RNA N6-methyladenosine modification in female reproductive biology and pathophysiology

Erqing Huang, Huang E, Lijuan Chen
Cell communication and signaling : CCS · 2023 · vol. 21(1) , pp. 53 · doi:10.1186/s12964-023-01078-4 · PMID:36894952 · PMC9996912 · W4323656104
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This review summarizes recent findings on N6-methyladenosine modification's roles in female reproductive biology and pathologies, including oogenesis, embryonic development, and gynecological diseases.

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This 2023 review by Huang and Chen surveyed recent evidence on N6-methyladenosine (m6A), the most abundant RNA modification, focusing on its roles in female reproductive biology and disease pathophysiology. It describes how m6A is regulated by “writers,” “erasers,” and “readers” (e.g., METTL3/METTL14/W TAP and others) and summarizes links between m6A-dependent posttranscriptional control and processes such as oogenesis, embryonic/fetal development, and pregnancy complications, while also compiling reported associations with conditions including endometriosis and adenomyosis. The authors note that the precise mechanisms of m6A function remain incompletely elucidated and that effects can be difficult to reconcile because they vary by cell type, environment, RNA features, and intracellular context. This paper is centrally about endometriosis and adenomyosis — it is a broad review that explicitly summarizes m6A involvement in endometriosis and adenomyosis among other female reproductive disorders.

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Abstract

Gene expression and posttranscriptional regulation can be strongly influenced by epigenetic modifications. N6-methyladenosine, the most extensive RNA modification, has been revealed to participate in many human diseases. Recently, the role of RNA epigenetic modifications in the pathophysiological mechanism of female reproductive diseases has been intensively studied. RNA m6A modification is involved in oogenesis, embryonic growth, and foetal development, as well as preeclampsia, miscarriage, endometriosis and adenomyosis, polycystic ovary syndrome, premature ovarian failure, and common gynaecological tumours such as cervical cancer, endometrial cancer, and ovarian cancer. In this review, we provide a summary of the research results of m6A on the female reproductive biology and pathophysiology in recent years and aim to discuss future research directions and clinical applications of m6A-related targets. Hopefully, this review will add to our understanding of the cellular mechanisms, diagnostic biomarkers, and underlying therapeutic strategies of female reproductive system diseases. Video Abstract.
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M

The TNM stage of gastric cancer is associated with METTL14 expression. According to an overall survival analysis, overall survival rates were higher for patients with higher levels of METTL14 expression. Based on multivariate analysis, METTL14 expression levels were associated with improved outcomes [ 159 ]. Non-small cell lung carcinoma cells undergo drug resistance and metastasis via diverse pathways when METTL3 increases m 6 A modification of both YAP and lncRNA MALAT1 [ 160 ]. FTO promotes cell proliferation of acute myeloid leukaemia in an m 6 A-dependent manner. Two inhibitors of FTO have been successfully developed by Huang and colleagues. These inhibitors, FB23 and FB23-2, bind directly to FTO and inhibit its m 6 A demethylase activity. The inhibitors display significantly improved inhibitory activity on FTO demethylation of m 6 A-RNA in vitro. Using these inhibitors, researchers inhibited the proliferation of a panel of AML cell lines and primary AML leukaemia stem cells in patient-derived xenotransplantation mice. Therefore, FTO and its analogues may be effective molecular targets for inhibiting leukaemogenesis in leukaemia stem cells [ 161 – 163 ]. Previous studies also indicated that YTHDF1 was strongly associated with a poor prognosis for ovarian cancer, breast cancer, and other female reproductive disorders [ 132 , 164 , 165 ]. The low expression of KIAA1429, an m 6 A methyltransferase, significantly increased dendritic cell infiltration. Researchers have shown that KIAA1429 expression affects immune checkpoint blockade therapeutic efficacy and boosts intratumoral antitumour immunity. Patients with low KIAA1429 expression experienced survival benefits from anti-PD-L1 immunotherapy [ 166 – 168 ]. It has been demonstrated that m 6 A regulators are associated with the prognosis of cervical cancer patients. m 6 A methylation regulators may be key regulators of PD-L1 expression and immune cell infiltration and may have an important impact on the TIME of cervical cancer [ 169 ]. In recent years, the role of m 6 A modification in PARP resistance in ovarian cancer has attracted the interest of several scientists. In BRCA-mutated ovarian cancer cells, m 6 A modification of FZD10 mRNA promoted PARP resistance through upregulation of the Wnt/β-catenin pathway [ 170 ]. Another study on olaparib resistance in ovarian cancer cells showed that m 6 A modifications of the olaparib pharmacogene were increased in resistant ovarian cancer cells [ 171 ]. These m 6 A modification sites could be used as potential pharmacoepitranscriptomics markers of drugs. Studies have confirmed that ALKBH5 expression is upregulated in cisplatin-resistant ovarian cancer and that overexpression of the ALKBH5-HOXA10 loop activates the JAK2/STAT3 signalling pathway, leading to chemoresistance in ovarian cancer [ 172 ]. In future studies, targeted blockade against the ALKBH5-HOXA10 loop may reverse chemoresistance in ovarian cancer cells. Based on the above studies, it is clear that m 6 A regulators are closely linked to clinical treatment and diagnosis.

