The Role and Clinical Significance of N6‑Methyladenosine

Methylation in Ovarian Cancer: Research Progress and Future

Prospects

Xuanyi Dai

Tianjin Farragut School, Tianjin, China

Keywords: N6‑methyladenosine (m6A), Ovarian Cancer, Progress, Future.

Abstract: Ovarian cancer (OC), often diagnosed late due to asymptomatic early stages, remains highly lethal despite

treatment advances. N6-methyladenosine (m6A) RNA methylation, regulated by writers, erasers, and readers,

plays a key role in OC progression, metastasis, and chemoresistance by modulating RNA stability and

translation. Dysregulated m6A modifications influence oncogenic pathways like PI3K/AKT and EMT, while

m6A-related proteins serve as diagnostic and prognostic biomarkers. Preclinical studies highlight the

therapeutic potential of targeting m6A regulators, though challenges like tumor heterogeneity hinder clinical

translation. Future research should clarify m6A's roles, develop diagnostics, and advance m6A-targeted

therapies. m6A methylation offers promising avenues for improving OC diagnosis, prognosis, and treatment.

1 INTRODUCTION

Among malignancies affecting the female

reproductive system, ovarian cancer (OC) is highly

prevalent, standing as the 18th most frequently

occurring cancer and the 14th leading cause of

cancer-related deaths (Stewart et al. 2019). Of all

the organs in the body, the ovary has the greatest

range of primary tumor types, and the composition

of ovarian tumor tissue is extremely complicated.

The biological behavior and histological structure

of various ovarian cancer types differ noticeably.

Sex cord-stromal tumors, germ cell tumors, and

epithelial ovarian cancer (EOC) are the three main

histological categories of OC (Siegel et al. 2023).

EOC is the most prevalent of these, making up

between 50% and 70% of all cases. EOC is further

subdivided into serous (52%), endometrioid (10%),

mucinous (6%), clear cell (6%), and other kinds

according to histological features. [3]. Most

patients are diagnosed at an advanced stage, which

leads to a dismal prognosis because of the disease's

subtle early signs and the absence of efficient

screening techniques. Common symptoms include

abdominal distension, abdominal pain, indigestion,

and frequent urination, but these symptoms are

often misdiagnosed as gastrointestinal disorders.

Diagnosis mainly relies on imaging examinations

(such as ultrasound, CT/MRI), tumor markers (such

as CA-125), and pathological examinations.

Treatment methods include surgery, chemotherapy,

targeted therapy, and immunotherapy. However,

the recurrence rate is high in advanced patients, and

the 5-year survival rate remains low.

Post-synthetic chemical modifications of DNA,

RNA, and proteins regulate gene expression and

cellular functions at the transcriptional, post-

transcriptional, and post-translational levels,

respectively. Specifically, DNA modifications

primarily affect the transcriptional level, RNA

modifications act at the post-transcriptional level,

and protein modifications regulate post-

translational processes. Among these, one of the

core mechanisms of post-transcriptional regulation

is RNA modification and its interaction with non-

coding RNAs (ncRNAs), commonly referred to

epitranscriptomics. More than 100 post-synthetic

RNA modifications have been discovered in the last

half-century, and they are present in almost all

known RNAs, with transfer RNA (tRNA) and

ribosomal RNA (rRNA) containing the great bulk

of these modifications (Sun et al. 2019). According

to recent research, RNA alterations have a

significant impact on a variety of molecular

processes, including splicing, translation, stability,

and RNA metabolism, which in turn affects gene

374

Dai, X.

The Role and Clinical Signiﬁcance of N6-Methyladenosine Methylation in Ovarian Cancer: Research Progress and Future Prospects.

DOI: 10.5220/0014493600004933

Paper published under CC license (CC BY-NC-ND 4.0)

In Proceedings of the 1st Inter national Conference on Biomedical Engineering and Food Science (BEFS 2025), pages 374-379

ISBN: 978-989-758-789-4

expression and cellular functioning. RNA

modifications predominantly consist of methylation

modifications, which represent both the most

prevalent and thoroughly investigated class.

