The Role of Lipid Metabolism in Cancer Progression: Molecular

Mechanisms and Therapeutic Strategies

Yuchen Han

College of Medical, Veterinary & Life Sciences, University Avenue, Glasgow, G12 8QQ, Scotland

Keywords: Lipid Metabolism, Cancer Progression, Therapeutic Targets.

Abstract: Cancer cells undergo significant metabolic reprogramming to support their rapid proliferation, survival, and

resistance to therapy. One key metabolic shift observed in tumors is the alteration in lipid metabolism,

particularly in fatty acid oxidation (FAO), fatty acid synthesis (FAS), lipid uptake, and lipid storage. Unlike

normal cells, cancer cells rely on FAO to sustain energy production under metabolic stress while also

upregulating lipid synthesis and up-take to fuel tumor growth and metastasis. This study explores how

targeting FAO, FAS, and li-pid uptake can provide new therapeutic opportunities. The article will discuss

FAO inhibitors (Etomoxir, ST1326, Perhexiline), FASN inhibitors (TVB-2640, C75, Orlistat), and lipid

uptake blockers (CD36 and FABP inhibitors) as emerging anti-cancer strategies. Additionally, it will analyze

how metabolic plasticity allows tumors to bypass these treatments, emphasizing the need for combination

therapies and personalized approaches. By addressing these aspects, the article aims to provide insights of

lipid metabolism in cancer progression, the latest therapeutic advances, and the challenges of translating these

strategies into clinical applications.

1 INTRODUCTION

Cancer is a major challenge for global health, and

there are 20 million new cases, and 9.7 million deaths

reported in 2022(Bray et al.,2021). With the high

resistance to conventional therapies such as

chemotherapy, radiotherapy, and immunotherapy, the

lethality of cancer will continuously rise. Therefore,

finding new targets for cancer treatment or reducing

chemo-radiotherapy sensitivity is essential. Lipid

metabolism is significant for maintaining cellular

homeostasis, energy providing, structural

components, and signaling molecules necessary for

cell survival and function. In normal cells, lipid

metabolism is tightly regulated to balance lipid

uptake, synthesis, storage and oxidation, ensuring

energy sufficiency and membrane integrity (Baenke

et al., 2013). However, cancer cells reprogram their

metabolism, including changes in lipid metabolism,

to meet the demands of rapid proliferation, increased

survival and metastasis. These changes allow cancer

cells to acquire and utilize lipids more efficiently than

normal cells, conferring advantages in growth, energy

production, and adaptation to stressful conditions

(Beloribi et al., 2016).

Cancer cells depend on glycolysis to generate

energy instead of oxidative phosphorylation, even in

the rich-oxygen condition, and this is called the

Warburg effect, which is one of the main features

distinguishing the normal cells and cancer cells.

Cancer cells also enhance de novo lipid biosynthesis

and lipid uptake to sustain their rapid proliferation

(Snaebjornsson et al., 2020). Cancer cells upregulate

key enzymes involved in lipid synthesis, such as fatty

acid synthetase (FASN) and acetyl-CoA carboxylase

(ACC), to ensure a continuous supply of fatty acids

for membrane biogenesis (Carracedo et al., 2013).

Additionally, increased expression of lipid

transporters, such as cluster of differentiation 36

(CD36), allows cancer cells to enhance fatty acid

uptake from the extracellular environment, further

supporting their metabolic flexibility (Pascual et al.,

2017).

Fatty acid oxidation (FAO) is the main energy

pathway for fatty acid synthesis (FAS) in cancer cells

(Carracedo et al., 2013). Lipid oxidation provides

energy for the metastasis and migration processes.

The metastatic cells generate ATP and evade immune

detection depending on the lipid metabolism. FAO is

closely linked to epithelial-mesenchymal transition

(EMT). FAO-induced reactive oxygen species (ROS)

Han, Y.

The Role of Lipid Metabolism in Cancer Progression: Molecular Mechanisms and Therapeutic Strategies.