The

Cell proliferation, differentiation, and metabolism and the cell cycle in the female reproductive system are regulated by m 6 A factors, according to many studies. Maternal factors accumulate in oocytes and play a major role in embryo maturation and development. Transcriptional activity is silenced during this time from fully developed GV oocytes to mid-blastula embryos [ 54 ]. In X. laevis oocyte maturation and later embryo development, RNA methylation has been found to be responsible for RNA translation regulation [ 55 ]. Oocyte maturation requires precise control over translation due to the lack of transcription during the early stages of embryogenesis [ 56 ]. High methylation levels of maternal RNA can interfere with translation and reduce the amount of protein available for embryo development and oocyte maturation. Postnatal oocyte maturation is influenced by YTHDC1. Knocking down YTHDC1 post-natally induces female mice to lose their sterility and ability to produce secondary and antral follicles. YTHDC1 deficiency led to RNA metabolism defects and granule accumulation in oocytes. Moreover, loss of YTHDC1 is lethal to embryos. To be precise, when the m 6 A reader YTHDC1 is lost, the 3'UTR length is changed by extensive alternative polyadenylation. microRNAs and protein binding sites have been demonstrated to be abundant in the 3'UTR. In the absence of YTHDC1, transcription and translation are affected, and therefore, oocyte development and female fertility are compromised [ 57 ]. Mice with YTHDC2 deficiency survived. However, mice of both sexes lacked fertility, and female mice had smaller ovaries. No germ cells were able to progress beyond the zygotene stage of prophase I of meiosis. Through its binding to m 6 A, YTHDC2 increases translation efficiency and stabilizes its targets [ 37 ]. YTHDC2 in the testes of male mice can ameliorate Mn-induced reproductive toxicity as well as cell cycle arrest [ 58 ]. YTHDF1 knockdown inhibited the self-renewal of female mouse germline stem cells. A significant difference was found in total m 6 A levels and METTL3, ALKBH5, YTHDF1, YTHDF2, YTHDC1, and YTHDC2 in female mouse germline stem cells compared to Sandos inbred mouse embryo-derived thioguanine and ouabain-resistant cells [ 59 ]. The m 6 A reader YTHDF2 post-transcriptionally regulates transcript degradation during mouse oocyte meiosis maturation, which is required for early embryo development. YTHDF2-deficient mice can survive normally; however, female mice are infertile [ 60 ]. Several m 6 A readers, including IGF2BP2 and IGF2BP3, are implicated in stabilizing maternal mRNAs involved in DNA repair and meiosis during oogenesis. In addition to contributing to mRNA stability, m 6 A is potentially involved in oocyte maturation through its involvement in other RNA metabolism processes [ 61 ]. A high level of METTL3 expression was observed during follicle development and oocyte maturation. Oocytes with inactivated METTL3 develop improperly, produce abnormal follicles, and fail to ovulate correctly. METTL3 interacts with ITSN2, a protein involved in oocyte meiotic resumption, to enhance its stability to act on oocyte meiosis in an m 6 A-dependent manner. MII oocytes and offspring are not produced in METTL3 knockdown females, and oocytes in the GV stage have smaller numbers and diameters than wild-type oocytes, suggesting that METTL3 is an m 6 A methyltransferase that promotes oocyte development by stabilizing maternal mRNAs during the GV stage [ 61 ]. Knockdown of METTL3 did not affect meiotic resumption. However, METTL3-deficient oocytes were unable to produce sufficient first polar bodies and normal spindles [ 62 ]. Many previous studies have confirmed that m 6 A regulators such as METTL3, METTL14, ALKBH5, and YTHDF2 regulate the differentiation of bone marrow mesenchymal stem cells, haematopoietic stem cells, and liver and breast cancer stem cells through Smad signalling, Notch signalling, and the oncogenes MYC and MYB [ 63 – 72 ]. Similarly, during embryonic development, the loss of METTL3 increases the expression of naïve pluripotency transcripts in murine pluripotent embryonic stem cells, hampering priming and differentiation competence [ 73 ]. IGF2BP3 binds to maternal mRNAs and inhibits their degradation during the transition between maternal and zygotic stages. Deficiency of IGFR2BP3 speeds up the degradation of maternal RNA. Cell division was impaired in IGF2BP3-mutant cells, but oocyte development was normal [ 74 ]. An in vitro experiment confirmed that deleting maternal IGF2BP2 causes interrupted embryonic development at the two-cell stage and impaired fertility. Oogenesis was not affected by IGF2BP2 deletion. In two-cell stage embryos, transcriptional and translational activity are both decreased. IGF2BP2 can significantly strengthen the ability