The evolving tumor microenvironment: From cancer initiation to metastatic outgrowth
Cancer Cell,
Journal Year:
2023,
Volume and Issue:
41(3), P. 374 - 403
Published: March 1, 2023
Language: Английский
The matrix in cancer
Nature reviews. Cancer,
Journal Year:
2021,
Volume and Issue:
21(4), P. 217 - 238
Published: Feb. 15, 2021
Language: Английский
The metabolism of cancer cells during metastasis
Nature reviews. Cancer,
Journal Year:
2021,
Volume and Issue:
21(3), P. 162 - 180
Published: Jan. 18, 2021
Language: Английский
The dormant cancer cell life cycle
Nature reviews. Cancer,
Journal Year:
2020,
Volume and Issue:
20(7), P. 398 - 411
Published: June 2, 2020
Language: Английский
Genomic characterization of metastatic patterns from prospective clinical sequencing of 25,000 patients
Cell,
Journal Year:
2022,
Volume and Issue:
185(3), P. 563 - 575.e11
Published: Feb. 1, 2022
Language: Английский
Metastasis
Stefanie Gerstberger,
No information about this author
Qingwen Jiang,
No information about this author
Karuna Ganesh
No information about this author
et al.
Cell,
Journal Year:
2023,
Volume and Issue:
186(8), P. 1564 - 1579
Published: April 1, 2023
Language: Английский
Metastasis-Initiating Cells and Ecosystems
Cancer Discovery,
Journal Year:
2021,
Volume and Issue:
11(4), P. 971 - 994
Published: April 1, 2021
Abstract
Metastasis
is
initiated
and
sustained
through
therapy
by
cancer
cells
with
stem-like
immune-evasive
properties,
termed
metastasis-initiating
(MIC).
Recent
progress
suggests
that
MICs
result
from
the
adoption
of
a
normal
regenerative
progenitor
phenotype
malignant
cells,
intrinsic
programs
to
survive
stresses
metastatic
process,
undergo
epithelial–mesenchymal
transitions,
enter
slow-cycling
states
for
dormancy,
evade
immune
surveillance,
establish
supportive
interactions
organ-specific
niches,
co-opt
systemic
factors
growth
recurrence
after
therapy.
Mechanistic
understanding
molecular
mediators
MIC
phenotypes
host
tissue
ecosystems
could
yield
therapeutics
improve
patient
outcomes.
Significance:
Understanding
origins,
traits,
vulnerabilities
capacity
initiate
metastasis
in
distant
organs,
microenvironments
support
ability
these
surveillance
regenerate
tumor,
critical
developing
strategies
prevention
treatment
advanced
cancer.
Leveraging
recent
our
here
we
review
nature
their
offer
perspective
on
how
this
knowledge
informing
innovative
treatments
cancers.
Language: Английский
Role of exosomal non-coding RNAs from tumor cells and tumor-associated macrophages in the tumor microenvironment
Zijie Xu,
No information about this author
Yi Chen,
No information about this author
Ling Ma
No information about this author
et al.
Molecular Therapy,
Journal Year:
2022,
Volume and Issue:
30(10), P. 3133 - 3154
Published: April 9, 2022
Exosomes
have
a
crucial
role
in
intercellular
communication
and
mediate
interactions
between
tumor
cells
tumor-associated
macrophages
(TAMs).
Exosome-encapsulated
non-coding
RNAs
(ncRNAs)
are
involved
various
physiological
processes.
Tumor-derived
exosomal
ncRNAs
induce
M2
macrophage
polarization
through
signaling
pathway
activation,
signal
transduction,
transcriptional
post-transcriptional
regulation.
Conversely,
TAM-derived
promote
proliferation,
metastasis,
angiogenesis,
chemoresistance,
immunosuppression.
MicroRNAs
gene
silencing
by
directly
targeting
mRNAs,
whereas
lncRNAs
circRNAs
act
as
miRNA
sponges
to
indirectly
regulate
protein
expressions.
The
of
tumor-host
is
ubiquitous.
Current
research
increasingly
focused
on
the
microenvironment.
