miR-143 and miR-145 inhibit stem cell characteristics of PC-3 prostate cancer cells

Huang, Shuai; Guo, Wei; Tang, Yubo; Ren, Dong; Zou, Xuenong; Peng, Xinsheng

doi:10.3892/or.2012.2015

Cited by 114 publications

(86 citation statements)

References 44 publications

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“…The miR-143 and miR-145 cluster also jointly suppresses tumor sphere formation and the expression of CSC markers (CD133 and CD44) and core pluripotency factors (Oct4, MYC, and KLF4) in PC3 cells (49). This study has further found that miR-143 and miR-145 inhibits bone metastasis progression of PCa using PC3 cells in vivo by regulating CSC characteristics.…”

Section: Mir-143 and Mir-145mentioning

confidence: 84%

Microdissecting the role of microRNAs in the pathogenesis of prostate cancer

2015

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Section: Mir-143 and Mir-145mentioning

confidence: 84%

Microdissecting the role of microRNAs in the pathogenesis of prostate cancer

2015

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“…Stabilized HIF1 protein is transported into the nucleus, where it binds to hypoxia response elements (HREs) on DNA and activates VEGF gene transcription. High expression of HIF1a has been reported in thyroid cancer and thyroid cancer cell lines (Huang et al 2012).…”

Section: Discussionmentioning

confidence: 99%

miR-145 suppresses thyroid cancer growth and metastasis and targets AKT3

Boufraqech¹,

Zhang²,

Jain³

et al. 2014

Endocrine-Related Cancer

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The expression and function of miR-145 in thyroid cancer is unknown. We evaluated the expression and function of miR-145 in thyroid cancer and its potential clinical application as a biomarker. We found that the expression of miR-145 is significantly downregulated in thyroid cancer as compared with normal. Overexpression of miR-145 in thyroid cancer cell lines resulted in: decreased cell proliferation, migration, invasion, VEGF secretion, and E-cadherin expression. miR-145 overexpression also inhibited the PI3K/Akt pathway and directly targeted AKT3. In vivo, miR-145 overexpression decreased tumor growth and metastasis in a xenograft mouse model, and VEGF secretion. miR-145 inhibition in normal primary follicular thyroid cells decreased the expression of thyroid cell differentiation markers. Analysis of indeterminate fine-needle aspiration samples showed miR-145 had a 92% negative predictive value for distinguishing benign from malignant thyroid nodules. Circulating miR-145 levels were significantly higher in patients with thyroid cancer and showed a venous gradient. Serum exosome extractions revealed that miR-145 is secreted. Our findings suggest that miR-145 is a master regulator of thyroid cancer growth, mediates its effect through the PI3K/Akt pathway, is secreted by the thyroid cancer cells, and may serve as an adjunct biomarker for thyroid cancer diagnosis.

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“…Consequently, miRNAs are involved in the initiation and progression of various human cancers including prostate cancer [4]. Several miRNAs, namely, miRNA (miR)-34a, miR-148a, miR-221, miR-222, miR-143, miR-145, miR-21, and miR-331-3p, are known to be involved in prostate cancer [5][6][7][8][9][10][11][12][13][14][15][16][17]. For example, miR-34a negatively regulates the tumor-initiating capacity of prostate cancer stem cells.…”

Section: Introductionmentioning

confidence: 99%

Syndecan-1 responsive microRNA-126 and 149 regulate cell proliferation in prostate cancer

Fujii

Shimada

Tatsumi

et al. 2015

Biochemical and Biophysical Research Communications

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MicroRNAs (miRNAs) are short (19-24 nt), low molecular weight RNAs that play important roles in the regulation of target genes associated with cell proliferation, differentiation, and development, by binding to the 3'-untranslated region of the target mRNAs. In this study, we examined the expression of miRNA-126 (miR-126) and miR-149 in prostate cancer, and investigated the molecular mechanisms by which they affect syndecan-1 in prostate cancer. Functional analysis of miR-126 and miR-149 was conducted in the prostate cancer cell lines, PC3, Du145, and LNCaP. The expression levels of SOX2, NANOG, Oct4, miR-126 and miR-149 were evaluated by quantitative RT-PCR. After silencing syndecan-1, miR-126, and/or miR-149 in the PC3 cells, cell proliferation, senescence, and p21 induction were assessed using the MTS assay, senescence-associated β-galactosidase (SA-β-Gal) assay, and immunocytochemistry, respectively. Compared to the Du145 and LNCaP cells, PC3 cells exhibited higher expression of syndecan-1. When syndecan-1 was silenced, the PC3 cells showed reduced expression of miR-126 and miR-149 most effectively. Suppression of miR-126 and/or miR-149 significantly inhibited cell growth via p21 induction and subsequently, induced senescence. The mRNA expression levels of SOX2, NANOG, and Oct4 were significantly increased in response to the silencing of miR-126 and/or miR-149. Our results suggest that miR-126 and miR-149 are associated with the expression of syndecan-1 in prostate cancer cells. These miRNAs promote cell proliferation by suppressing SOX2, NANOG, and Oct4. The regulation of these factors by miR-126 and miR-149 is essential for syndecan-1-mediated development of androgen-refractory prostate cancer.

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miR-143 and miR-145 inhibit stem cell characteristics of PC-3 prostate cancer cells

Cited by 114 publications

References 44 publications

Microdissecting the role of microRNAs in the pathogenesis of prostate cancer

Microdissecting the role of microRNAs in the pathogenesis of prostate cancer

miR-145 suppresses thyroid cancer growth and metastasis and targets AKT3

Syndecan-1 responsive microRNA-126 and 149 regulate cell proliferation in prostate cancer

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