of embryos to develop into blastocysts and improve embryo quality by regulating IGF2 [ 75 ]. In addition to mRNA methylation, in recent years, it has been reported that rRNA methylation also plays an important regulatory role in embryonic differentiation. Zebrafish that lose snoRNA-guided rRNA modification undergo developmental defects and die during embryogenesis [ 76 ]. Likewise, there is evidence that METTL5 methylates 18S rRNA. By deleting METTL5, the pluripotency of mouse embryonic stem cells (mESCs) is lost, and germ layer specification is impaired. Mechanistically, METTL5-deposited m 6 A promotes the translation of FBXW7, which plays a significant role in regulating cell differentiation. The absence of METTL5 delays the onset of mESC differentiation by inducing abnormal translation of FBXW7 and accumulation of its substrate, c-MYC [ 77 ]. All these studies indicate that m 6 A modification in mammals regulates germ cell differentiation by balancing the overall levels of m 6 A regulators, providing new insight into the functions and regulatory mechanisms of oocyte development. In addition to being involved in the regulation of female germ cell development and embryonic development, the growth of the foetus has been shown to be affected by the m 6 A demethylase FTO. Placenta from newborns with a large head circumference or heavy birth weight is reported to express higher levels of the m 6 A demethylase FTO. This is consistent with the research about birth weight mentioned below, which showed that samples from heavy-for-date newborns had conspicuously reduced methylation. Maternal parity influences the expression level of the FTO gene in the human term placenta and its association with foetal and placental weights. In comparison to appropriate-for-date children, both the small birth weight and heavy birth weight groups showed high levels of m 6 A modifications at the 5'UTR but lower levels near stop codons [ 78 , 79 ]. In low-birth-weight placentas of pigs with maternal obesity, FTO protein levels and m 6 A modification of FTO mRNA are higher. In addition, in low-birth-weight foetuses, genes related to lipid metabolism and angiogenesis are expressed differently than in normal foetuses. It is thought that increased m 6 A modification may play a role in regulating the expression of key genes in the low-birth-weight placenta [ 80 ]. Although the exact mechanism by which FTO impacts the head size of the foetus remains unclear, we presume that FTO may regulate foetal growth by m 6 A methylation [ 81 ]. Previous studies have shown that DNA methylation may be involved in the development of metabolic diseases in offspring through complex epigenetic effects. In a study of the risk of developing obesity in rodent offspring, scientists found that the expression of METTL3 and FTO genes was higher in the offspring of parents who ate a low-fat diet despite hypothalamic m 6 A modification levels being reduced. Notably, a ubiquitously expressed transcriptional coactivator, CREBBP, has elevated m 6 A modifications and increased mRNA expression in the offspring hypothalamus. CREBBP is known to be involved in the regulation of the body's nutritional status and energy balance by the hypothalamus. Therefore, it is possible to understand why low-fat parental diets result in a higher level of weight and insulin resistance in their offspring [ 82 ]. Table 1 summarizes the physiological functions of m 6 A RNA methylation in the female reproductive system. Table 1 The physiological function of m6A RNA methylation in female reproductive system Physiological function m 6 A regulator Type Mechanism References Germ cell development YTHDC1 Reader Change 3'UTR length by extensive alternative polyadenylation [ 57 ] YTHDC2 Reader Influence translation efficiency and stabilize its targets [ 37 ] YTHDF1 Reader Associated with self-renewal of female mouse germline stem cells [ 59 ] YTHDF2 Reader Post-transcriptionally regulate transcript degradation during mouse oocyte meiosis [ 60 ] METTL3 Writer Interact with Itsn2 to act on oocyte meiosis in an m 6 A-dependent manner and involved in producing first polar bodies and normal spindles [ 61 , 62 ] IGF2BP2/IGF2BP3 Reader Stabilize maternal mRNAs involved in DNA repair and meiosis during oogenesis [ 61 ] Embryo development METTL3 Writer Associated with the expression of naïve pluripotency transcripts [ 73 ] IGF2BP3 Reader Deficiency speeds up the degradation of maternal RNA [ 74 ] IGF2BP2 Reader Strengthen the ability of embryos to develop into blastocysts [ 75 ] METTL5 Writer Improve pluripotency of mouse embryonic stem cells and promote germ layer specification [ 77 ] Foetal growth FTO Eraser Regulate the genes that control nutrient metabolism [ 79 , 82 ] The physiological function of m6A RNA methylation in female reproductive system