On
basis
"cancer-immunity
cycle"
hypothesis,
we
discuss
effects
immune
T
cell
exhaustion,
overexpression
programmed
death
ligands,
create
immunosuppressive
Furthermore,
potential
applications
prospects
clinical
biomarkers
drug
delivery
systems.
Non-coding
do
not
encode
proteins
but
control
expression
function.1Hombach
S.
Kretz
M.
RNAs:
classification,
biology
functioning.Adv.
Exp.
Med.
Biol.
2016;
937:
3-17Crossref
PubMed
Scopus
(346)
Google
Scholar,
2Chan
J.J.
Tay
Y.
Noncoding
RNA:RNA
regulatory
networks
cancer.Int.
J.
Mol.
Sci.
2018;
19:
1310Crossref
(608)
3Guil
Esteller
RNA-RNA
regulation:
coding
noncoding
players.Trends
Biochem.
2015;
40:
248-256Abstract
Full
Text
PDF
Scholar
Several
types
ncRNAs,
including
microRNAs
(miRNAs),
long
(lncRNAs),
circular
(circRNAs),
affect
growth,
metabolism
multiple
mechanisms.3Guil
4Anastasiadou
E.
Jacob
L.S.
Slack
F.J.
RNA
cancer.Nat.
Rev.
Cancer.
18:
5-18Crossref
(900)
5Goodall
G.J.
Wickramasinghe
V.O.
2021;
21:
22-36Crossref
(337)
miRNAs
20–25
nucleotide
that
at
level
binding
3′
untranslated
region
(3′
UTR)
target
thus
regulating
other
cellular
processes.6Ha
Kim
V.N.
Regulation
microRNA
biogenesis.Nat.
Cell
2014;
15:
509-524Crossref
(3372)
Scholar,7Dong
H.
Lei
Ding
L.
Wen
Ju
Zhang
X.
MicroRNA:
function,
detection,
bioanalysis.Chem.
2013;
113:
6207-6233Crossref
(823)
longer
than
200
nucleotides
regulation
nucleus
cytoplasm.8Chen
L.L.
Linking
localization
function.Trends
41:
761-772Abstract
(592)
Scholar,9Quinn
Chang
H.Y.
Unique
features
biogenesis
function.Nat.
Genet.
17:
47-62Crossref
(2150)
modulate
stability,
translation,
translocation
mRNAs.9Quinn
Scholar,10Statello
Guo
C.J.
Chen
Huarte
Gene
its
biological
functions.Nat.
22:
96-118Crossref
(817)
increase
mRNA
expressions
sponging
competitive
endogenous
(ceRNAs),
secreted
either
alone
or
bound
proteins.11Tay
Rinn
Pandolfi
P.P.
multilayered
complexity
ceRNA
crosstalk
competition.Nature.
505:
344-352Crossref
(2450)
Scholar,12Lin
C.
Yang
Long
cancer:
wiring
circuitry.Trends
28:
287-301Abstract
(330)
characterized
covalently
closed-loop
structure
without
5′
cap
poly(A)
tail.13Yu
C.Y.
Kuo
H.C.
emerging
roles
functions
their
generation.J.
Biomed.
2019;
26:
29Crossref
(167)
Scholar,14Kristensen
Andersen
M.S.
Stagsted
L.V.W.
Ebbesen
K.K.
Hansen
T.B.
Kjems
biogenesis,
characterization
RNAs.Nat.
20:
675-691Crossref
(1539)
These
implicated
spongings,
interactions,
nuclear
transcription
pre-mRNA
splicing.15Wang
R.
Li
N.
Jia
Pan
Liang
CircNT5E
acts
sponge
miR-422a
glioblastoma
tumorigenesis.Cancer
Res.
78:
4812-4825Crossref
(199)
Scholar,16Qian
Yu
Z.
Meng
Huang
Wang
P.
significance
human
cancers.Biochim.
Biophys.
Acta
1870:
247-260Crossref
(0)
40–150
nm
extracellular
vesicles
pathological
processes
mediating
communication.17Hessvik
N.P.
Llorente
A.
knowledge
exosome
release.Cell
Life
75:
193-208Crossref
(1112)
Scholar,18Pegtel
D.M.
