MiR-23a induced the activation of CDC42/PAK1 pathway and cell cycle arrest in human cov434 cells by targeting FGD4

Lin, Jinpiao; Huang, Huijuan; Lin, Liheng; Li, Weiwei; Huang, Jianfen

doi:10.1186/s13048-020-00686-9

Cited by 12 publications

(6 citation statements)

References 27 publications

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“…In this study, we identified miR-23a as a novel miRNA that induces pGC apoptosis in pigs. Previous studies showed that miR-23a promotes cell apoptosis in hGCs via the FasL-Fas, ERK1/2, and CDC42/PAK1 signaling pathways, which are related to ovarian reserve function and premature ovarian failure [ 18 , 28 , 29 ]. In hGCs, miR-23a has also been shown to block the cell cycle on the G0/G1 phase and suppress cell proliferation [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies showed that miR-23a promotes cell apoptosis in hGCs via the FasL-Fas, ERK1/2, and CDC42/PAK1 signaling pathways, which are related to ovarian reserve function and premature ovarian failure [ 18 , 28 , 29 ]. In hGCs, miR-23a has also been shown to block the cell cycle on the G0/G1 phase and suppress cell proliferation [ 28 ]. In addition to GCs, miR-23a is also an important regulator in many cell types such as human acute lymphoblastic T-cells [ 30 ], airway epithelial cells and fibroblasts [ 31 ], and oral squamous cell carcinoma cells [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

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A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress

Wang

Zeng

et al. 2022

Antioxidants

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Phenotypes are the result of the interaction between the gene and the environment, so the response of individuals with different genotypes to an environment is variable. Here, we reported that a mutation in miR-23a influences granulosa cells (GCs) response to oxidative stress, a common mechanism of environmental factors affecting female reproduction. We showed that nuclear miR-23a is a pro-apoptotic miRNA in porcine GCs through the activation of the transcription and function of NORHA, a long non-coding RNA (lncRNA) induces GC apoptosis and responses to oxidative stress. Mechanistically, miR-23a acts as an endogenous small activating RNA (saRNA) to alter histone modifications of the NORHA promoter through the direct binding to its core promoter. A C > T mutation was identified at −398 nt of the miR-23a core promoter, which created a novel binding site for the transcription factor SMAD4 and recruited the transcription repressor SMAD4 to inhibit miR-23a transcription and function in GCs. Notably, g.−398C > T mutation in the miR-23a promoter reduced GCs response to oxidative stress. In addition, g.−398C > T mutation was significantly associated with sow fertility traits. In short, our findings preliminarily revealed the genetic basis of individual differences in the response to oxidative stress from the perspective of a single mutation and identified miR-23a as a candidate gene for the environmental adaptation to oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress

Wang

Zeng

et al. 2022

Antioxidants

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“…Furthermore, a high expression of miR-93 [22] and lower miR-23a have been identified in the GCs from PCOS patients. They indicated that miR-23a induces cell cycle arrest via the inhibition of FGD4 signalling [23]. Another group has also demonstrated a significantly lower expression of miR-126-5p and miR-29a in the GCs of PCOS patients when compared with healthy individuals, which were indicated to induce GC apoptosis in PCOS [24].…”

Section: Mirnas In Granulosa Cells (Gcs) and Pcosmentioning

confidence: 98%

The Novelty of miRNAs as a Clinical Biomarker for the Management of PCOS

Alhamdan¹,

Hernandez-Medrano²

2022

Polycystic Ovary Syndrome - Functional Investigation and Clinical Application

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Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects around 5–10% of women of reproductive age. The aetiology of PCOS is not fully understood with various genetics, iatrogenic (e.g. chemotherapy) and environmental factors have been proposed. microRNAs (miRNAs) are small non-coding single-stranded RNAs which are known to act as a regulator to gene expression at the post-transcriptional levels. Altered expression of miRNAs has been linked to several disorders including infertility. Recent reports demonstrated the expression of differential levels of miRNAs in the serum, ovarian follicular cells and follicular fluid of PCOS patients when compared with healthy women. Therefore, miRNAs may play important role in the pathogenesis of PCOS. The aim of this chapter is to summarise the current understanding pertaining to miRNAs and PCOS and to expedite its possible role in the diagnosis and management of this disorder.

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“… 81 In human ovarian granulosa tumour cells, miR‐23a induced cell cycle arrest via the CDC42/PAK1 pathway. 82 Clinical trials have also observed that increasing CDC42 expression in granulosa cells from patients with polycystic ovary syndrome improves fertility. 83 Further studies have shown that granulosa cell CDC42 expression is significantly associated with pregnancy outcome and is a potential follicle marker associated with embryos.…”

Section: Cdc42 and Granulosa Cellsmentioning

confidence: 99%

Advances in the study of CDC42 in the female reproductive system

Mei

Liu

et al. 2021

J Cellular Molecular Medi

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Cell division cycle 42 (CDC42) is a member of the Rho-GTPase family. It is 191 amino acids in length, located on chromosome 1p36.12, and it contains a molecular weight of 21.33 kDa. 1 CDC42 was first identified in budding yeast in 1997, and it plays an integral role in the regulation of cell motility, cell proliferation, cytoskeleton and in particular, microfilament-dependent cell polarity. 2-5 CDC42 is highly homologous and conserved in human and yeast, and can be hypothesized to play a fundamental role in cell biology. 6 CDC42 also plays a central role in the establishment of cell polarity. 7 The first evidence of the involvement of CDC42 in the establishment of cell polarity came from a study by Adams et al. in yeast, 8 which showed that a novel effector domain of CDC42 is involved in triggering the yeast G2/M transition and can couple the cell cycle to play a role in cytoskeletal rearrangements. 9 Later, in Drosophila oocytes, it was found that Drosophila maternal effector proteins interact with both actin through the WH2 structure and CDC42, thereby localizing GTPase to the actin cytoskeleton. 10 It is noteworthy that the multifactor-controlled 'inactivation-activation' process of CDC42 also makes it play an important role in the combined regulation of multiple genes and signalling pathway network, and the synergistic effect of multiple genes makes the process of female gametogenesis more precise. Thus, the role of CDC42 in female vertebrate gametogenesis has been gradually unveiled. In this context, the aim of this paper is to review the role played by CDC42 in controlling female gametogenesis and to summarize the related mechanisms. We will describe how CDC42 regulates female gametogenesis (including four chapters on follicular reserve and primordial follicle activation, meiosis, fertilization and embryo formation); similarly, we will briefly

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MiR-23a induced the activation of CDC42/PAK1 pathway and cell cycle arrest in human cov434 cells by targeting FGD4

Cited by 12 publications

References 27 publications

A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress

A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress

The Novelty of miRNAs as a Clinical Biomarker for the Management of PCOS

Advances in the study of CDC42 in the female reproductive system

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