N6-methyladenosine Modifications in Cervical Cancer:

The Molecular and Clinical Perspective

Ziqi Xu

Shanghai Experimental School International Division, Shanghai, China

Keywords: N6-methyladenosine, Cervical Cancer, Therapeutic Targeting.

Abstract: N6-methyladenosine (m6A) is closely associated with cervical cancer. m6A is responsible for the

stability, transport, and splicing of RNA, which regulates apoptosis, cell proliferation, RNA metabolism,

the tumor immune microenvironment, and metastasis. The m6A modification process is found in both

mRNA and non-coding RNAs (ncRNAs). A group of enzymes called writers, erasers, and readers are

involved in controlling m6A.These enzymes act as oncogene promoters in cervical cancer by upregulating

or downregulating oncogenes. m6A modifications hold future potential to be used as biomarkers. Several

drugs and inhibitors targeting m6A modulators have been discovered. This review explores the molecular

mechanisms of m6A modifications, as well as their perspectives and potentials.

1 INTRODUCTION

Cervical cancer (CC) ranks as one of the most

common cancers and leading cause of cancer-

related death among women, with approximately

660,000 new cases and 350,000 deaths reported

globally in 2022. One major contributing factor to

CC is the persistent infection with human

papillomavirus (HPV). Typically, it takes 15 to 20

years for cells to become abnormal and progress to

cervical cancer. Prevention strategies for CC

include vaccination between the ages of 9 and 14,

as well as cervical screening every 5 to 10 years

beginning at age 30. CC can be treated with radical

hysterectomy, radiotherapy, chemoradiation, or

excisional cone biopsy, depending on the disease's

stage. Epigenetics is a field of study that regulates

gene expression without altering the underlying

DNA sequence. One form of epigenetic

modification is RNA modification. N6-

methyladenosine (m6A) is a subtype of RNA

modification (Jiang et al. 2021). The most widely

accepted consensus sequence for m6A modification

is RRACH (where R = A or G, and H = A, C, or U).

m6A plays a crucial role in RNA stability, transport,

and splicing. The m6A modification process is

catalyzed by a set of enzymes categorized as

“writers” (e.g., METTL3, METTL14), “erasers”

(e.g., FTO, ALKBH5), and “readers” (e.g.,

YTHDF1, YTHDC1).

m6A is closely associated with cervical cancer.

Studies have shown that m6A regulatory factors are

abnormally overexpressed in cervical cancer (CC),

such as methyltransferase-like 13 (METTL3).

Additionally, m6A regulates key pathways

involved in cervical cancer, including immune

response, cell proliferation, and cancer cell

survival. One example is through modifying the

stability and translation of mRNAs that encode

immune checkpoint proteins (e.g., PD-1, PD-L1)

(Mao et al. 2023). Despite growing interest in the

field of m6A research and significant progress

made by scientists, the exact mechanisms and

functions of m6A remain poorly understood. In this

review, the biological processes and enzyme

functions involved in m6A modification are

elucidated. Next, the link between m6A and

cervical cancer is explored, including the role of

m6A dysregulation in cervical cancer (CC).

Moreover, the clinical relevance and therapeutic

potential of m6A are discussed, such as its use as a

biomarker and the potential for m6A modulation in

CC treatment. Finally, recent advances in m6A

research and future directions are examined.

Xu, Z.

N6-methyladenosine Modiﬁcations in Cervical Cancer: The Molecular and Clinical Perspective.

DOI: 10.5220/0014486600004933

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

In Proceedings of the 1st International Conference on Biomedical Engineering and Food Science (BEFS 2025), pages 281-286

ISBN: 978-989-758-789-4

281

2 ENZYMES INVOLVED IN M6A

RNA METHYLATION

There are three methyltransferase complexes (MTCs)

involved in the regulation of m6A modifications on

RNA: writers, erasers, and readers.

Writers promote methylation. Some key

enzymes include METTL3, METTL14, and WTAP.

Methyltransferase-like 3 (METTL3), the first

identified m6A methyltransferase, plays dual roles

as both an oncogene and a tumor suppressor in

cancer (Fang et al. 2022). METTL3 is involved in

numerous physiological processes, such as

embryonic and brain development (Jiang et al.

2021). METTL3 primarily functions together with

METTL14 as a heterodimeric complex. METTL14

aids METTL3 in identifying and interacting with

RNA substrates. WTAP guides the METTL3/14

heterodimer core complex into nuclear speckles via

a nuclear localization signal (Huang et al. 2022).

