p16INK4a Translation Suppressed by miR-24

Lal, Ashish; Kim, Hyeon-Ho; Abdelmohsen, Kotb; Kuwano, Yuki; Pullmann, R; Srikantan, Subramanya; Subrahmanyam, Ramesh; Martindale, Jennifer L.; Yang, Xiaoling; Ahmed, Fahad; Navarro, Francisco; Dykxhoorn, Derek M.; Lieberman, Judy; Gorospe, Myriam

doi:10.1371/journal.pone.0001864

Cited by 242 publications

(210 citation statements)

References 39 publications

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“…As reported recently, miRNAs are abundant, small non-coding RNAs that mediate sequence-specific, posttranscriptional gene expression by binding to the target 3 0 UTR of mRNA, and have been implicated in the regulation of certain cancer-related processes, including development, differentiation, apoptosis and proliferation (Merkerova et al, 2008;Ruan et al, 2009;Yang et al, 2009). To date, miR-24 has been implicated in the regulation of hematopoietic differentiation and cell proliferation (Lal et al, 2008(Lal et al, , 2009Wang et al, 2008). For example, miR-24 downregulates the expression of human dihydrofolate reductase and expression of miR-24 is upregulated during differentiation of human leukemia cells.…”

Section: Discussionmentioning

confidence: 99%

Induction of anion exchanger-1 translation and its opposite roles in the carcinogenesis of gastric cancer cells and differentiation of K562 cells

Zhang

et al. 2010

Oncogene

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Anion exchanger-1 (AE1), an erythroid-specific membrane protein, mediates the Cl À /HCO À 3 exchange across the plasma membrane and regulates intracellular pH. We have found that AE1 was unexpectedly expressed in gastric cancer cells and participated in the tumorigenesis of the cancer. Here, we focus on the induction of AE1 expression and its role in gastric carcinogenesis as well as in the differentiation of K562 cells. The results show that expression of AE1 is not related to genetic mutation or the mRNA level, but rather, that it is modulated by miR-24. miR-24 decreases the expression of AE1 through binding to the 3 0 UTR of AE1 mRNA. Transfection of an miR-24 into gastric cancer cells reduced the elevation of the AE1 protein, which resulted in return of AE1-sequestrated p16 to the nucleus, thereby inhibiting proliferation of the cells. Furthermore, the miR-24 inhibitor cooperated with hemin to induce the expression of AE1 in K562 cells and differentiation of the cells, which is consistent with results obtained from the cells cultured at pH 7.6 or from forced stable expression of AE1. These findings establish a novel regulation of miR-24-related AE1 expression in gastric carcinogenesis and erythropoiesis.

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Section: Discussionmentioning

confidence: 99%

Induction of anion exchanger-1 translation and its opposite roles in the carcinogenesis of gastric cancer cells and differentiation of K562 cells

Zhang

et al. 2010

Oncogene

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“…Total cellular RNA was prepared directly from cells using TRIzol (Invitrogen) or was isolated after immunoprecipitation (IP) from cellular RNAprotein complexes by IP [using anti-HuR, anti-HA or IgG, as described (21,33)]. After reverse transcription (RT) using random hexamers and SSII reverse transcriptase (Invitrogen), real-time quantitative (q)PCR analysis was performed using gene-specific primer pairs (Table S1) and SYBR Green PCR master mix (Applied Biosystems), as described (21).…”

Section: Methodsmentioning

confidence: 99%

miR-519 reduces cell proliferation by lowering RNA-binding protein HuR levels

Abdelmohsen

Srikantan

Kuwano

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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196

177

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Gene expression is potently regulated through the action of RNAbinding proteins (RBPs) and microRNAs (miRNAs). Here, we present evidence of a miRNA regulating an RBP. The RBP HuR can stabilize and modulate the translation of numerous target mRNAs involved in cell proliferation, but little is known about the mechanisms that regulate HuR abundance. We identified two putative sites of miR-519 interaction on the HuR mRNA, one in its coding region (CR), one in its 3 -untranslated region (UTR). In several human carcinoma cell lines tested, HeLa (cervical), HCT116 and RKO (colon), and A2780 (ovarian

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“…The p27 and p57 proteins are regulated by miR-221/222 [52,53] and miR92b [54] . The INK family member p16 is regulated by miR-24 [55] . The number of miRNAs regulating the entry and progression through G 2 /M is much fewer than those regulating the G 1 /S transition.…”

Section: Mir-34 Familymentioning

confidence: 99%

Macro-management of microRNAs in cell cycle progression of tumor cells and its implications in anti-cancer therapy

Liang

2011

Acta Pharmacol Sin

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The cell cycle, which is precisely controlled by a number of regulators, including cyclins and cyclin-dependent kinases (CDKs), is crucial for the life cycle of mammals. Cell cycle dysregulation is implicated in many diseases, including cancer. Recently, compelling evidence has been found that microRNAs play important roles in the regulation of cell cycle progression by modulating the expression of cyclins, CDKs and other cell cycle regulators. Herein, the recent findings on the regulation of the cell cycle by microRNAs are summarized, and the potential implications of miRNAs in anti-cancer therapies are discussed.

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p16INK4a Translation Suppressed by miR-24

Cited by 242 publications

References 39 publications

Induction of anion exchanger-1 translation and its opposite roles in the carcinogenesis of gastric cancer cells and differentiation of K562 cells

Induction of anion exchanger-1 translation and its opposite roles in the carcinogenesis of gastric cancer cells and differentiation of K562 cells

miR-519 reduces cell proliferation by lowering RNA-binding protein HuR levels

Macro-management of microRNAs in cell cycle progression of tumor cells and its implications in anti-cancer therapy

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