Other

Based on the deepening of m 6 A modifications and transcriptome-wide mapping approaches, other posttranscriptional modifications of RNAs have also received attention, including N 1 -methyladenosine (m 1 A), 5-methylcytidine (m 5 C), N 7 -methylguanosine (m 7 G), and pseudouridine (Ψ) [ 140 – 142 ]. Although research on these chemical modifications is not as intensive as that on m 6 A, the role of these chemical modifications in female reproductive disorders deserves attention and has great therapeutic potential. m 5 C is a conserved and common RNA modification. It is primarily found in eukaryotic tRNAs and rRNAs [ 143 ]. In an animal experiment, deletion of the m 5 C methyltransferase Nsun5 resulted in suppression of ovarian function and embryonic development arrest in mice [ 144 ]. In several bioinformatics studies on ovarian and endometrial cancers, m 5 C-related genes were closely associated with tumour chemotherapy sensitivity and overall survival [ 145 – 147 ]. In addition, abnormal m 5 C modification may be involved in TRDMT1-mediated granulosa cell death, which in turn causes premature ovarian failure [ 148 ]. Another study in Drosophila confirmed that YPS promotes the proliferation and differentiation of germinal stem cells in the Drosophila ovary by binding RNA containing m 5 C modifications [ 149 ]. However, the role of m 5 C in human ovarian function remains to be further investigated. m 1 A and m 7 G modifications are also present in eukaryotic mRNAs [ 150 ]. m 1 A modifications may produce their biological effects by enhancing RNA‒protein interactions or by altering RNA secondary structures [ 151 ]. m 7 G modification is usually catalysed by METTL1 and located at the 5’ caps and internal positions of eukaryotic mRNA [ 152 ]. Several studies on endometrial cancer have found that m 1 A- and m 7 G-related lncRNAs and miRNAs can be used to construct tumour-related prognostic models and are associated with different immune infiltration phenotypes and drug susceptibility in endometrial cancer [ 153 – 156 ]. Pseudouridine is the most abundant modified nucleotide in RNA [ 157 ]. In a study on ovarian cancer, a pseudouridine synthase, PUS7, was considered a potential diagnostic marker for ovarian cancer [ 158 ].