Erasers are demethylases that remove m6A

modifications from RNA (Jiang et al. 2021). The

two major erasers are FTO and ALKBH5. FTO

functions by adding a hydroxyl group (–OH) to the

N6 position, converting m6A to hm6A, f6A, and

ultimately to adenosine. This process requires

cofactors such as iron (Fe²⁺) and α-ketoglutarate (α-

KG) (Mao et al. 2023). FTO has been shown to

remove m6A modifications from the mRNA of

specific genes, thereby controlling the expression of

targets such as ASB2 and RARA. The second m6A

demethylase, ALKBH5, removes m6A marks from

PD-L1 mRNA, stabilizing the mRNA and

preventing its degradation (Fang et al. 2022).

ALKBH5 also modulates mRNA export, RNA

metabolism (Jiang et al. 2021), and the tumor

immune microenvironment (Fang et al. 2022). Like

METTL3, ALKBH5 can function as both an

oncogene and a tumor suppressor (Qu et al. 2022).

ALKBH5 is important for acquired immunity and

natural immunity. ALKBH5 demethylase gene

transcripts that encode for molecules of the natural

immune system, such as TRAF3 and TRAF6. Thus,

it affects viral infection and antiviral immune

responses. ALKBH5 removes the m6A

modifications on NR4A1 mRNA, increasing the

expression of NR4A1 protein. NR4A1 is required

for gut immunity and homeostasis of ILC3s.

Moreover, ALKBH5 regulates the function of

CD4+ T cells during induced neuroinflammation by

enhancing interferon-γ (IFN-γ) and C-X-C motif

chemokine ligand 2 (CXCL2) mRNA stability.

Therefore, there is an increased activation of CD4+

T cells, and more neutrophils to the central nervous

system (CNS) (Qu et al. 2022).

Readers are proteins that bind to and recognize

m6A-modified RNA molecules (Fang et al. 2022).

They control gene expression by influencing

various aspects of RNA metabolism, such as mRNA

stability and translation efficiency. Some examples

of readers include IGF2BP1 and YTHDC1/2 (Jiang

et al. 2021, Mao et al. 2023). IGF2BP1 is highly

expressed in tumor cells but downregulated in adult

tissues (Huang et al. 2021). One of its functions is

to stabilize specific mRNAs necessary for cell

proliferation and metastasis. YTHDC1/2 are

readers containing a YTH domain. They affect

cancer progression by regulating multiple genes

(Fang et al. 2022). YTHDC1 promotes the splicing

of m6A-modified RNA by interacting with splicing

factors to facilitate exon inclusion in target mRNAs

(Mao et al. 2023). The helicase domain of

YTHDC2, an RNA helicase, aids in RNA binding

and controls mRNA translation (Fang et al. 2022).

3 THE ROLE OF M6A

DYSREGULATION IN

CERVICAL CANCER

Studies have shown that METTL3, WTAP, FTO,

ALKBH5, IGF2BP1/2/3, and several other enzymes

act as oncogenic drivers in cervical cancer (Fang et

al. 2022). These enzymes promote tumor growth by

downregulating tumor suppressor genes or

upregulating oncogenes. For instance, METTL3 adds

m6A marks to FOXD2-AS1, thereby promoting the

progression of cervical cancer. FOXD2-AS1,

stabilized by m6A modification, inhibits the

expression of p21 (Gao et al. 2024). One study found

that METTL3 downregulates the expression of

RAGE in cervical cancer. RAGE signaling promotes

carcinogenesis by causing abnormal activation of cell

survival pathways, chronic inflammation, and

impaired cell communication. RAGE is also reported

to inhibit apoptosis in cervical cells (Li et al. 2021).

Abnormal expression of WTAP is closely associated

with cell cycle regulation, metabolic vulnerabilities,

and drug resistance, all of which may contribute to

cancer development. In a WTAP knockdown

experiment, reduced WTAP expression in

nasopharyngeal carcinoma (NPC) cells induced G1

phase cell cycle arrest and apoptosis. Convincing

evidence indicates that WTAP targets HK2 in

multiple cancer cell types. Induction of HK2 enables

aerobic glycolysis in tumor cells (Ju et al. 2023).

