8 , 12 , 13 , 14 , 15 …”

mentioning

confidence: 99%

The Fra-1–miR-134–SDS22 feedback loop amplifies ERK/JNK signaling and reduces chemosensitivity in ovarian cancer cells

Sun

Zhang

et al. 2016

Cell Death Dis

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The Fra-1 transcription factor is frequently upregulated in multiple types of tumors. Here we found that Fra-1 promotes miR-134 expression. miR-134 activates JNK and ERK by targeting SDS22, which in turn induces Fra-1 expression and leads to miR-134 upregulation. In addition, miR-134 augmented H2AX S139 phosphorylation by activating JNK and promoted non-homologous end joining (NHEJ)-mediated DNA repair. Therefore, ectopic miR-134 expression reduced chemosensitivity in ovarian cancer cells. Furthermore, miR-134 promotes cell proliferation, migration and invasion of ovarian cancer cells, and enhances tumor growth in vivo. Of particular significance, both Fra-1 and miR-134 are upregulated in ovarian cancer tissues, and Fra-1 and miR-134 expression is positively correlated. High levels of miR-134 expression were associated with a reduced median survival of ovarian cancer patients. Our study revealed that a Fra-1-miR-134 axis drives a positive feedback loop that amplifies ERK/JNK signaling and reduces chemosensitivity in ovarian cancer cells.

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Decreased miR-134 expression and its tumor-suppressive function in human osteosarcoma

Cited by 6 publications

References 24 publications

MicroRNA-134 suppresses cell proliferation in gastric cancer cells via targeting of GOLPH3

MicroRNA-134 suppresses cell proliferation in gastric cancer cells via targeting of GOLPH3

miR-134: A Human Cancer Suppressor?

The Fra-1–miR-134–SDS22 feedback loop amplifies ERK/JNK signaling and reduces chemosensitivity in ovarian cancer cells

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