MicroRNA‐133b stimulates ovarian estradiol synthesis by targeting Foxl2

Dai, Anyi; Sun, Haixiang; Fang, Ting; Zhang, Qun; Wu, Shaogen; Jiang, Yue; Ding, Lijun; Yan, Guijun; Hu, Yali

doi:10.1016/j.febslet.2013.06.023

Cited by 105 publications

(82 citation statements)

References 42 publications

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“…As it has been previously reported that miR-133b acts as a tumor suppressor in lung cancer, the expression levels of miR-133b in A549 cells were measured following radiation treatment (13)(14)(15)(16)(17)(18). The expression of miR-133b was significantly reduced following radiation treatments of 0.2 to 0.6 Gy (Fig.…”

Section: Mir-133b Is Negatively Correlated With Radioresistancementioning

confidence: 57%

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Overexpression of microRNA-133b sensitizes non-small cell lung cancer cells to irradiation through the inhibition of glycolysis

Liu

Gao

2016

Oncology Letters

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Abstract. Non-small cell lung cancer (NSCLC) accounts for 85% of all types of lung cancer and is the leading cause of world-wide cancer-associated mortalities. Radiation therapy has long been regarded as a fundamental therapeutic treatment strategy for NSCLC. However, alternative therapies for NSCLC remain insufficient, with the majority of cancers developing a high incidence of radioresistance. MicroRNAs (miRNAs/miRs) are endogenous oligonucleotide RNAs that serve an important role in carcinogenesis and tumor progression. In the present study, a novel function of miR-133b that is associated with the radiosensitivity of lung cancer cells is reported. miR-133 was downregulated in radioresistant lung cancer cells, which exhibited an elevated glycolysis rate when compared with radiosensitive cells. Additionally, it was observed that pyruvate kinase isoform M2 (PKM2) is a target of miR-133b, and that the expression of PKM2 is positively correlated with radioresistance. Finally, it was demonstrated that overexpression of miR-133b resensitizes radioresistant lung cancer cells through the inhibition of PKM2-mediated glycolysis. The current study may indicate a novel function of miR-133b, potentially aiding the development of anticancer therapeutics.

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Section: Mir-133b Is Negatively Correlated With Radioresistancementioning

confidence: 57%

“…Discussion miR-133b has been reported as a tumor suppressor functioning in numerous types of cancer that demonstrate low miR-133b expression, as noted in colorectal (13), gastric (14), bladder (15), lung (16), esophageal (17), ovarian (18) and breast (19) cancer. However, the role of miR-133b within radiosensitivity remains under investigation.…”

mentioning

confidence: 91%

Overexpression of microRNA-133b sensitizes non-small cell lung cancer cells to irradiation through the inhibition of glycolysis

Liu

Gao

2016

Oncology Letters

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“…Moreover, physiological changes in the expression of miRNAs supporting putative roles during follicle development have often not been demonstrated , Yang et al 2012, Dai et al 2013, and detailed spatiotemporal miRNA profiles during development are not available. In a previous study (McBride et al 2012), we used sequencing to characterize the developmental changes in miRNA expression in ovine follicles, although our focus was on terminal differentiation (follicle-luteal transition) rather than on follicle growth and atresia.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have already reported effects of specific miRNAs on different aspects of granulosa cell function , including steroidogenesis (Yao et al 2010, Xu et al 2011, Yin et al 2012, Dai et al 2013, proliferation (Yao et al 2010, Yan et al 2012, Dai et al 2013, survival (Carletti et al 2010, Yang et al 2012, terminal differentiation (Kitahara et al 2013), and cumulus expansion (Yao et al 2014). With a few exceptions (Carletti et al 2010, Kitahara et al 2013, most evidence on follicular roles of miRNAs has been obtained using cultured cells, particularly rodent cells, and in some cases actual changes in the expression of these miRNAs during follicle development have not been demonstrated.…”

Section: Introductionmentioning

confidence: 99%

Characterization of microRNAs differentially expressed during bovine follicle development