Background

As a result of the growing interest in understanding how DNA and RNA modifications function, epigenomics has become a cutting-edge field [ 1 ]. Scientists have identified numerous layers of epigenetic modulation that are derived from the modification of DNA and proteins; however, RNA modification remains elusive [ 2 ]. Over 160 RNA chemical modifications have been discovered thus far [ 3 ]. The multitude of RNA modifications has added a new level of complexity to gene regulation. In eukaryotic mRNA, m 6 A RNA modification is the most abundant modification, which is defined as the methylation of adenosine 6 positions in mRNA and some noncoding RNA. N 6 -methyladenosine has been proven to be connected with various metabolic and physiologic processes, such as RNA transcript splicing, translation efficiency, nuclear export, stability, and decay [ 4 ]. m 6 A shares the same base pairing with unmodified adenosine, which prevents it from being detected by conventional sequencing or hybridization methods. A mystery surrounded the transcriptome distribution of m 6 A until a combination of m 6 A-specific methylated RNA immunoprecipitation and next-generation sequencing was devised. By employing these methods, scientists were able to determine that m 6 A residues were located in evolutionarily conserved regions within humans and mice. m 6 A residues were found to be contained primarily within internal mRNA sequences and appeared in the poly A tail, especially in the 3'UTR of mRNAs near the stop codon, and they always share a consensus motif of RRACH (R = A/G, H = A/C/U), and a terminal U is dominant part of the consensus [ 5 – 8 ]. The process of RNA methylation is controlled by methyltransferases, demethylases, and recognition factors. A methyltransferase and a demethylase catalyse the methylation of RNA dynamically, and the m 6 A function is determined by its recognition factor. Regulators may also be referred to as ''writers'', ''erasers'', and ''readers''. Although these regulators have been identified, the specific function of this process has not been well established. Cell types and environmental conditions may affect the expression level and biological function of m 6 A effectors. Furthermore, these factors can also be influenced by RNA species, abundances, secondary structures, intracellular location, translation state, and other heterogeneous factors. Taking these factors into account, it may be difficult to explain the exact function of m 6 A [ 9 ]. The normal physiological functions of the female reproductive system depend on the gonadal axis of the reproductive endocrine system, which regulates ovulation and the menstrual cycle. The maintenance of normal pregnancy depends on the establishment of endometrial receptivity, normal embryogenesis, and the formation of an immune microenvironment at the maternal-foetal interface. Several studies have shown that m 6 A modification is related to the regulation of physiological functions of the female reproductive system [ 10 ]. For example, by controlling the translation of Pgr mRNA through m 6 A modification, METTL3 is crucial for efficient P4 signaling during embryogenesis. m 6 A‑RNA immunoprecipitation‑qPCR showed that Pgr mRNA transcript was a target for METTL3-dependent m 6 A mRNA methylation [ 11 ]. In the process of ovarian aging, researchers found that the ovarian aging can be alleviated by up-regulating the FTO level in ovarian granulosa cells to reduce the m 6 A level of FOS-mRNA-3′UTR [ 12 ].However, the subtle mechanism of m 6 A modification involved in the physiological function of the female reproductive system remains to be elucidated. Common disorders of the female reproductive system include benign diseases, such as inflammatory diseases of the reproductive organs, infertility, endometriosis, and polycystic ovarian syndrome; complications of pregnancy, such as miscarriage, preeclampsia, and gestational diabetes mellitus; and some malignant diseases, such as cervical cancer, endometrial cancer, and ovarian cancer. In recent years, it has been found that epigenetic abnormalities may be associated with the development of several female reproductive disorders. For example, epigenetic modifications such as DNA methylation, histone methylation and acetylation and long noncoding RNAs are involved in regulating follicular granulosa cell proliferation, endometrial receptivity and decidualization in early pregnancy, which affect ovulation, embryo implantation, and labour initiation [ 13 ]. Abnormalities in these epigenetic modifications may be associated with polycystic ovary syndrome, infertility due to repeated embryo implantation failure, and pregnancy complications. Some patients with endometriosis may be born with congenital epigenetic molecular abnormalities, and the recurrent bleeding and repair processes of endometriosis lesions may also trigger acquired epigenetic events [ 14 ]. In addition, some chemical toxicants, such as Bisphenol A (BPA), can affect ovarian function, embryonic development, and gamete quality during fertilization through epigenetic modifications such as CpG island methylation, histone modifications, and noncoding RNA production [ 15 ]. The function of epigenetic modification in the female reproductive system has received increasing attention over the last few years. Despite this, research on m 6 A modification and the female reproductive system is still in its infancy. A comprehensive review of recent research advances in m 6 A modification and its roles in pathogenesis, diagnosis, and molecular targeted therapies for gynaecological reproductive disease is presented in this paper. We discuss the potential directions of m 6 A modification for future research in obstetrical and gynaecological disorders, aiming to clarify the role played by RNA methylation in female reproductive system diseases and malignant tumours. In doing so, we can gain a novel perspective on these diseases.