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FTO promotes the progression of cervical

cancer, as higher expression levels of FTO are

observed in late-stage patients (stages III and IV)

compared to early-stage patients (stages I and II)

and normal cervical tissues. Overexpression of FTO

enhances the migration and proliferation of cervical

cancer cells by targeting the translation of E2F1 and

Myc. Overexpression of E2F1 and Myc, in turn,

encourages cell division. ALKBH5 inhibits cell

apoptosis, increases the migration and invasion

capabilities of cervical cancer (CC) cells, promotes

cell division in HeLa and SiHa cells, and

encourages angiogenesis. ALKBH5 enhances the

expression of PAK5, a protein kinase linked to

chemoresistance and cancer aggressiveness.

Additionally, PAK5 is associated with HPV

infection. In a study where ALKBH5 was silenced,

ectopic expression of PAK5 partially restored the

inhibited malignant characteristics, thereby

promoting tumorigenesis and metastasis of cervical

cancer (Huo et al. 2023). IGF2BP2 interacts with

circARHGAP12 at exon 3. Overexpression of

IGF2BP2 may stabilize circARHGAP12 and

FOXM1 when binding to them. circARHGAP12 is

an unfavorable circular RNA for cervical cancer,

while FOXM1 is identified as a driver of

oncogenesis in this disease. circARHGAP12

promotes cell proliferation, migration, colony

formation, and in vivo tumor growth of cervical

cancer cells (Ji et al. 2021).

4 M6A ASSOCIATING WITH

NONCODING RNA

RNA sequences that do not encode proteins are

known as noncoding RNAs (ncRNAs). Research has

demonstrated that m6A methylation was present on

ncRNA as well. Circular RNAs (circRNAs),

microRNAs (miRNAs), and long non-coding RNAs

(lncRNAs) are the three most prevalent forms of non-

coding RNAs (ncRNAs) (Mao et al. 2023). Long non-

coding RNAs (lncRNAs) control a large percentage

expression of genes by interactions between

DNA/RNA/protein, and involves in cancer

development (Modi et al.2024). LncRNA has four

subtypes of molecules that are involved in the

development or occurrence of tumors: signal, bait,

guide, or scaffold (Mao et al. 2023). lncRNA DARS-

AS1 is an oncogene in cervical cancer.

Cytoprotective autophagy in the hypoxic tumor

microenvironment is regulated by DARS-AS1.

Hypoxia-inducible factor 1-alpha (HIF1α)

transcriptionally upregulates DARS-AS1 expression

in CC cells. DARS-AS1 recruits METLL3 and

METTL14 to promote the translation of the DARS

mRNA in CC cells, and it binds with DARS mRNA

to make it more stable. FOXD2-AS1 is linked to

cancer cell migration, proliferation, and a bad

prognosis. METTL3 is in charge of FOXD2-AS1.

Through the attraction and promotion of lysine-

specific demethylase 1 (LSD1), FOXD2-AS1 can

decrease p21 mRNA expression. CC cell migration

and proliferation are inhibited by FOXD2-AS1

knockdown, which also encourages CC cell death

(Modi et al. 2024).

MicroRNAs (miRNAs) are another small non-

coding RNAs with approximate 22 nucleotides

long. It specifically prevents target mRNA

molecules from translating by attaching to their 3′

UTR, so then the mRNA molecules will break

down. Studies on METTL3 and recognition protein

HNRNPA2B1 manifests m6A participate in

synthesis of miRNA through pri-miRNA

modification. Similarly other m6A

methyltransferases, for example METTL14 affects

miRNA synthesis. It has been discovered an

abnormal amount of miRNA is expressed in

cervical cancer, inducing miR-139-3p, and miR-

532- 5p (Mao et al. 2023). High levels of the

lncRNA ZNFX1 anti-sense RNA 1 (ZF-AS1) in CC

are indicative of advanced FIGO stage, increased

risk of metastasis, and poor patient survival. ZF-

AS1 suppresses miR-647 in a METTL3-mediated

way to encourage CC growth and metastasis. A

poor prognosis for patients with CC is linked to the

highly expressed lncRNA KCNMB2-AS1, although

CC cells undergo apoptosis and proliferation

suppression when KCNMB2-AS1 is inhibited.

MiR-130b-5p and miR-4294 are silenced by

KCNMB2-AS1. As a result, IGF2BP3 is

unregulated. It improves stability and expression by

interacting with m6A mutations on KCNMB2-AS1.

Thus, tumorigenicity of CC cells increases (Modi et

al. 2024).