DOI: 10.5220/0014431600004933

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 117-123

ISBN: 978-989-758-789-4

117

upregulate key EMT markers such as vimentin and

snail, promoting cancer cell invasion and lymph node

metastasis. (Li, et al., 2021).

Additionally, FAO can cause the loss of cellular

attachment, which promotes cancer cell detachment

from the primary tumor and facilitates metastatic

dissemination. (Carracedo, et al., 2013). FAO has

multiple functions and plays a significant role in

various metabolic pathways in cancer, so it is a

crucial target of tumor progression and a promising

therapeutic target for improving radiotherapy and

chemotherapy outcomes.

Lipid metabolism also crosses with other

metabolic pathways, such as glutamine metabolism

and glycolysis. (Baenke et al., 2013). Glutamine

metabolism supports energy production and

biosynthesis to sustain the rapid growth of cancer

cells (Currie et al., 2013). Glutamine is converted to

alpha-ketoglutarate (α-KG), which enters the TCA

cycle and provides a carbon source and energy to

cancer cells (Schulze&Harris, 2012). Glutamine is

converted to lactate in cancer cells to produce

NADPH, which is essential for FAS.

2 METABOLIC PLASTICITY

AND THE INTERACTION OF

LIPID METABOLISM WITH

GLYCOLYSIS AND

GLUTAMINE METABOLISM

THE TEMPLATE FILE

Metabolic plasticity is a hallmark of cancer cells,

allowing them to adapt to environmental stresses such

as hypoxia and nutrient deprivation to ensure

continued proliferation and survival (Schulze and

Harris, 2012). Cancer cells reprogramme metabolic

pathways to optimize the use of glucose, glutamine

and lipids to form an interconnected metabolic

network.

Glutamine metabolism is critical in maintaining

lipid biosynthesis, supporting the tricarboxylic acid

(TCA) cycle and reductive carboxylation pathways

(Son et al., 2013). DeBerardinis et al. (2007)

demonstrated, using 13C NMR spectroscopy, that

glioblastoma cells exhibit a high rate of

glutaminolysis, where glutamine-derived α-KG

enters the TCA cycle, replenishes citrate, and fuels

fatty acid biosynthesis. Their study found that even

though these cancer cells primarily rely on glycolysis

(Warburg effect), approximately 60% of fatty acyl

carbon was glucose derived. At the same time, the rest

was supplied by glutamine metabolism (Son et al.,

2013).

Similarly, Son et al. (2013) provided evidence that

KRAS-mutant pancreatic ductal adenocarcinoma

(PDAC) cells use a non-canonical glutamine

metabolism pathway to fuel biosynthetic and redox

processes. Unlike normal cells, which primarily

convert glutamine to α-KG via glutamate

dehydrogenase (GLUD1), PDAC cells rely on

aspartate transaminase (GOT1) to convert glutamine-

derived aspartate into oxaloacetate (OAA), which is

then metabolized into malate and, subsequently,

pyruvate. This pathway increases NADPH

production, which supports FAS and redox

homeostasis. The knockdown of GOT1 in PDAC

cells resulted in a 50% reduction in the

NADPH/NADP+ ratio, demonstrating its essential

role in supporting lipid biosynthesis under oxidative

stress conditions.

Glutamine-derived α-KG is a key metabolite for

sustaining lipid biosynthesis in cancer cells.

DeBerardinis et al. observed that blocking glutamine

metabolism led to a 40% reduction in FAS in

glioblastoma cells, indicating that glutamine

metabolism is required to maintain the lipogenic flux.

Additionally, NADPH, which is generated from the

pentose phosphate pathway (PPP) and malic enzyme

1 (ME1), provides reducing power for FAS. Son et al.

(2013) further demonstrated that ME1 inhibition in

PDAC cells reduces NADPH levels by 35% and

impairs lipid synthesis, leading to increased oxidative

stress and reduced tumor growth.