Eukaryotic RNAs predominantly feature four major

internal methylation modifications: N6-

methyladenosine (m6A), 5-methylcytosine (m5C),

7-methylguanosine (m7G), and N1-

methyladenosine (m1A). Of these, m6A represents

the predominant internal modification found in

messenger RNA molecules (mRNA) and one of the

most widely studied RNA modifications (Sun et al.

2019). m6A modification is achieved through

methylation of the adenosine nitrogen at position 6,

a process catalyzed by methyltransferases and

reversible by demethylases, forming a dynamic and

reversible regulatory network. m6A modification

has multiple functions in RNA metabolism. It can

regulate RNA stability, splicing, nuclear export,

translation efficiency, and degradation processes,

thereby profoundly influencing gene expression.

Additionally, m6A modification plays a critical role

in various biological processes, particularly in

cancer-related mechanisms.

2 THE MECHANISMS OF M6A

METHYLATION

MODIFICATION

N6-methyladenosine (m6A) constitutes a

predominant RNA modification in eukaryotes,

occurring extensively across diverse RNA species

including messenger RNA (mRNA), long non-coding

RNA (lncRNA), ribosomal RNA (rRNA), and

microRNA (miRNA) (Zhang et al. 2020). m6A

modification is achieved by adding a methyl group (-

CH3) to the nitrogen atom at the sixth position of

adenosine (A). This process is dynamically regulated

by three types of regulatory factors: writers, erasers,

and readers, which play a critical role in RNA

metabolism and function (Fang et al. 2022). Writers

are a group of methyltransferase complexes, with

core components including METTL3 (the main

catalytic enzyme), METTL14 (assisting in substrate

RNA recognition), WTAP (localizing the complex to

nuclear speckles), VIRMA (guiding the complex to

specific RNA regions), and RBM15 and ZC3H13

(regulating the stability and specificity of the

complex) (Yang et al. 2023). Together, they

recognize specific RNA sequences (such as RRACH)

and catalyze methylation reactions. Erasers are a

group of demethylases, primarily including FTO and

ALKBH5, which remove methyl groups through

oxidation reactions, making the m6A modification

process reversible and thereby regulating mRNA

stability, translation efficiency, and nuclear-

cytoplasmic transport. Readers are a class of proteins

that recognize and bind to m6A modifications,

including the YTH domain protein family (e.g.,

YTHDF1 promotes translation, YTHDF2 mediates

degradation, YTHDC1 regulates splicing and

nuclear-cytoplasmic transport), the IGF2BP family

(enhancing mRNA stability and translation

efficiency), and the HNRNP family (regulating pre-

mRNA processing and miRNA processing). These

readers mediate the functions of m6A modifications,

regulating RNA metabolic processes such as RNA

stability, splicing, translation efficiency, nuclear-

cytoplasmic transport, and the functions of non-

coding RNAs (Yang et al. 2023).

Through this dynamic and reversible regulatory

network, m6A modifications play a key role in gene

expression, cellular functions, and various

biological processes. They regulate stem cell

differentiation and embryonic development during

development and differentiation, influence immune

cell activation and function in immune responses,

and modulate malignant cell growth, migration,

invasion, and chemoresistance in cancer (Zhao et al.

2020). For example, in ovarian cancer, the

abnormal expression of writers such as METTL3,

WTAP, and VIRMA, as well as erasers such as FTO

and ALKBH5, is closely related to tumorigenesis

and prognosis. METTL3 demonstrates promoter

hypomethylation and upregulated expression in

OC, with extensive evidence supporting its

oncogenic role in disease pathogenesis. Low

expression of FTO and ALKBH5 is associated with

shorter overall

survival and progression-free

survival (PFS) in patients. Additionally, readers

such as YTHDF1, IGF2BP1, and HNRNPA2B1

regulate RNA metabolism, affecting cancer cell

proliferation, invasion, and chemoresistance.