Circular RNAs (circRNAs) have a closed-loop

structure. CircRNA participates in transcription,

splicing, gene expression, sequestering miRNA,

and RNA-binding proteins (Deng et al. 2022).

When circRNA is formed, it is very stable and

increases in the cytoplasm by moving out of the

nucleus. Additionally, circRNA can be found in

extracellular vesicles. Recent studies showed some

circRNA is able to encode mRNA, and be modified

by m6A (Mao et al. 2023). In CC, low levels of

ALKBH5 allow for m6A alterations on

circCCDC134, which significantly improves its

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expression and stability in a way that is reliant on

YTHDF2. Through its interactions with miR-503-

5p and p65, circCCDC134 regulates MYB

expression. Increased HIF1α transcription or

overexpression of ALKBH5 as a result of this

regulation promotes the growth, survival, and

metastasis of cancer cells. Additionally, stability is

increased and CXC motif chemokine ligand 1

(CXCL1) is overexpressed when circRNF13 is

overexpressed, which leads to radiation resistance.

Overexpression of METTL3 leads to more m6A

modifications on circRNF13. Then YTHDF2 binds

to circRNF13 and promotes breakdown. The

degradation of circRNF13 leads to a decrease in its

expression. As a result, radiosensitivity in CC cells

improved (Modi et al. 2024).

5 CLINICAL RELEVANCE AND

THERAPEUTIC POTENTIAL

m6A regulators have garnered increasing attention in

recent years. Although research in this area is still

limited, there have been some notable breakthroughs.

Selberg et al. conducted a structure-based virtual

screening of compound databases and identified four

small molecules capable of enhancing the activity of

the METTL3-METTL14 complex. Additionally,

Bedi et al. discovered a promising adenosine analog

that exhibited significant inhibitory activity against

METTL3. Inhibiting METTL3 reduces the

expression of CXCL1 by stabilizing circRNF13,

thereby decreasing radioresistance in cervical cancer

(Shen et al. 2025). Similarly, ALKBH5 modulates

immune responses in the tumor microenvironment

through chemokine signaling. Inhibiting ALKBH5

results in decreased recruitment of tumor-associated

macrophages (TAMs), making tumors more

susceptible to immune surveillance.

m6A modifications hold potential as biomarkers,

including prognostic, diagnostic, and predictive

biomarkers (Mao et al. 2023). One potential

prognostic biomarker is the METTL3/YTHDF1/HK2

axis. HK2 is a key enzyme involved in the Warburg

effect, a hallmark of cancer characterized by the

preferential use of aerobic glycolysis over

mitochondrial oxidative phosphorylation for energy

production. Measuring the activity of the

METTL3/YTHDF1/HK2 axis can help determine

tumor aggressiveness and cancer prognosis. FTO

levels can also serve as prognostic markers to predict

disease progression. Patients with late-stage cervical

cancer (as classified by the FIGO staging system)

typically exhibit higher FTO levels (Mao et al. 2023).

Several prediction models integrating multiple m6A

regulators have been developed. For instance, Ji et al.

constructed a risk score system based on METTL16,

YTHDF1, and ZC3H13, which demonstrated high

predictive performance for the prognosis of cervical

cancer patients (Ji et al. 2021). Wang et al. analyzed

33 m6A regulators and developed a diagnostic and

prognostic model for cervical cancer. They calculated

an m6A score and identified seven diagnostic

elements and one prognostic factor from 20 pairs of

population tissues. RBM15, NSUN2, METTL3,

CBLL1, RBMX, and ZC3H13 were found to be

upregulated in cervical cancer, while HNRNPAB and

YTHDF3 were downregulated (Wang et al.

2022).

Regarding predictive biomarkers, overexpression of

FTO in the β-catenin pathway leads to

chemoradiotherapy resistance both in vitro and in

vivo. YTHDF3 is also upregulated in cervical cancer

and positively correlates with radioresistance in

cancer cells (Gao et al. 2024). The identification of

these biomarkers could help predict the overall

efficacy of treatments.

6 FUTURE RESEARCH

DIRECTIONS

Recently, there have been multiple drug discoveries

targeting m6A modulators. Curcumin is used to

decrease ALKBH5 expression, leading to an increase

in methylation of TRAF4's mRNA. Thus YTHDF1

will bind to TRAF, and results in better translation of

the TRAF4 protein. Quercetin bind with FTO through

hydrophobic interactions and hydrogen bonds.