Gould
S.J.
Exosomes.Annu.
88:
487-514Crossref
(793)
content
exosomes
released
donor
protected
from
enzymatic
hydrolysis.19Abels
E.R.
Breakefield
X.O.
Introduction
vesicles:
cargo
selection,
content,
release,
uptake.Cell.
Neurobiol.
36:
301-312Crossref
(713)
20Mathieu
Martin-Jaular
Lavieu
G.
Théry
Specificities
secretion
uptake
for
cell-to-cell
communication.Nat.
9-17Crossref
(1420)
21Mashouri
Yousefi
Aref
A.R.
Ahadi
A.M.
Molaei
F.
Alahari
S.K.
Exosomes:
composition,
mechanisms
cancer
metastasis
resistance.Mol.
75Crossref
(410)
fundamental
resistance.21Mashouri
22van
Niel
D'Angelo
Raposo
Shedding
light
vesicles.Nat.
213-228Crossref
(2898)
23Zhang
D.
development,
immunity.Biochim.
1871:
455-468Crossref
(215)
Tumoral
secrete
microenvironment
(TIME).23Zhang
Scholar,24Kalluri
function
cancer.J.
Clin.
Invest.
126:
1208-1215Crossref
(967)
(TEXs)
immunological
activities,
polarization,
regulation,
inhibition
natural
killer
(NK)
activity.25Whiteside
T.L.
progression.Adv.
Chem.
74:
103-141Crossref
(402)
26Kok
V.C.
C.C.
Cancer-derived
exosomes:
biomarker
development.Int.
Nanomed.
2020;
8019-8036Crossref
(50)
27Greening
D.W.
Gopal
Xu
Simpson
R.J.
W.
cancer.Semin.
Dev.
72-81Crossref
(401)
TEXs
also
malignancy,
suggesting
key
tumoral
cells.28Xie
Zhou
Fang
Su
Tu
Extracellular
immunotherapy.Adv.
6:
1901779Crossref
(103)
29Veerman
R.E.
Güçlüler
Akpinar
Eldh
Gabrielsson
Immune
cell-derived
-
therapeutic
applications.Trends
25:
382-394Abstract
(110)
30Yan
Jiang
cancer-immunity
cycle.Trends
506-517Abstract
(46)
development
immunosuppression
attracted
increasing
attention.31Sun
Shi
K.
Liu
Q.
Song
Yuan
Effect
applications.Mol.
147Crossref
32Cheng
Zhu
Peng
Exosomal
Glioma:
66Crossref
(131)
33Xie
Dang
Yue
Zhai
Yan
Lu
cancer.Mol.
37Crossref
(134)
can
be
used
because
high
encapsulation
efficiency
ability
transport
anti-cancer
drugs,
agents,
nucleic
acids,
gene-editing
systems
such
CRISPR-Cas9.34Pullan
J.E.
Confeld
M.I.
Osborn
J.K.
Sarkar
Mallik
carriers
therapy.Mol.
Pharm.
16:
1789-1798Crossref
(76)
35Liu
Cheng
Delivery
strategies
CRISPR-Cas9
system
applications.J.
Control.
Release.
2017;
266:
17-26Crossref
(257)
36Ghaemi
Bagheri
Abnous
Taghdisi
S.M.
Ramezani
Alibolandi
CRISPR-cas9
genome
editing
targeted
therapy.Life
267:
118969Crossref
(7)
Macrophages
phagocytic
cells,
phenotypes
influenced
cytokines
factors
TIME.37Belgiovine
D'Incalci
Allavena
Frapolli
Tumor-associated
anti-tumor
therapies:
complex
links.Cell.
73:
2411-2424Crossref
assume
classically
activated
pro-inflammatory
(M1)
phenotype
an
alternatively
anti-inflammatory
(M2)
phenotype.38Orecchioni
Ghosheh
Pramod
A.B.
Ley
Macrophage
polarization:
different
signatures
M1(LPS+)
vs.
Classically
M2(LPS-)
Alternatively
macrophages.Front.
Immunol.
