IGF-1-mediated PKM2/β-catenin/miR-152 regulatory circuit in breast cancer

Wen, Yiyang; Liu, Weitao; Sun, Haoran; Shi, Zhumei; Wang, Min; Li, Wei; Zhang, Jianying; Liu, Lingzhi; Jiang, Bing-Hua

doi:10.1038/s41598-017-15607-y

Cited by 34 publications

(21 citation statements)

References 46 publications

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“…In support of our results, the association between IGF-1 and miR-152 expression has been previously demonstrated in human oocytes, since the culturing of immature oocytes in the presence of IGF-1 signi cantly reduced the expression of miR-152 [47]. Moreover, in cancer research, it was suggested that miR-152 is involved in the IGF-1-mediated miR-152/PKM2/β-catenin regulatory circuit that regulates cell proliferation and angiogenesis [48]. Additionally, the overexpression of miR-152 inhibits breast cancer cell proliferation via targeting IGF1R and IRS1 and suppressing their downstream AKT and MAPK/ERK signaling pathways [37].…”

Section: Discussionsupporting

confidence: 89%

Inhibition of miR-152 During in Vitro Maturation Enhances the Developmental Potential of Porcine Embryos

Gad

Murín

Němcová

et al. 2020

Preprint

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Background Oocyte developmental competence is regulated by various mechanisms and molecules including microRNAs (miRNAs). However, the functions of many of these miRNAs in oocyte and embryo development are still unclear. In this study, we managed to manipulate the expression level of miR-152 during oocyte maturation to figure out its potential role in determining the developmental competence of porcine oocytes.Results The inhibition of miR-152 during oocyte maturation does not affect the MII and cleavage rates, however it significantly enhances the blastocyst rate compared to the mimic and control groups. Pathway analysis identified several signaling pathways (including PI3K/AKT, TGFβ, Hippo, FoxO, and Wnt signaling) that are enriched in the predicted target genes of miR-152. Gene expression analysis revealed that IGF1 was significantly up-regulated in the inhibitor group and downregulated in the mimic group of oocytes. Moreover, IGF1R was significantly upregulated in the inhibitor group compared to the control one and IGFBP6 was downregulated in the inhibitor group compared to the other groups. Blastocysts developed from the mimic-treated oocytes exhibited an increase in miR-152 expression, dysregulation in some quality-related genes, and the lowest rate of blastocyst formation. Conclusions Our results demonstrate a negative correlation between miR-152 expression level and blastocyst rate in pigs. This correlation could be through targeting IGF system components during oocyte development.

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Section: Discussionsupporting

confidence: 89%

Inhibition of miR-152 During in Vitro Maturation Enhances the Developmental Potential of Porcine Embryos

Gad

Murín

Němcová

et al. 2020

Preprint

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“…Some microRNAs have organ specification, such as miRNA-122 [84], miRNA-124 [85], miRNA-133-3p [86], miRNA-137 [84], miRNA-20 [68] [4, 87] and miRNA-3662 [88] etc., which regulate the expression of PKM subunits by directly targeting polypyrimidine bundle binding protein 1 (PTBP1), while polypyrimidine bundle binding protein 1 (PTBP1) is a splice that regulates PKM2 dominant expression. Similar to: miRNA-29b [89], miRNA-99a [90], miRNA-133b [91], miRNA-145 [92], miRNA-148a [93], miRNA-152 [93, 94], miRNA-290 [95], miRNA-326 [96], miRNA-338-3P [97], miRNA-340 [98], miRNA-369 [99], miRNA-371 [95], miR-379 [100], miRNA-675 [101], miRNA-4417 etc. [102].…”

Section: The Splicing Of Pmk2mentioning

confidence: 99%

PKM2, function and expression and regulation

et al. 2019

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Pyruvate kinase (PK), as one of the key enzymes for glycolysis, can encode four different subtypes from two groups of genes, although the M2 subtype PKM2 is expressed mainly during embryonic development in normal humans, and is closely related to tissue repair and regeneration, with the deepening of research, the role of PKM2 in tumor tissue has received increasing attention. PKM2 can be aggregated into tetrameric and dimeric forms, PKM2 in the dimer state can enter the nuclear to regulate gene expression, the transformation between them can play an important role in tumor cell energy supply, epithelial–mesenchymal transition (EMT), invasion and metastasis and cell proliferation. We will use the switching effect of PKM2 in glucose metabolism as the entry point to expand and enrich the Warburg effect. In addition, PKM2 can also regulate each other with various proteins by phosphorylation, acetylation and other modifications, mediate the different intracellular localization of PKM2 and then exert specific biological functions. In this paper, we will illustrate each of these points. Electronic supplementary material The online version of this article (10.1186/s13578-019-0317-8) contains supplementary material, which is available to authorized users.

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“…Arrays were deparaffinized, hydrated, pretreated for epitope unmasking, incubated with hydrogen peroxide, blocked with 10% goat serum (according to the manufacturer's instructions), and then arrays were incubated with the indicated antibodies at 4°C overnight. After washing, arrays were treated as previously reported ( 23 ).…”

Section: Methodsmentioning

confidence: 99%

HB-EGF Activates the EGFR/HIF-1α Pathway to Induce Proliferation of Arsenic-Transformed Cells and Tumor Growth

Wang

et al. 2020

Front. Oncol.

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Arsenic was recently identified as a pollutant that is a major cause of lung cancer. Since heparin-binding EGF-like growth factor (HB-EGF) was reported to be a promising therapeutic target for lung cancer, we investigated the role and mechanism of HB-EGF during arsenic-induced carcinogenesis and development of lung cancer. HB-EGF expression were upregulated in As-T cells, lung cancer cell lines, and in most lung cancer tissue samples; and HB-EGF activated the EGFR/p-ERK/HIF-1α pathway and induced VEGF by regulating HIF-1α transcription. HIF-1α transcriptional stimulation by HB-EGF was facilitated by PKM2 and played an important role in HB-EGF's effect on cells. An HB-EGF inhibitor(CRM197, cross-reacting material 197) slowed cell proliferation and inhibited migration of As-T and A549 cells, and inhibited tumor growth. PKM2 also played an important role in the proliferation and migration in As-T cells. The positive staining ratios of EGFR phosphorylation (Y1068) and PKM2 were significantly higher in most cases of lung cancer than in paired normal tumor-adjacent lung tissues; and HB-EGF expression levels strongly correlated with p-EGFR expression levels. Thus, HB-EGF drives arsenic-induced carcinogenesis, tumor growth, and lung cancer development via the EGFR/PKM2/HIF-1α pathway.

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IGF-1-mediated PKM2/β-catenin/miR-152 regulatory circuit in breast cancer

Cited by 34 publications

References 46 publications

Inhibition of miR-152 During in Vitro Maturation Enhances the Developmental Potential of Porcine Embryos

Inhibition of miR-152 During in Vitro Maturation Enhances the Developmental Potential of Porcine Embryos

PKM2, function and expression and regulation

HB-EGF Activates the EGFR/HIF-1α Pathway to Induce Proliferation of Arsenic-Transformed Cells and Tumor Growth

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