Cancer cells reprogram lipid metabolism to

sustain survival in response to metabolic stressors

such as hypoxia or nutrient deprivation (Schulze &

Harris, 2012). Hypoxia-inducible factor-1α (HIF-1α)

is crucial in promoting lipid droplet accumulation,

enhancing fatty acid uptake, and shifting metabolism

away from oxidative phosphorylation (OXPHOS)

towards glycolysis. Furthermore, Son et al. (2013)

demonstrated that in PDAC cells, glutamine-derived

malate generates NADPH through malic enzyme

activity to counteract oxidative stress. When ME1 or

GOT1 was knocked down, the PDAC cells exhibited

a significant accumulation of ROS, demonstrating the

importance of glutamine-derived NADPH in

maintaining redox balance.

The interplay between lipid metabolism,

glycolysis, and glutamine metabolism is critical for

cancer cells to adapt to metabolic stress and sustain

proliferation (Schulze & Harris, 2012). α-KG and

NADPH play essential roles in FAS and redox

BEFS 2025 - International Conference on Biomedical Engineering and Food Science

118

balance, supporting tumor survival under hypoxic and

nutrient-deprived conditions (Son et al., 2013). The

reprogramming of glutamine metabolism to sustain

lipid biosynthesis further underscores the importance

of targeting these metabolic pathways as a potential

therapeutic strategy in cancer.

3 LIPID UPTAKE IN CANCER

Cancer cells have the capacity to perform metabolic

reprogramming, which is different from how healthy

cells do it. They can quickly modify their metabolic

pathways to get the energy needed for their growth

and development. The mechanism of the key pathway

of fatty acid survival in cancer cells is the increased

uptake of exogenous fatty acids. For example, cancer

cells are known for using mitochondrial β-oxidation

to produce ATP by taking up fatty acids, which are

shown to be more effective than glycolysis and are

especially essential in low-nutrient or hypoxic

conditions (Butler et al., 2021). Also, nitrous oxide is

thought to help the cancer cell survive and become

more resistant to chemotherapy and radiation therapy.

However, the production of NADPH during the lipid

oxidation pathway will help cells resist oxidative

stress and further reduce the risk of oxidative damage,

resulting in apoptosis. Lipid does not only act as an

energy source. It is also a necessary component of the

tumor cell membrane. The excessive influx of fatty

acids into cancer cells drives the synthesis of

phospholipids and sphingolipids, resulting in the

development of highly flexible membranes that will

enable the cells to proliferate, migrate and also

metastasize effectively (Furman et al., 2019).

Exogenous fatty acids in the tumor

microenvironment (TME) give oxygen radicals,

promoting cell proliferation and facilitating immune

evasion; thus, cancer cells have a metabolic

advantage. High intake of dietary fat and a lipid

microenvironment rich in content allow cancer cells

to elevate the process of oxidative phosphorylation

(OXPHOS) and the formation of lipid storage, which

consequently leads to higher energy production and a

diminished reliance on glucose metabolism (Butler et

al., 20-21). The two sets of metabolisms are easily

distinguishable. The same techniques can be used to

direct drugs to cancer cells or perfect the sensitivity

of chemotherapy and radiotherapy.

Lipid transfer by cancer cells is mostly done

through specific fatty acid transporters like cluster of

differentiation 36 (CD36) and fatty acid binding

proteins (FABPs), acting as mediators for the entry

and movement of lipids inside cells. CD36 is a cell-

bound scavenger receptor that emerges as a factor in

lipid metabolism and has been shown to have a huge

impact on the metastatic potential of various cancers,

such as breast cancer, ovarian cancer, and melanoma

(Pascual et al., 2017). In lung adenocarcinoma

(LUAD), the high-fat diet (HFD) conditions are

driving the tumor growth as well as the metastatic

potential. The signal transduction pathway,

predominantly driven by CD36, has been shown to

play a prominent role in producing HFD- fueled

CD36-Src signaling axis. Data from experiments

suggest that PA as a stimulus for cells can lead to the

movement of CD36 to the cell membrane and

activation of the Src kinase pathway, which activates

the Akt/ERK pathway that eventually leads to

migration and invasion. The use of the fatty acid

analog blocker sulfo-N-succinimidyl oleate (SSO)

restricted LUAD metastasis in vivo and demonstrated

its efficacy as a therapeutic target (Liu, et al., 2023).