Quercetin inhibits the expression of METTL3,

leading to decreased cancer cell proliferation,

migration, and invasion. When Quercetin is used with

a chemotherapeutic drug cisplatin, it’s more effective

in targeting cervical cancer cells like HeLa and SiHa

(Deng et al. 2022). Researchers have been studying

screening numerous 2OG analogues and linked

molecules as inhibitors of FTO and ALKBH5.

Cofactors 2OG and Fe2+ regulates the demethylation

activity of FTO and ALKBH5. Numerous 2OG

oxygenases generic inhibitors inhibit FTO

demethylation. The inhibitors are based on

compounds like pyridyl, hydroxyquinoline, and

isoquinoline. A high-throughput fluorescence

polarization (FP) assay was carried out for

FTO/ALKBH5. Meclofenamic acid (MA) can

function as a selective inhibitor of FTO over

ALKBH5. Combining data from ligand-protein

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complex crystal structures with structure-based drug

designs was another effective method for finding

inhibitors with chemical scaffolds (You et al. 2022).

Rhein, a Rheum rhabarbarum-rich anthraquinone,

was discovered to be one of the most competitive,

cell-active, reversible inhibitors of FTO. Rhein

inhibited FTO by either competitively binding to the

2-oxoglutarate (2-OG) cofactor at the active site,

directly binding to nucleic acids, or both.

Traditional medicine sources have recently been a

new way of finding new agents targeting m6A, with

the assistant of AI and traditional medicines

databases. For instance, the TCM Systems

Pharmacology Database and Analysis Platform

(TCMSP) has approximately 30 thousand ingredients

of five hundred kinds of Chinese herbal medicine, and

more than three thousand targets. Moreover, with the

combination of AI, it could collect and analyze data

of different demethylases and methylases, such as the

site of modification, and the antigen it downregulates,

the side effect it exhibits, etc. Then AI will give a

prediction of the targeted drugs based on this

information. Scientists are able to use these designs

and perhaps make changes based on the models. Thus

the costs of developing drugs and inhibitors of such

methylates and demethylases will significantly

decrease, and the time will shorten. More and more

effective m6A inhibitors and drugs targeting them

will be approved in the future (Deng et al. 2022).

7 CONCLUSION

m6A modification is actively involved in the

development of cervical cancer, through regulating

RNA stability, translation, and degradation.

Methyltransferase complexes (MTC) such as writers

(METTL3, METTL14, WTAP), erasers (FTO,

ALKBH5), and readers (IGF2BP1, YTHDC1/2)

promote tumor growth, translation, immune response,

cell proliferation, metastasis, and drug resistance.

These enzymes promote tumor growth by

downregulating tumor suppressor genes or

upregulating oncogenes. For instance, METTL3

stabilizes FOXD2-AS1, inhibiting the expression of

p21, while FTO and ALKBH5 enhances

tumorgenesis by controlling cell apoptosis,

proliferation, and metastasis. m6A modifications

exist on noncoding RNAs (ncRNAs), such as

lncRNAs, circRNAs, and miRNAs. Oncogenic

lncRNAs like DARS-AS1 and FOXD2-AS1 promote

tumor growth, knockdown of these genes inhibit

proliferation and induces apoptosis. Abnormal

miRNA expression linked to cervical cancer.

circRNAs contribute to regulation of genes and

therapeutic resistance.

m6A regulators offers a promising therapeutic

strategy. For instance, small molecules enhancing

METTL3-METTL14 activity, and METTL3

inhibitors are being discovered. Furthermore, m6A

modifications serve as prognostic, diagnostic, and

predictive biomarkers. The METTL3/YTHDF1/HK2

axis links m6A to cancer metabolism, and FTO levels

correlate with advanced-stage cervical cancer.

Discoveries of drugs targeting m6A modulators

include Curcumin, Quercetin, Meclofenamic acid and

Rhein. Curcumin reduces ALKBH5 expression.

Quercetin inhibits expression of METTL3, leading to

decreased cancer cell proliferation. Meclofenamic

acid and Rhein are inhibitors of FTO. AI and

traditional medicine databases aid in finding new

inhibitors through analyzing demethylases,

methylases, and drug interactions, reducing costs and

accelerating drug development. The continued

research in this field holds great promise for

improving diagnosis, prognosis, and treatment

strategies for cervical cancer patients.

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