Hyperglycaemia-induced miR-301a promotes cell proliferation by repressing p21 and Smad4 in prostate cancer

Li, Xiaojuan; Li, Jun; Cai, Yi; Peng, Shubin; Wang, Jun; Xiao, Zhaoming; Wang, Yu; Tao, Yiran; Leng, Qu; Wu, Dinglan; Yang, Shaodong; Ji, Zhonghua; Han, Yuefu; Li, Liren; Gào, Xīn; Zeng, Chengbo; Wen, Xin

doi:10.1016/j.canlet.2018.01.031

Cited by 41 publications

(35 citation statements)

References 38 publications

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“…miR-301a represses the expression of SMAD4, promoting the proliferation of prostate cancer cells in vitro and tumor growth in vivo. Interestingly, the expression of miR-301a is regulated by high glucose levels [308], which fits the known association between hyperglycemia and the development of prostate cancer, as well as the prostate cancer grade, Gleason score, and increased risk of prostate cancer recurrence [315,316]. MicroRNAs also regulate the expression of SMAD2.…”

Section: Prostate Cancersupporting

confidence: 66%

“…Transfection of PC3 prostate cancer cells with miR-34b mimics results in the inhibition of cell growth, migration, and invasion [306]. The expression of SMAD4 is also regulated by multiple other microRNAs, including miR-1260b, miR-301a, miR-888, and miR-183 [307][308][309][310][311]. Interestingly, expression of miR-1260b is downregulated by genistein, an isoflavone naturally occurring in plants (e.g., lupin, fava beans, soybeans, and coffee), exerting chemopreventive and anticancer activities [312][313][314].…”

Section: Prostate Cancermentioning

confidence: 99%

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TGF-β and microRNA Interplay in Genitourinary Cancers

Bogusławska¹,

Kryst

Poletajew

et al. 2019

Cells

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Genitourinary cancers (GCs) include a large group of different types of tumors localizing to the kidney, bladder, prostate, testis, and penis. Despite highly divergent molecular patterns, most GCs share commonly disturbed signaling pathways that involve the activity of TGF-β (transforming growth factor beta). TGF-β is a pleiotropic cytokine that regulates key cancer-related molecular and cellular processes, including proliferation, migration, invasion, apoptosis, and chemoresistance. The understanding of the mechanisms of TGF-β actions in cancer is hindered by the “TGF-β paradox” in which early stages of cancerogenic process are suppressed by TGF-β while advanced stages are stimulated by its activity. A growing body of evidence suggests that these paradoxical TGF-β actions could result from the interplay with microRNAs: Short, non-coding RNAs that regulate gene expression by binding to target transcripts and inducing mRNA degradation or inhibition of translation. Here, we discuss the current knowledge of TGF-β signaling in GCs. Importantly, TGF-β signaling and microRNA-mediated regulation of gene expression often act in complicated feedback circuits that involve other crucial regulators of cancer progression (e.g., androgen receptor). Furthermore, recently published in vitro and in vivo studies clearly indicate that the interplay between microRNAs and the TGF-β signaling pathway offers new potential treatment options for GC patients.

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Section: Prostate Cancersupporting

confidence: 66%

Section: Prostate Cancermentioning

confidence: 99%

TGF-β and microRNA Interplay in Genitourinary Cancers

Bogusławska¹,

Kryst

Poletajew

et al. 2019

Cells

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“…First, to investigate whether miR301a-3p targets and alters p21 levels in vivo, we transfected HNSCC cells UMSCC74B (Fig 5B) Figs 5C, S5B and S5H). Similarly, others have shown that inhibition of miR301a-3p increases the levels of p21 and severely blocked prostate cancer cell growth, both in vitro and in vivo [45]. Second, our previous findings demonstrate that FXR1 knockdown leads to an increased p21 3'-UTR luciferase activity [34].…”

Section: P21 Is a Target Of Mir301a-3psupporting

confidence: 68%

RNA binding protein FXR1-miR301a-3p axis contributes to p21WAF1 degradation in oral cancer

Majumder

Palanisamy

2020

PLoS Genet

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RNA-binding proteins (RBPs) associate with the primary, precursor, and mature micro-RNAs, which in turn control post-transcriptional gene regulation. Here, by small RNAseq, we show that RBP FXR1 controls the expression of a subset of mature miRNAs, including highly expressed miR301a-3p in oral cancer cells. We also confirm that FXR1 controls the stability of miR301a-3p. Exoribonuclease PNPT1 degrades miR301a-3p in the absence of FXR1 in oral cancer cells, and the degradation is rescued in the FXR1 and PNPT1 coknockdown cells. In vitro, we show that PNPT1 is unable to bind and degrade the miRNA once the FXR1-miRNA complex forms. Both miR301a-3p and FXR1 cooperatively target the 3'-UTR of p21 mRNA to promote its degradation. Thus, our work illustrates the unique role of FXR1 that is critical for the stability of a subset of mature miRNAs or at least miR301a-3p to target p21 in oral cancer.

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“…6 In recent years, microRNAs have been defined as regulators and potential biomarkers, playing a crucial role in the oncogenesis, metastasis and development of RCC. 7,8 Previous studies have revealed that miR-301a is an onco-miRNA in various types of tumor, such as pancreatic cancer, 9 breast cancer, 10 prostate cancer, 11 and malignant melanoma. 12 However, research on miR-301a in RCC has not yet been reported.…”

Section: Introductionmentioning

confidence: 99%

<p>MiR-301a Promotes Cell Proliferation by Repressing PTEN in Renal Cell Carcinoma</p>

Li¹,

Jiang²,

Zhang³

et al. 2020

CMAR

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Renal cell carcinoma (RCC) displays an increasing incidence and mortality rate worldwide in recent years. More and more evidence demonstrated microRNAs function as positive or negative regulatory factors in many cancers, while the role of miR-301a in RCC is still unclear. Material and Methods: The expression and clinical significance of miR-301a were assessed via bioinformatic software on open microarray datasets of the Cancer Genome Atlas (TCGA) and then confirmed by quantitative real-time PCR (qRT-PCR) in RCC cell lines. Loss of function assays were performed in RCC cell lines both in vitro and in vivo. Cell Counting Kit-8 (CCK-8), flow cytometry, luciferase reporter assays, Western blotting, and immunohistochemistry were employed to explore the mechanisms of the effect of miR-301a on RCC. Results: By analyzing RCC clinical specimens and cell lines, we found a uniform increased miR-301a in expression in comparison with normal renal tissue or normal human proximal tubule epithelial cell line (HK-2). In addition, miR-301a upregulation correlated advanced stage and poor prognosis of clear cell RCC (ccRCC). Anti-miR-301a could inhibit growth and cell cycle G1/S transition in RCC cell lines. Moreover, we found that PTEN was identified as a direct target of miR-301a that might partially interrupt miR-301a-induced G1/S transition. Importantly, nude-mouse models revealed that knockdown of miR-301a delayed tumor growth. Conclusion: These results indicate that miR-301a functions as a tumor-promoting miRNA through regulating PTEN expression, representing a novel therapeutic target for RCC.

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Hyperglycaemia-induced miR-301a promotes cell proliferation by repressing p21 and Smad4 in prostate cancer

Cited by 41 publications

References 38 publications

TGF-β and microRNA Interplay in Genitourinary Cancers

TGF-β and microRNA Interplay in Genitourinary Cancers

RNA binding protein FXR1-miR301a-3p axis contributes to p21WAF1 degradation in oral cancer

<p>MiR-301a Promotes Cell Proliferation by Repressing PTEN in Renal Cell Carcinoma</p>

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