Conclusion

The actions of m 6 A modification have gradually become apparent in recent years as high-throughput sequencing technologies and highly specific antibodies against m 6 A have been developed. In the field of m 6 A RNA methylation, great progress has been made in revealing potential mechanisms of the onset and progression of female reproductive system disorders. Differentially expressed m 6 A regulator genes are found in a large number of gynaecological cells compared to normal cells and serve as triggers in gynaecological disease progression. Additionally, imbalanced RNA m 6 A has also been identified in these diseases. To clarify the molecular mechanisms underlying certain refractory obstetrics and gynaecology diseases, such as endometriosis and preeclampsia, abnormal RNA m 6 A modification is an important research direction. Various female reproductive cancers are known to be affected by m 6 A modification and its regulators. Crystal structure data, for example, have provided insight into cancer-associated mutations in METTL14. Mutations in METTL14 that cause an inefficient RNA-binding domain are found in endometrial cancers, and the mutated form of the enzyme shows partially reduced activity. It has also been found that m 6 A mRNA methylation modulates AKT activity, which is necessary for endometrial cancer proliferation and tumorigenicity [ 126 ]. By binding to a locus of the MYC gene, IGF2BP2 enhances the proliferation, metastasis, and aerobic glycolysis of cervical cancer cells [ 173 ]. These findings indicate that the role of m 6 A regulators in female reproductive organs is different based on cell type, therapeutic issues, and pathological conditions. Clinical diagnostics and therapeutics can also target m 6 A regulators in disorders of the female reproductive system. The oncogenic mechanism of mRNA m 6 A modification in gynaecologic malignant tumorigenesis may become a direction for future research. m 6 A regulators and their upstream and downstream signalling pathways may provide certain methods to elucidate the pathophysiological mechanisms of gynaecologic malignant tumours and establish prognostic models. Modification of pharmacogene mRNAs may alter their pharmacokinetics and pharmacodynamics, thus affecting drug efficacy. In future studies, not only do the pathophysiological mechanisms of female reproductive system diseases in which m 6 A is involved deserve attention but also the m 6 A modifications occurring in the pharmacodynamic gene targets corresponding to drugs need to be considered. For the successful design of tissue- or cell-specific RNA methylation agonists or inhibitors, more multicentre and large-scale studies are needed. Many essential issues must be addressed in a detailed manner. A very limited number of cell and animal models are used in all cited papers, and the results are hence subject to variation. First, although METTL4, FTO, and ALKBH5 are commonly known and well-studied m 6 A regulatory factors, the role of less studied m 6 A regulatory factors, such as RBM15/15B and ZC3H13, may only be the tip of the iceberg. Further research is needed on the interactions between RNA modification regulators and their downstream targets in the female reproductive system. Second, the reproductive-endocrine system plays a pivotal role in the progression of gynaecological diseases. Research currently focuses on the influence of m 6 A on cellular behaviour. The interplay between the hormonal milieu and endocrine system related to m 6 A modification remains a mystery and should be addressed in the future. Finally, the majority of published studies have concentrated only on the molecular mechanism of m 6 A modification. A greater focus should be placed on the diagnostic and therapeutic properties of m 6 A. According to a large body of evidence, m 6 A modifications are related to clinical phenotypes and prognoses. m 6 A is involved in the common pathological features shared by benign and malignant diseases of the female reproductive system, and different m 6 A phenotypes in these diseases may be involved in the transformation between benign and malignant diseases and between different pathological types in the same disease. Compared with other reviews in this field, our article provides a more comprehensive overview of the relationship between m 6 A and the physiology and pathology of the female reproductive system. Whether it is germ cell genesis, embryonic development or benign and malignant diseases of the female reproductive system, we searched for appropriate literature to address them. In particular, we briefly outlined other RNA modifications. The connection between these RNA modifications and m 6 A modifications may become a new direction in future studies. In addition, we look forward to the involvement of m 6 A modifications in the diagnosis and treatment of female reproductive system diseases. m 6 A modifications deserve to be noticed for their clinical applications in female reproductive system diseases. Undoubtedly, the pathogenesis of female reproductive system diseases is quite complex, and changes in the levels of m 6 A regulators dynamically regulate the level of m 6 A modifications in the female reproductive system, altering the abundance and function of related mRNAs and proteins and ultimately determining the onset of disease. However, the application of m 6 A regulators to clinical diagnosis and treatment requires improving the sensitivity and specificity of the relevant biomarkers. RNA m 6 A modification can likely be used to classify clinical phenotypes of several female reproductive disorders and to predict the mutual transformation of these disorders.

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Condition tags

endometriosisadenomyosis

MeSH descriptors

Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous Abortion, Spontaneous

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