YTHDF1 and YTHDF2 show elevated expression

in ovarian cancer with potential prognostic value.

IGF2BP1 promotes invasion by counteracting

miRNA-mediated gene suppression, while

HNRNPA2B1 enhances malignancy through

Lin28B upregulation (Zhu et al. 2022).

The Role and Clinical Signiﬁcance of N6-Methyladenosine Methylation in Ovarian Cancer: Research Progress and Future Prospects

375

3 THE ROLES OF m6A

METHYLATION IN OVARIAN

CANCER

3.1 m6A RNA Modification

Modulating mRNA to Influence the

Progression of Ovarian Cancer

Elevated expression levels of METTL3 demonstrate

a significant and independent correlation with

diminished survival outcomes and enhanced

malignant characteristics in endometrioid epithelial

ovarian cancer (EEOC) patients. Experimental

evidence reveals that targeted suppression of

METTL3 through knockdown methodologies

effectively curbs cellular proliferation and migratory

capacity while simultaneously inducing programmed

cell death (apoptosis) in both CRL-11731D and TOV-

112D ovarian cancer cell models (Fan et al. 2020).

Notably, the observed phenotypic alterations

following METTL3 depletion exhibit substantially

greater magnitude than those resulting from

comparable knockdown interventions targeting either

WTAP or METTL14 proteins. At the molecular level,

experimental reduction of METTL3 expression leads

to a significant decrease in m6A methylation patterns

specifically within ovarian cancer-associated genes

including CSF-1, AXL, EIF3C, and FZD10, thereby

demonstrating that the m6A modification profile

mediated by METTL3 exhibits unique characteristics

that differentiate it from those modifications

catalyzed by either WTAP or METTL14 (Zhang et al.

2021). Furthermore, in the COV362 ovarian cancer

cell line model, genetic silencing of METTL3

expression results in a pronounced accumulation of

cells in the G0/G1 phase of the cell cycle

accompanied by a marked increase in cellular

mortality through apoptotic pathways. In vivo

investigations employing METTL3 conditional

knockout (cKO) murine models demonstrate

enhanced ovarian cancer cell proliferation concurrent

with altered macrophage polarization from the pro-

inflammatory M1 phenotype to the tumor-promoting

M2 phenotype, collectively indicative of accelerated

neoplastic progression. Therapeutically, sulforaphene

(Sul) reverses METTL3 overexpression, reducing OC

cell viability and promoting apoptosis via the

FAS/FADD and Bax/Bcl-2 pathways (Zhang et al.

2021). METTL14 exhibits a dual role in OC.

Molecular analyses reveal context-dependent roles

for RNA methylation regulators in epithelial ovarian

cancer (EOC). In specific tumor subsets, METTL14

demonstrates reduced expression accompanied by

decreased global m6A levels relative to normal

ovarian tissues, where it exhibits tumor suppressive

activity through m6A-mediated downregulation of

TROAP expression, thereby inhibiting EOC cell

proliferation. Paradoxically, distinct EOC

populations display METTL14 overexpression,

which functionally promotes malignant behaviors

including enhanced proliferation, migration and

invasion in A2780 and SKOV3 cellular models.

Similarly, ALKBH5 shows consistent overexpression

in ovarian carcinoma specimens, where it drives

aggressive tumor phenotypes via TLR4/NF-κB

pathway-mediated transcriptional activation of the

stemness factor NANOG. Hypoxia-inducible factor

(HIF)-1α induces ALKBH5 expression, which

stabilizes RMRP and promotes OC growth and

migration (Zhang et al. 2021).