10:
1084Crossref
(541)
(TAMs)
M1
early
stages
cancer.37Belgiovine
In
later
stage,
growth
mediators,
IL-4,
IL-10,
TGF-β,
expressed
TIME,
inducing
polarization.37Belgiovine
M1-M2
highly
dynamic
reversible.
TAMs
produce
inhibit
activity
TIME.39Yin
Han
Zheng
B.
Zhao
SALL4-mediated
upregulation
miR-146a-5p
drives
T-cell
exhaustion
HCC.Oncoimmunology.
8:
1601479Crossref
(3)
TAM
infiltration
solid
tumors
underscores
these
progression
immunosuppression.39Yin
40Ruffell
Coussens
L.M.
resistance
cancer.Cancer
Cell.
27:
462-472Abstract
(800)
41Sica
Erreni
Porta
pathology.Cell.
72:
4111-4126Crossref
(352)
divided
into
M2a,
M2b,
M2c,
M2d.42Rőszer
T.
Understanding
mysterious
activation
markers
effector
mechanisms.Mediators
Inflamm.
2015:
816460Crossref
M2a
subgroup
IL-4
IL-13
produces
CD163,
CD206,
IL1Ra.42Rőszer
M2b
stimulated
complexes
bacterial
lipopolysaccharide
CD86,
IL-6,
TNF-α.42Rőszer
M2c
induced
glucocorticoids,
TGF-β
TGF-β;
addition,
this
active
against
apoptotic
cells.42Rőszer
M2d
subgroup,
IL-6
adenosine,
secretes
(high
levels
IL-10
low
IL-12)
vascular
endothelial
factor
(VEGF)
angiogenesis.42Rőszer
Some
pathways
switch.41Sica
Scholar,43Shapouri-Moghaddam
Mohammadian
Vazini
Taghadosi
Esmaeili
S.A.
Mardani
Seifi
Mohammadi
Afshari
J.T.
Sahebkar
plasticity,
health
disease.J.
Physiol.
233:
6425-6440Crossref
(1441)
Pro-inflammatory
malignant
behavior,
promotes
tumorigenesis
evasion.41Sica
Therefore,
fine-tuned
TIME.
Tumor
tissues
may
contain
mixed
populations
with
spectrum
states.
However,
review,
assumed
phenotype,
described
literature.37Belgiovine
Increased
attention
has
been
given
TAMs.
polarized
support
forming
cycle
which
(Figure
1).
This
review
discusses
during
initiation
controlled
influence
formation
TIME
based
model,
application
diagnostic
prognostic
targets.
involves
networks.38Orecchioni
phosphatidylinositol
3-kinase
(PI3K)/AKT
JAK/STAT
factors,
transducer
activator
(STAT)
family,
peroxisome
proliferator-activated
receptor-γ
(PPARγ),
interferon
polarization.44Czimmerer
Daniel
Horvath
Rückerl
Nagy
Kiss
Peloquin
Budai
M.M.
Cuaranta-Monroy
I.
Simandi
et
al.The
STAT6
mediates
direct
repression
inflammatory
enhancers
limits
macrophages.Immunity.
48:
75-90.e76Abstract
(112)
Scholar,45Vergadi
Ieronymaki
Lyroni
Vaporidi
Tsatsanis
Akt
M1/M2
polarization.J.
198:
1006-1014Crossref
(398)
Tumors
controlling
factors.
For
instance,
HPV+
head
neck
squamous
carcinoma
(HNSCC),
miR-9
was
enriched
transported
macrophages,
downregulating
PPARδ.46Tong
Mao
Xie
Sun
Wei
HPV
+
HNSCC-derived
induces
increases
radiosensitivity.Cancer
Lett.
478:
34-44Crossref
(23)
miR-451/miR-21
were
detected
primary
multiforme
(GBM)
taken
up
brain
mice,
decreasing
c-Myc
levels.
miR-21
miR-451
increased
microglia
co-cultured
GBM
heparin
reduced
effect.47van
der
Vos
K.E.
Abels
Lai
Carrizosa
Oakley
Prabhakar
Mardini
O.
Crommentuijn
M.H.