Not only that, but CD36-mediated fatty acid uptake is

a key factor in AML that is not changeable, and AML

cells depend on it for the survival of the cancer stem

cells. Newly found small-molecule inhibitor SMS121

reduces the uptake of fatty acids by AML cells,

thereby stifling their survival, especially in the cells

over-expressing CD36. When AML cells were

exposed to adipocytes, lipid transfer was observed,

which

facilitated leukemia particle growth. When the

function of CD36 is blocked with SMS121, the

metabolic adaptation is interrupted; thereby, SMS121

becomes a potential anti-leukemia drug, as shown in

the above case (Ábacka, et al., 2024).

A-FABP is another fatty acid transporter. A-

FABP is largely present in tumor-associated

macrophages (TAMs), which are the primary

producers of a pro-tumorigenic environment. It will

promote the disease via IL-6/STAT3. This will

increase the growth, and metastasis is seen as the

outcome (Hao, et al.,2018). By means of a certain

study, it was found that TAMs with blocked A-FABP

show a decrease in mammary tumor growth and

metastasis, which in turn indicates A-FABP as a

master regulator in these processes'

microenvironment (Hao, et al.,2018). Small-molecule

inhibitors of A-FABP already have proven anticancer

effects in preclinical models with them, reducing the

tumor burden and suppressing the tumor-promoting

functions of TAMs. These molecules, originally

invented for treating metabolic diseases, are now

being examined for their possible use in cancer

therapy (Hao, et al.,2018). Also, high levels of A-

FABP in obesity predict an elevated risk of breast

The Role of Lipid Metabolism in Cancer Progression: Molecular Mechanisms and Therapeutic Strategies

119

cancer. Thus, it is evident that metabolic dysfunction

is a contributing factor to cancer progression (Hao, et

al.,2018). Targeting A-FABP can be a potential

strategy for novel cancer therapies that are especially

effective in addressing obesity-related cancers, given

its strong links with the tumor-promoting pathways

and the success of its inhibition in the preclinical

models.

There has been an increase in evidence to support

the idea that tumor growth is accelerated by the fat-

rich high-fat diet (HFD) because it provides more

fatty acids to cancer cells. Pascual et al. (2017)

revealed that CD36-expressing metastatic cells can

take in more fatty acids under a high-fat diet than

normal conditions. That is the reason why they can

persistently move from one part of the body to

another. This might be a new way to treat cancer with

dietary lipids by blocking the lipid uptake pathways

which might have to be explored further on this.

4 LIPID SYNTHESIS OF LIPID

METABOLISM

The de novo synthesis of lipids specific for cancer

cells allows them to multiply and grow at far higher

rates than normal cells, which rely on dietary lipids.

Adhering to an extracellular lipid supply or a de novo

lipid synthesis pathway is key to cancer cell viability.

Cancer cells use de novo lipid synthesis as the

exclusive pathway to the biosynthesis of fatty acids

when there is no help from an outside supply. FASN

is the main enzyme in the de novo synthesis of lipids.

It is responsible for converting acetate to palmitate

and synthesizing fatty acids from acetyl-CoA and

malonyl-CoA. However, because most tissues have

high-fat diets, FASN is rarely expressed in normal

tissues. Across different types of cancer, including

prostate cancer, it is highly expressed and is

responsible for tumorigenesis, metabolic adaptation,

and resistance to apoptosis. It is the main cause of the

carcinogenic effects of the protein FASN, as it is

involved in the production of crucial fatty acids for

the synthesis of membranes, energy production, and

signaling involving lipids. FASN seems to be a

potential target in cancer treatment due to its

exceptional part in the metabolism of the cancerous

cells and the result of the FASN blocking is the

apoptosis of the tumor cells, and the result of this

influences the proliferation (Baron et al.,2004).