Additionally, ALKBH5 suppression in SKOV3

cells enhances autophagy and inhibits proliferation

and invasion by modulating the EGFR-PIK3CA-

AKT-mTOR axis. FTO expression is decreased in

OC and OC stem cells (OCSCs). Overexpression of

FTO inhibits OCSC self-renewal and tumorigenesis

by demethylating PDE4B and PDE1C, leading to

cAMP accumulation. The RNA demethylase FTO

demonstrates additional tumor-suppressive effects

in ovarian cancer through induction of reactive

oxygen species accumulation and programmed cell

death pathways, ultimately inhibiting xenograft

tumor growth in immunocompromised murine

models. Concurrently, the m6A reader protein

YTHDF1 exhibits significant upregulation in

ovarian carcinomas and shows strong clinical

correlation with adverse patient outcomes.

Mechanistically, YTHDF1 facilitates

malignant

progression by selectively enhancing the

translational efficiency of EIF3C through

recognition of m6A-modified EIF3C transcripts

(Han et al. 2020). Similarly, elevated expression of

IGF2BP2 promotes multiple oncogenic phenotypes

including tumor expansion, migratory capacity and

invasive potential via its m6A-dependent regulation

of CKAP2L protein synthesis. YTHDC1 is

downregulated in OC, and its overexpression

inhibits OC development by stabilizing PIK3R1

and downregulating GANAB via the STAT3

pathway.

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3.2 m6A RNA Modification

Modulating Non-Coding RNA to

Influence the Progression of

Ovarian Cancer

Non-coding RNAs (ncRNAs) are broadly categorized

into housekeeping ncRNAs (rRNA, tRNA, snRNA)

and regulatory ncRNAs (miRNA, circRNA, lncRNA).

m6A modification critically regulates ncRNA

metabolism by controlling RNA stability, splicing

processes, and degradation rates. METTL3 promotes

OC progression by targeting miR-1246, leading to the

suppression of CCNG2. It also enhances miR-126-5p

maturation via m6A methylation, activating the

PI3K/Akt/mTOR pathway by targeting PTEN. m6A

writer METTL3 mediates RHPN1-AS1 stabilization

to trap miR-596 and stimulate FAK/PI3K/Akt

signaling (Tan et al. 2023). The METTL3-IGF2BP1

axis maintains circASXL1 stability through m6A

modification, driving ovarian cancer development by

modulating the miR-320/RACGAP1 pathway. In

EOC, reduced METTL16 expression promotes

MALAT1 decay and blocks β-catenin nuclear

translocation, inhibiting tumorigenesis. WTAP is

upregulated under hypoxia and promotes OC

proliferation and invasion by modulating miR-200

expression in an m6A-dependent manner. YTHDF2 is

upregulated in EOC and inversely correlated with

miR-145 levels. It enhances EOC growth and

migration by reducing the level of m6A mRNA.

CACNA1G-AS1 promotes OC growth and migration

by upregulating FTH1 via the IGF2BP1 axis,

inhibiting ferroptosis. UBA6-AS1 inhibits OC growth

and invasion by enhancing UBA6 mRNA stability via

RBM15-mediated m6A modification. MEG3, which

is downregulated in OC, inhibits VASH1 degradation

by suppressing miR-885-5p. YTHDF2 promotes

MEG3 RNA decay in a METTL3-dependent manner.

circRAB11FIP1 promotes OC progression by

sponging miR-129 and regulating ATG14 and ATG7

expression in an FTO-dependent m6A modification

manner (Tan et al. 2023).