Skog
al.Directly
visualized
glioblastoma-derived
transfer
microglia/macrophages
brain.Neuro
Oncol.
58-69Crossref
(207)
prostate
(PCa),
let-7a-5p
let7-b,
-g,
-i
downregulated
integrin-β3,
causing
PCa
migration.48Ferguson
Lee
Deci
Nguyen
phenotypic
distinct
sources:
comparative
study
composition.AAPS
67Crossref
lncRNA
TUC339
hepatocellular
(HCC)
promoted
leading
cytokine
production,
compromised
phagocytosis,
decreased
co-stimulatory
molecule
macrophages.49Kogure
I.K.
Lin
W.L.
Patel
vesicle-mediated
novel
TUC339:
mechanism
cancer.Genes
4:
261-272Crossref
(239)
Scholar,50Li
Wu
HCC-derived
TUC339.Int.
2958Crossref
(36)
receptor
CXCR
chemokine
pathways,
explain
underlying
regulation.50Li
miR-21-5p
colorectal
(CRC)
cells.51Shao
Shen
al.Colorectal
cancer-derived
small
establish
premetastatic
niche
liver
metastasis.Carcinogenesis.
39:
1368-1379Crossref
(6)
CRC
lines
SW480,
SW620,
LoVo
injected
nude
mice
significantly
macrophages.
via
TLR7
pre-metastatic
survival
colonization,
ultimately
metastasis.51Shao
metabolic
enzymes.
melanoma
miR-125b-5p
lysosomal
acid
lipase
A
switching
survival.52Gerloff
Lützkendorf
Moritz
R.K.C.
Wersig
Mäder
Müller
L.P.
Sunderkötter
Melanoma-derived
educates
associated
(LIPA).Cancers.
12:
464Crossref
BMP-7,
PI3K/AKT
pathway.45Vergadi
Scholar,53Covarrubias
A.J.
Aksoylar
H.I.
Horng
Control
mTOR
signaling.Semin.
286-296Crossref
(189)
Scholar,54Zhao
Kong
F.Q.
Jie
A.D.
Y.Q.
D.D.
Z.Q.
al.Macrophage
MSR1
BMSC
osteogenic
differentiation
M2-like
activating
PI3K/AKT/GSK3β/β-catenin
pathway.Theranostics.
17-35Crossref
(37)
Phosphatase
tension
homolog
deleted
chromosome
ten
(PTEN)
inhibits
AKT
dephosphorylating
PIP3.45Vergadi
Scholar,55Lu
PTEN/PI3k/AKT
regulates
emphysematous
mice.Scand.
85:
395-405Crossref
(38)
bladder
regulated
inhibiting
PTEN
enhanced
STAT3
expression,
promoting
migration
invasion.56Lin
Yin
H.B.
X.Y.
G.M.
He
W.Y.
Gou
Bladder
cell-secreted
activates
progression.Int.
56:
151-164PubMed
miR-130b-3p,
miR-425-5p,
miR-25-3p
pathway.
epithelial-mesenchymal
transition
(EMT)
VEGF
metastasis.57Wang
Si
Cui
Qu
contribute
CXCL12/CXCR4-induced
enhancing
macrophages.Cancer
474:
36-52Crossref
(108)
Scholar,58Wang
Corrigendum
"Exosome-encapsulated
macrophages"
[Canc.
474
(2020)
36-52].Cancer
2022;
525:
200-202Crossref
circFARSA
upregulated
non-small
lung
(NSCLC)
exosomes.59Chen
PTEN/PI3K/AKT
metastasis.Cancer
Treat.
Commun.
100412Crossref
(11)
ubiquitination
degradation
PTEN,
polarization.59Chen
RNA-binding
eIF4A3
triggered
cyclization
EMT
NSCLC
cells.59Chen
STAT1/5
STAT
3/6
respectively.60Zhao
Bian
Y.Y.
Y.J.
Ma
Y.T.
Pei
Zeng
HuoXueTongFu
formula
alleviates
intraperitoneal
adhesion
SOCS/JAK2/STAT/PPAR-γ
signalling
pathway.Mediators
2019:
1769374Crossref
(14)
Scholar,61Hu
Ivashkiv
L.B.