FASN has emerged as a promising therapeutic

target because it plays a key role in cancer

metabolism. Its presence inhibits the occurrence of

apoptosis in tumor cells and it changes their

proliferation, hands down. (Baron et al., 2004). Some

potential targets can be tumor metabolism and

control, such as FASN that can have its inhibitors,

e.g., TVB-2640, BI 99179, C75, cerulenin, and

orlistat (Kley et al., 2011) (Kelly et al., 2023). TVB-

2640 is a first-in-class selective, reversible FASN

inhibitor that has proven effective in many cancers by

decreasing biosynthesis of lipid and overall tumor cell

survival. Phase II trial found that TVB-2640, with the

participation of bevacizumab, can significantly

prolonged progression-free survival in kids with

malignant tumors in comparison with standard

treatment (Kelly, W. et al., 2023). BI 99179 is a

potent and selective non-covalent FASN inhibitor

that has been researched in central nervous system

tumors and has preclinically shown potent anticancer

activity (Kley, et al., 2011). Cancer cells' dependence

on de novo lipid synthesis is what makes targeting

FASN such an attractive therapeutic strategy to

disrupt tumor metabolism.

ACC is the other vital enzyme in the fatty acid

metabolism that plays a major role in the neo-FAS

process of tumor cells. ACC is usually upregulated in

cancer cells to boost membrane lipid need for cell

proliferation that is fast and rapid. Data showed that

ACC is the protein that is behind the higher cancer

cell survival by an increase in the number of cell

membrane lipids, that is why they grow faster. Also,

the upregulation of these enzymes is an essential part

of the oncogenic signaling pathways (e.g.,

PI3K/AKT/mTOR and SREBP1) that promote

lipogenesis synthetics. Research has also proved that

ACC1 gene deletion or pharmacological inhibition of

ACC1 induces comprssion of cancer cell proliferation

and tumor growth. This finding was further supported

by in vivo lung cancer model, where the ACC

inhibitor ND-646 was able to reduce the size of the

tumor through blocking neoadipogenesis while

enhancing apoptosis (Svensson, R. U. et al., 2016).

By the same token, knockdown of ACC1 on acute

myeloid leukemia (AML) cells was corresponding to

higher levels of ROS and NADPH depletion, which

means the cells were under metabolic stress and easy

to eliminate. Recently designed medication, sorbitol

A, was found out to act as a macrocyclic ACC

inhibitor through the interference of lipogenesis and

the modification of the lipid bilayer composition, thus

making the cancer cell fleeted in an oxidative

environment.

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5 ROLE OF FAO IN CANCER

FAO is an important contributor to the diversion of

energy toward tumor cells. It is a process through

which cells receive ATP synthesis and survival under

dead humidity; it also maintains their redox

equilibrium. Additionally, FAO has been suggested

to be a critical process in EMT which is a necessary

action for cancer cells to become more malignant and

capable of moving cells. Therefore, FAO could

promote tumor metastasis and tumor invasiveness in

a cancer cell population by effecting the EMT

process. Fatty acids, in turn, were shown to be

associated with the immunosuppressive milieu of

tumors. It was discovered that lipid droplet-dependent

fatty acid metabolism in TAMs preserved the

immune-suppressive phenotype of those cells. This

suggests that FAO is responsible for the immune

escape of tumours by altering the function of

macrophages. This suggests that FAO may promote

the tumor's immune escape by modulating the TAMs'

function.

FAO is suggested to be one therapeutic target in

cancer by virtue of the notable metabolic differences

between tumor and normal cells. It is thought that the

increased FAO competence of cancer cells may be

one of the factors behind their decreased sensitiveness

to these treatments. Thus the FAO can be used as an

effective personification, which considerably can be

used for detecting cancer and for cancer therapy.

Selective inhibitors of FAO have been plumbed in

preclinical directions with satisfactory outcomes.