Sontakke¹,

Mohammed²,

McNeilly³

et al. 2014

Reproduction

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Several different miRNAs have been proposed to regulate ovarian follicle function; however, very limited information exists on the spatiotemporal patterns of miRNA expression during follicle development. The objective of this study was to identify, using microarray, miRNA profiles associated with growth and regression of dominant-size follicles in the bovine monovular ovary and to characterize their spatiotemporal distribution during development. The follicles were collected from abattoir ovaries and classified as small (4-8 mm) or large (12-17 mm); the latter were further classified as healthy or atretic based on estradiol and CYP19A1 levels. Six pools of small follicles and individual large healthy (nZ6) and large atretic (nZ5) follicles were analyzed using Exiqon's miRCURY LNA microRNA Array 6th gen, followed by qPCR validation. A total of 17 and 57 sequences were differentially expressed (greater than or equal to twofold; P!0.05) between large healthy and each of small and large atretic follicles respectively. Bovine miRNAs confirmed to be upregulated in large healthy follicles relative to small follicles (bta-miR-144, bta-miR-202, bta-miR-451, bta-miR-652, and bta-miR-873) were further characterized. Three of these miRNAs (bta-miR-144, bta-miR-202, and bta-miR-873) were also downregulated in large atretic follicles relative to large healthy follicles. Within the follicle, these miRNAs were predominantly expressed in mural granulosa cells. Further, body-wide screening revealed that bta-miR-202, but not other miRNAs, was expressed exclusively in the gonads. Finally, a total of 1359 predicted targets of the five miRNAs enriched in large healthy follicles were identified, which mapped to signaling pathways involved in follicular cell proliferation, steroidogenesis, prevention of premature luteinization, and oocyte maturation.

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“…Another miR shown to modulate estrogen synthesis is miR-133b, which increases estrogen synthesis in the ovaries by targeting Foxl2, a negative regulator of the steroidogenic enzymes, STAR protein and CYP19A1. miR-133b was shown to associate with FOXL2 3 0 -UTR, reducing FOXL2 protein levels, and its binding to STAR and CYP19A1 promoter sequences in granulosa cells, thereby increasing estrogen synthesis and secretion (Dai et al 2013). It is likely that further miRs will emerge as regulating hormone synthesis enzymes, and given the clinical importance of intratumoural steroid synthesis for both breast and prostate cancer it will be of major interest to determine whether these are disregulated in both tumour types and whether they are regulated by steroid signalling themselves.…”

Section: Estrogen Modulation Of Mir Biogenesismentioning

confidence: 99%

Interplay between steroid signalling and microRNAs: implications for hormone-dependent cancers

Fletcher¹,

Dart²,

Bevan³

2014

Endocrine Related Cancer

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Hormones are key drivers of cancer development. To date, interest has largely been focussed on the classical model of hormonal gene regulation, but there is increasing evidence for a role of hormone signalling pathways in post-translational regulation of gene expression. In particular, a complex and dynamic network of bi-directional interactions with microRNAs (miRs) at all stages of biogenesis and during target gene repression is emerging. miRs, which act mainly by negatively regulating gene expression through association with 3 0 -UTRs of mRNA species, are increasingly understood to be important in development, normal physiology and pathogenesis. Given recent demonstrations of altered miR profiles in a diverse range of cancers, their ability to function as oncogenes or tumour suppressors, and hormonal regulation of miRs, understanding mechanisms by which miRs are generated and regulated is vitally important. miRs are transcribed by RNA polymerase II and then processed in the nucleus by the Drosha-containing Microprocessor complex and in the cytoplasm by Dicer, before mature miRs are incorporated into the RNA-induced silencing complex. It is increasingly evident that multiple cellular signalling pathways converge upon the miR biogenesis cascade, adding further layers of regulatory complexity to modulate miR maturation. This review summarises recent advances in identification of novel components and regulators of the Microprocessor and Dicer complexes, with particular emphasis on the role of hormone signalling pathways in regulating their activity. Understanding hormone regulation of miR production and how this is perturbed in cancer are critical for the development of miR-based therapeutics and biomarkers.

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MicroRNA‐133b stimulates ovarian estradiol synthesis by targeting Foxl2

Cited by 105 publications

References 42 publications

Overexpression of microRNA-133b sensitizes non-small cell lung cancer cells to irradiation through the inhibition of glycolysis

Overexpression of microRNA-133b sensitizes non-small cell lung cancer cells to irradiation through the inhibition of glycolysis

Characterization of microRNAs differentially expressed during bovine follicle development

Interplay between steroid signalling and microRNAs: implications for hormone-dependent cancers

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