PGC-1 alpha interacts with microRNA-217 to functionally regulate breast cancer cell proliferation

Zhang, Shaohui; Liu, Xinguo; Liu, Jianming; Guo, Heng; Xu, Hongfeng; Zhang, Geng

doi:10.1016/j.biopha.2016.11.062

Cited by 26 publications

(20 citation statements)

References 38 publications

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“…However, miR-217 has been reported to promote breast cancer cell proliferation [29, 30, 35]. To determine the functions of miR-217 in TNBC, we over-expressed miR-217 in HCC1937 and HCC1806 cells.…”

Section: Resultsmentioning

confidence: 99%

“…Overexpression of miR-217 induces drug resistance and invasion of MCF-7 and SKBR-3 cells through activating AKT by downregulation of PTEN [35]. Furthermore, downregulation of miR-217 in MCF7 and MDA-MB-231 cells inhibits cell proliferation through targeting PGC-1α and DACH1 [29, 30]. These studies suggest an oncogenic role of miR-217 in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

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miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

et al. 2017

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Triple negative breast cancer (TNBC) is one of the most aggressive breast cancers without effective targeted therapies. Numerous studies have implied that KLF5 plays an important roles in TNBC. How is KLF5 regulated by microRNAs has not been well studied. Here, we demonstrated that miR-217 down-regulates the expression of KLF5 and KLF5’s downstream target gene FGF-BP and Cyclin D1 in TNBC cell lines HCC1806 and HCC1937. Consequently, miR-217 suppresses TNBC cell growth, migration, and invasion. MiR-217 suppresses TNBC, at least partially, through down-regulating the KLF5 expression. These results suggest that the miR-217-KLF5 axis might serve as a potential target for treatment of TNBC.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

et al. 2017

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“…Many other studies have reported roles for miR-23a in cancer without investigating PGC1α; interestingly, this miR is often downregulated in tumors [ 84 ]. Similarly, miR-217, which inhibits proliferation and induces apoptosis, was found to bind to PGC1α mRNA in breast cancer cell lines and downregulate its expression [ 85 ]. Together, these as yet scant reports on miRNAs and PGC1α reinforce the notion that PGC1α expression levels in cancer may vary greatly.…”

Section: Pgc1α In Cancermentioning

confidence: 99%

“…PGC1α downregulation may be due to promoter methylation or ubiquitinylation of the PGC1α protein; both mechanisms are seen also in non-cancer cells [ 25 , 70 ]. Transcriptional repression may occur via high levels of MYC [ 60 , 61 ], active BRAF [ 39 ], or hypoxia-induced factor 1α (HIF1α) [ 29 ], miRNA regulation [ 82 , 83 , 84 , 85 ], or cytokine effects [ 75 , 76 , 77 , 78 , 79 ]. Inactivation of the PGC1α protein is also possible, notably by acetylation and phosphorylation [ 1 , 86 ].…”

Section: Figurementioning

confidence: 99%

PGC1α: Friend or Foe in Cancer?

Mastropasqua

Girolimetti

Shoshan

2018

Genes

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The PGC1 family (Peroxisome proliferator-activated receptor γ (PPARγ) coactivators) of transcriptional coactivators are considered master regulators of mitochondrial biogenesis and function. The PGC1α isoform is expressed especially in metabolically active tissues, such as the liver, kidneys and brain, and responds to energy-demanding situations. Given the altered and highly adaptable metabolism of tumor cells, it is of interest to investigate PGC1α in cancer. Both high and low levels of PGC1α expression have been reported to be associated with cancer and worse prognosis, and PGC1α has been attributed with oncogenic as well as tumor suppressive features. Early in carcinogenesis PGC1α may be downregulated due to a protective anticancer role, and low levels likely reflect a glycolytic phenotype. We suggest mechanisms of PGC1α downregulation and how these might be connected to the increased cancer risk that obesity is now known to entail. Later in tumor progression PGC1α is often upregulated and is reported to contribute to increased lipid and fatty acid metabolism and/or a tumor cell phenotype with an overall metabolic plasticity that likely supports drug resistance as well as metastasis. We conclude that in cancer PGC1α is neither friend nor foe, but rather the obedient servant reacting to metabolic and environmental cues to benefit the tumor cell.

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“…Previous research has found that miRNAs are involved in various cellular processes, including cell proliferation, apoptosis, migration and invasion, the cell cycle and stem cell renewal (4,5). In addition, evidence suggests that miRNAs are aberrantly expressed in various cancers, and they play oncogenic or tumor-suppressive roles in these cancers (6)(7)(8). Differentially expressed miRNAs may also offer novel therapeutic approaches for the more successful treatment of HPAC (9,10).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-217 inhibits cell proliferation, invasion and migration by targeting Tpd52l2 in human pancreatic adenocarcinoma

Chen

Wang

et al. 2017

Oncol Rep

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MicroRNAs (miRNAs) play important roles in the regulation of various tumor biological processes including proliferation and apoptosis. miR-217 has been implicated in many types of cancer, whereas its expression and potential biological function in human pancreatic adenocarcinoma (HPAC) remain unclear. We aimed to investigate the clinical significance of miR-217 in patients with pancreatic carcinoma and its role and underlying molecular mechanism in HPAC. We collected 15 pairs of pancreatic cancer and normal pancreas tissues to evaluate the expression of miR-217 and tumor protein D52-like 2 (Tpd52l2). Then, we transfected AsPC-1 cells with miR-217 mimics or Tpd52l2 siRNA to detect the effect on cell proliferation, apoptosis, invasion, migration and the cell cycle. In addition, miR-217 mimics and Tpd52l2 expression plasmids were co-transfected into AsPC-1 cells to further investigate the mechanism of miR-217 and Tpd52l2 in HPAC tumorigenesis. Finally, exploration of related signaling pathways was carried out. Herein, we found that the expression of miR-217 was significantly downregulated in HPAC tissues as compared with that observed in adjacent normal tissues. Further functional assays showed that restoration of the expression of miR-217 inhibited cell proliferation, invasion and migration, induced apoptosis, and caused cell cycle arrest of HPAC cells. Notably, Tpd52l2 was identified as a functional target of miR-217 in HPAC. Furthermore, an inverse correlation between miR-217 and Tpd52l2 expression was observed in the HPAC tissues. Downregulation of Tpd52l2 had an effect similar to that following overexpression of miR-217, and upregulation of Tpd52l2 reversed the effects of the overexpression of miR-217. Finally, we found that overexpression of miR-217 or knockdown of Tpd52l2 suppressed the PIK3CA/AKT signaling pathways. In addition, this may explain the effect of miR-217/Tpd52l2 on HPAC development. Taken together, these results suggest a critical role of miR-217 in suppressing proliferation, migration and invasion of HPAC cells by targeting Tpd52l2. Targeting the miR-217/Tpd52l2 axis may be a new therapeutic application with which to treat patients with HPAC in the future.

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PGC-1 alpha interacts with microRNA-217 to functionally regulate breast cancer cell proliferation

Cited by 26 publications

References 38 publications

miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

PGC1α: Friend or Foe in Cancer?

MicroRNA-217 inhibits cell proliferation, invasion and migration by targeting Tpd52l2 in human pancreatic adenocarcinoma

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