Etomoxir is the lead of CPT1A inhibitors whose

capability to block the oxidation of fatty acids was

proven to entailing the effect of suppressing tumor

cell proliferation while enhancing chemosensitivity

to colorectal cancer (CRC) in animal models

(Mozolewska, et al., 2020). ST1326 (Teglicar) is

another CPT1 inhibitor, which has a lower toxicity

rate when compared with that of the etomoxir

treatment. This is why it might be appealing as an

alternative for clinical conditions. Perhexiline, a dual

CPT1/CPT2 inhibitor, has also been the mediator of

the anticancer skill to CRC cells by fostering its

sensitivity through oxaliplatin-based therapy

(Mozolewska, et al., 2020).

FAO is the pathway regulator for cancer cell

survival and TME formation. FAO also supports

immunosuppressive cells such as regulatory T cells

(Tregs) and myeloid-derived suppressor cells

(MDSCs), which allow cancer cells to escape

immune control. (Li, M. et al. 2021). The opposite,

i.e., the blocking of FAO, has been also shown to

rejuvenate tumour immunity and an assistance to the

effectiveness of immune checkpoint inhibitors like

anti-PD-1 therapy (Li, et al.,2021). The other side, it

is an appealing metabolic hole to intervene in the

offensive process, to create life for the tumor, and to

enable them to emigrate and metastasize easily. The

corpus of experimental evidence formulating several

studies undergone the proposition that FAO

inhibition is a potentially effective treatment for

cancer. Among CPT1 inhibitors, such as Etomoxir,

ST1326, and Perhexiline either individually or in

combination with immunotherapy and chemotherapy

showed notable the anticancer potential and thus can

be the subject of further clinical investigations

required for the validation of persuasive efficiency as

a basis of the cancer treatment (Mozolewska, et al.,

2020).

6 CONCLUSION

This study investigates the crucial role of lipid

metabolism in cancer progression, in particular its

influence on tumour growth, resistance to therapy and

immune evasion. By exploring FAO, lipid synthesis

and lipid uptake, this review provides insights into

how metabolic intervention can be used to disrupt

tumor survival mechanisms and highlights the

clinical potential of CPT1 inhibitors, FASN

inhibitors, and CD36 targeting therapies,

demonstrating their promise in both preclinical and

clinical settings. It also suggests that combining

metabolic inhibitors with chemotherapy or

immunotherapy may help overcome drug resistance

and improve outcomes.

Essential clinical demonstrations have brought

alongside that CPT1 inhibitors, such as Etomoxir,

ST1326, and Perhexiline, have so far exhibited

enormous potentials in anti-cancer implications either

as a standalone or as part of combined therapies but

have not been well absorbed due to their high toxicity

and metabolic adaptation. In addition, the solution

needs to go deeper into ways of developing more

selective and targeted medications against next-

generation CPT1 inhibitors and combining FAO with

chemotherapy and immunotherapy to overcome the

resistance mechanism. It is also pointed out that

cancer stem cells (CSCs), which are under the

influence of FAO, are the cells in the carcinogenic

process that can lead to relapse and resistance. The

strength of FAO inhibition might be a new approach

to wipe out CSCs and avert tumor recurrence. Cancer

cells exhibit enhanced de novo lipid synthesis,

The Role of Lipid Metabolism in Cancer Progression: Molecular Mechanisms and Therapeutic Strategies

121

making FASN (FASN) and ACC promising

therapeutic targets’ inhibitors (e.g., TVB-2640, C75

and orlistat, among others) have shown preclinical

efficacy, but their clinical translation remains

challenging due to metabolic compensation. The

future of lipid synthesis inhibition should focus on

combination therapies, where lipid synthesis-

targeting drugs are combined with glycolysis

inhibitors to prevent metabolic escape or impair

oncogenic signaling pathways by disrupting lipid raft

integrity.

These findings provide a valuable reference for

future studies, particularly in the refinement of lipid-

targeting drugs to increase specificity and reduce

toxicity, and in the development of combination

strategies to counteract metabolic compensation. To

address these limitations and advance cancer

therapies targeting lipid metabolism, future research

should focus on safer, more selective inhibitors of

lipid metabolism to minimise toxicity, improve

efficacy, and combine metabolic inhibitors with

immune checkpoint inhibitors or chemotherapy to

improve treatment response.

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