Crosstalk
among
Jak-STAT,
Toll-like
receptor,
ITAM-dependent
activation.J.
Leukoc.
2007;
82:
237-243Crossref
(157)
members
suppressor
(SOCS)
family.60Zhao
miR-29a-3p
oral
SOCS1/STAT6
signaling.62Cai
Qiao
Gao
Oral
carcinoma-derived
subtype
mediated
exosome-enclosed
miR-29a-3p.Am.
316:
C731-C740Crossref
co-culture
system,
miR-223
cervical
(CSCC)
CSCC
creating
positive
feedback
loop.63Zhang
Qian
STAT3-miR-223-TGFBR3/HMGCS1
axis
modulates
carcinoma.Mol.
14:
2313-2331Crossref
Moreover,
repressed
TGFBR3
HMGCS1
UTRs,
resulting
anchorage-independent
growth.63Zhang
Hypoxia
stimulates
secretion,
hypoxic
trigger
HIF1α-
HIF2α-dependent
manner.64Escribese
Casas
Corbí
A.L.
Influence
oxygen
tensions
polarization.Immunobiology.
2012;
217:
1233-1240Crossref
Scholar,65Díaz-Bulnes
Saiz
M.L.
López-Larrea
Rodríguez
R.M.
hypoxia
ER
stress
res
Language: Английский
Revealing the transcriptional heterogeneity of organ‐specific metastasis in human gastric cancer using single‐cell RNA Sequencing
Haiping Jiang,
No information about this author
Dingyi Yu,
No information about this author
Penghui Yang
No information about this author
et al.
Clinical and Translational Medicine,
Journal Year:
2022,
Volume and Issue:
12(2)
Published: Feb. 1, 2022
Abstract
Background
Deciphering
intra‐
and
inter‐tumoural
heterogeneity
is
essential
for
understanding
the
biology
of
gastric
cancer
(GC)
its
metastasis
identifying
effective
therapeutic
targets.
However,
characteristics
different
organ‐tropism
metastases
GC
are
largely
unknown.
Methods
Ten
fresh
human
tissue
samples
from
six
patients,
including
primary
tumour
adjacent
non‐tumoural
organs
or
tissues
(liver,
peritoneum,
ovary,
lymph
node)
were
evaluated
using
single‐cell
RNA
sequencing.
Validation
experiments
performed
histological
assays
bulk
transcriptomic
datasets.
Results
Malignant
epithelial
subclusters
associated
with
invasion
features,
intraperitoneal
propensity,
epithelial–mesenchymal
transition‐induced
stem
cell
phenotypes,
dormancy‐like
discovered.
High
expression
first
three
subcluster‐associated
genes
displayed
worse
overall
survival
than
those
low
in
a
cohort
containing
407
samples.
Immune
stromal
cells
exhibited
cellular
created
pro‐tumoural
immunosuppressive
microenvironment.
Furthermore,
20‐gene
signature
node‐derived
exhausted
CD8
+
T
was
acquired
to
forecast
node
validated
cohorts.
Additionally,
although
anti‐NKG2A
(KLRC1)
antibody
have
not
been
used
treat
patients
even
clinical
trials,
we
uncovered
only
malignant
but
one
endothelial
subcluster,
mucosal‐associated
invariant
cells,
cell‐like
B
plasmacytoid
dendritic
macrophages,
monocytes,
neutrophils
may
contribute
HLA‐E‐KLRC1/KLRC2
interaction
cytotoxic/exhausted
and/or
natural
killer
(NK)
suggesting
novel
opportunities
GC.
our
findings
suggested
that
PD‐1
might
predict
responses
blockade
therapy
Conclusions
This
study
provided
insights
into
heterogeneous
microenvironment
tumours
organ‐specific
provide
support
precise
diagnosis
treatment.
Language: Английский
Somatic cell-derived organoids as prototypes of human epithelial tissues and diseases
Nature Materials,
Journal Year:
2020,
Volume and Issue:
20(2), P. 156 - 169
Published: Aug. 17, 2020
Language: Английский