4 THE CLINICAL

SIGNIFICANCE OF m6A

METHYLATION IN OVARIAN

CANCER

Ovarian cancer continues to pose significant

diagnostic and therapeutic challenges in clinical

oncology. Current treatment modalities, including

surgical intervention and cytotoxic chemotherapy,

have shown limited efficacy in improving patient

outcomes, underscoring the urgent demand for novel

biomarkers and molecular targets. Recent studies

have identified

Epitranscriptomic alterations, especially m6A

RNA methylation, as pivotal gene expression

modulators that are increasingly investigated in

ovarian cancer studies (Zhu et al. 2022). Dysregulated

m6A modifications in OC tissues compared to normal

ovaries alter gene expression profiles, contributing to

ovarian tumorigenesis. These modifications influence

key oncogenic pathways, including PI3K/AKT,

Wnt/β-catenin, and EMT (epithelial-mesenchymal

transition), promoting tumor growth, invasion, and

metastasis. Additionally, m6A methylation

modulates the expression of oncogenes (MYC,

EGFR) and tumor suppressors (PTEN), driving

cancer progression. Furthermore, m6A modifications

play a role in maintaining cancer stem cells (CSCs),

which are associated with tumor initiation, drug

resistance, and recurrence. m6A-altered RNA

molecules in blood/tissue demonstrate potential as

minimally invasive OC diagnostic markers (Zhu et al.

2022). Early detection of these modifications could

improve patient outcomes through timely

intervention. Abnormal expression of m6A-related

proteins (FTO, METTL14, METTL3, ALKBH5) in

OC tissues compared to normal ovaries provides

potential diagnostic markers. Increased expression of

m6A methyltransferases (METTL14, METTL3)

correlates with higher tumor grades, lymphatic

spread, and unfavorable clinical outcomes, while

decreased levels of demethylases (FTO) are linked to

better patient survival. Additionally, high expression

of KIAA1429 and YTHDC2 is associated with poorer

prognoses, while IGF2BP1 enhances invasive growth

and is linked to unfavorable outcomes. m6A

modifications also regulate miRNAs (miR-145, miR-

126-5p) and lncRNAs, influencing OC cell

proliferation, apoptosis, and migration (Tan et al.

2023).

Pharmacological agents directed against m6A

regulatory machinery (METTL3, FTO, ALKBH5)

demonstrate therapeutic potential in experimental

models, effectively suppressing ovarian cancer cell

growth, motility and metastatic capacity. These

RNA epigenetic alterations additionally modulate

chemotherapeutic sensitivity to platinum-based

agents and PARP inhibitors. Notably, YTHDF1

binding to m6A-marked TRIM29 enhances protein

synthesis in platinum-resistant ovarian cancer cells,

The Role and Clinical Signiﬁcance of N6-Methyladenosine Methylation in Ovarian Cancer: Research Progress and Future Prospects

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underscoring its clinical relevance, whereas FZD10

m6A methylation mediates PARP inhibitor

responsiveness (Han et al. 2020). Modulating m6A

levels can enhance OC cell sensitivity to existing

therapies, offering new avenues for combination

treatments. Additionally, m6A modifications

modulate the tumor microenvironment and immune

response, suggesting potential synergies with

immunotherapy (Fan et al. 2020). m6A methylation

affects mRNA stability, translation efficiency, and

degradation, influencing key signaling pathways in

OC. It also regulates the function of miRNAs and

lncRNAs, which play critical roles in OC

progression and metastasis. Furthermore, m6A

modifications interact with other epigenetic

mechanisms, contributing to the complexity of OC

biology. Detection of m6A-modified RNAs in

circulating tumor cells or exosomes offers a non-

invasive method for OC diagnosis and monitoring

(Tan et al. 2023). Understanding the m6A landscape

in individual tumors could guide the development

of personalized therapeutic strategies. Ongoing

research aims to translate m6A-targeted therapies

into clinical practice, with promising results in

preclinical models.

5 CONCLUSION

The research on m6A RNA methylation has revealed

its critical role in the occurrence, progression,

metastasis, and therapeutic resistance of ovarian

cancer (OC). The dynamic regulation of m6A

modifications by writers, erasers, and readers

influences gene expression, offering new

opportunities for the diagnosis, prognosis, and

treatment of ovarian cancer. However, challenges

such as tumor heterogeneity, contradictory findings,

and methodological limitations still need to be

addressed. m6A modifications affect the occurrence,

progression, and drug resistance of ovarian cancer by

regulating the stability, translation, and degradation

of mRNA and non-coding RNA (ncRNA). m6A-

related genes (METTL3, FTO, YTHDF1) exhibit

significant expression abnormalities in ovarian

cancer and are closely associated with tumor

progression, metastasis, and patient prognosis. m6A

modifications promote the progression and

chemoresistance of ovarian cancer by regulating key

signaling pathways (PI3K/AKT, Wnt/β -catenin) and

epithelial-mesenchymal transition (EMT). m6A-

modified RNA transcripts and related regulatory

proteins (METTL3, FTO, YTHDF1) can serve as

early diagnostic and prognostic markers for ovarian

cancer. High expression of m6A writers (METTL3,

METTL14) is associated with poor prognosis, while

low expression of erasers (FTO) is linked to better

survival rates. Small molecule inhibitors targeting

m6A regulators (METTL3, FTO, ALKBH5) have

shown potential in preclinical studies to suppress

tumor growth and overcome chemoresistance. m6A

modifications influence treatment response by

regulating chemoresistance-related pathways, such as

the FTO-mediated RP5-991G20.1/hsa-miR-

1976/MEIS1 axis.

Tumor heterogeneity and the diversity of m6A

modifications complicate the development of

universal diagnostic and therapeutic strategies.

Contradictory findings regarding certain m6A

regulators (FTO, ALKBH5, METTL14) in different

studies require further validation. The lack of

standardized methods for detecting m6A

modifications hinders clinical translation.

Developing high-throughput, standardized

techniques for detecting m6A modifications will

promote research reproducibility and clinical

application. Integrating multi-omics data (genomics,

transcriptomics, proteomics) can provide a

comprehensive understanding of the role of m6A

modifications in ovarian cancer. In-depth research is

needed to elucidate the specific roles of m6A

modifications in different ovarian cancer subtypes

and clarify their functions in various molecular

contexts. Developing novel inhibitors targeting m6A

regulators (METTL3, FTO, ALKBH5) and

evaluating their efficacy in preclinical and clinical

trials is essential. Exploring the mechanisms by

which m6A modifications contribute to

chemoresistance and developing strategies to reverse

resistance, such as targeting YTHDF1 or FTO, is

crucial. Investigating the interactions between m6A

modifications and other molecular pathways

(immune checkpoints, DNA repair pathways) can

lead to the development of synergistic treatment

strategies.

Using m6A modification profiles to guide

personalized treatment and tailoring therapies based

on patients' molecular characteristics is a promising

approach. Developing liquid biopsy techniques to

detect m6A-modified RNA in circulating tumor cells

(CTCs) or exosomes enables non-invasive diagnosis

and dynamic monitoring. Studying the interactions

between m6A modifications, DNA methylation, and

histone modifications can reveal their synergistic

regulatory mechanisms in ovarian cancer. Exploring

the regulatory effects of histone modifications on

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m6A modifications, such as H3K27me3 influencing

m6A levels by regulating METTL14 expression, is

also important. Advancing clinical trials of m6A-

targeted therapies to evaluate their safety and efficacy

in ovarian cancer patients is critical. Combining

epigenetic therapies (DNMT inhibitors, HDAC

inhibitors) with m6A-targeted therapies offers

potential for combination treatments. The role of

m6A methylation in ovarian cancer is increasingly

recognized, and its potential in diagnosis, prognosis,

and treatment provides new hope for improving

patient outcomes. Despite challenges such as tumor

heterogeneity, contradictory findings, and

methodological limitations, the advancement of

standardized techniques, mechanistic research, and

clinical trials holds promise for establishing m6A

modifications as a key target for precision therapy in

ovarian cancer. Future research should focus on

elucidating the molecular mechanisms of m6A

modifications, developing novel targeted drugs, and

exploring their synergistic effects with other

epigenetic modifications, thereby providing more

effective treatment strategies for ovarian cancer

patients.

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