Breast carcinoma is a global health problem that
affects women's quality of life. The World Health Organization
estimates that there are >2.26 million new cases and >684,000
deaths worldwide each year (1).
The incidence of breast carcinoma varies widely across populations
and regions and is influenced by factors such as age, ethnicity and
socioeconomic status (2). Despite
advances in diagnostic imaging and biomarker research, limitations,
such as the low sensitivity of dense breast tissue and variations
in screening accessibility, hinder its early detection (3). Furthermore, treatment resistance and
metastatic recurrence pose major challenges, emphasizing the need
for new diagnostic and therapeutic strategies. In this context,
exosomal microRNAs (miRNAs) have emerged as critical regulators of
breast carcinoma progression, with potential applications in early
diagnosis, prognosis and targeted therapy (4,5).
Previous studies have shown that exosomes are small
extracellular vesicles secreted by cells that play a key role in
intercellular communication by transporting biologically active
molecules including proteins, lipids and nucleic acids (6,7).
Among them, miRNAs, short non-coding RNA involved in
post-transcriptional gene regulation, have been identified as key
mediators of tumor growth, metastasis and therapy resistance
(8). There is growing evidence
that exosomal miRNAs secreted by breast cancer cells act as
oncogenes that promote malignant tumor behavior by inhibiting tumor
suppressor genes or activating pro-tumor signaling pathways. For
example, miR-221/222 can mediate endocrine therapy resistance
(9) and high expression of
miR-10b is closely associated with distant metastasis in breast
cancer (10). The secretion and
uptake of these exosomal miRNAs are highly specific and can reshape
the tumor microenvironment and drive disease progression.
Furthermore, their presence in biological fluids and
disease-specific expression patterns make exosomal miRNAs promising
non-invasive biomarkers for breast carcinoma (11).
Building on previous findings, recent studies have
explored the mechanistic roles of exosomal miRNAs in modulating the
tumor microenvironment (TME), facilitating drug resistance and
promoting calcification in breast carcinoma. Moreover, the
integration of nanotechnology and exosome-based drug delivery
systems, such as synthetic miRNA mimics and inhibitors, has opened
new avenues for miRNA-targeted therapies. These emerging insights
bridge the gap between basic research and clinical applications,
bringing exosomal miRNAs closer to becoming practical oncology
tools. The aim of the present review was to provide a comprehensive
overview of the role of exosomal miRNAs in breast carcinoma,
summarize past studies, highlight recent advances and assess their
potential in precision medicine. By exploring their diagnostic,
prognostic and therapeutic applications, this study contributes to
the development of novel strategies to improve breast carcinoma
management and patient prognosis.
A variety of risk factors associated with breast
carcinoma development have been identified. Germline pathogenic
variants in the BRCA1 and BRCA2 genes confer a
markedly elevated risk of breast carcinoma development (12). Endogenous hormonal factors,
particularly elevated estrogen and progesterone levels or prolonged
exposure to these hormones through early menarche (<12 years),
late menopause (>55 years), nulliparity, or advanced maternal
age at first childbirth (>30 years), have been mechanistically
linked to oncogenesis (13). In
addition, lifestyle factors, including physical inactivity, obesity
(body mass index ≥30 kg/m2), smoking and excessive
alcohol consumption (>three drinks/day), have been linked to an
increased risk of breast carcinoma development (14). Furthermore, environmental factors,
including ionizing radiation and exposure to certain chemicals, are
associated with the development of breast carcinoma (15).
The primary diagnostic modalities for the early
detection of breast carcinoma include histopathological analysis,
radiographic imaging and molecular biomarker assays. Conventional
mammography demonstrates limited sensitivity (58-72%) in dense
breast tissue (Breast Imaging Reporting and Data System density
category C/D) (16), leading to
false-negative result interpretations and diagnostic delays.
Radiographically dense parenchyma, characterized by >50%
fibroglandular tissue composition, not only obscures tumor
visualization but also demonstrates an independent correlation with
2-6-fold increased breast carcinoma risk through stromal-epithelial
interactions (17). While
population-based screening programs have reduced mortality rates by
15-40%, they incur substantial healthcare expenditures and induce
screening-related anxiety (18).
Moreover, equitable implementation remains challenging in
low-resource settings due to infrastructure limitations and trained
personnel shortages, compounded by heterogeneous international
guidelines. Therefore, current early diagnostic technologies for
breast cancer are limited by imaging sensitivity and the stability
of molecular markers. Future diagnostic strategies should be a
combination of imaging and liquid biopsy models, in which exosomal
miRNAs are expected to be a key bridge between the two.
Exosomes are a class of small membranous vesicles
secreted by cells, usually 30-150 nm in diameter and belong to a
subgroup of extracellular vesicles. They are found in various body
fluids, including blood, saliva and urine and are secreted by a
wide range of cell types (19).
Proteomic profiling has revealed the complexity of the exosomal
cargo, including thousands of proteins, various miRNAs and lipids.
The protein composition of exosomes varies depending on their
cellular origin and includes cytoplasmic enzymes, fusion proteins,
membrane transporter proteins, molecular chaperones and structural
proteins (20). The main function
of exosomes is to mediate intercellular communication and influence
the function of recipient cells. In breast carcinoma, exosomes have
been shown to be involved in tumor progression, metastasis and
immune evasion.
Studies have revealed several key mechanisms
underlying exosome formation, including endosomal sorting complexes
required for transport (ESCRT)-dependent and ESCRT-independent
pathways, the role of quadruple transmembrane proteins and the
formation of atypical exosomes (21,22). Fig.
1 illustrates the process of exosome formation.
Exosome formation primarily relies on the ESCRT
mechanism. This process begins with t early endosomes, which are
formed through the endocytosis of the plasma membrane. As the
endosomes mature into multivesicular bodies (MVBs), their membrane
folds inwards to form intraluminal vesicles (ILVs). These ILVs
become exosomes when MVBs fuse with the plasma membrane and are
released into the extracellular space (23).
Exosomes are rich in cholesterol,
phosphatidylcholine, phosphatidylserine and other lipids that are
not only involved in exosome biosynthesis, but also affect their
uptake and function (24).
Intracellular cholesterol levels regulate exosome release through
the PI3K/AKT signaling pathway: elevated intracellular cholesterol
inhibits this pathway, resulting in decreased exosome release,
whereas decreased intracellular cholesterol activates this pathway
and increases exosome release (25). Additionally, neutral
sphingomyelinase 2 promotes ILV and exosome formation by converting
sphingomyelin into sphingosine. Moreover, the autophagy-related
protein LC3 promotes sphingosine-mediated ILV formation by
recruiting the nSMase activator onto endosomal membranes (26).
Tetraspanins, such as CD9, CD63 and CD81 not only
play crucial roles in endosomal membrane invagination and ILV
formation but also influence exosome stabilization and facilitate
cell-cell communication (27). In
terms of cargo sorting, tetraspanins can recognize and bind to
specific proteins and nucleic acids and regulate the cargo loading
of exosomes (28).
Studies have revealed some mechanisms underlying
atypical exosome formation. For instance, certain cell types can
generate exosomes via the Golgi pathway or calcium-dependent
secretory autophagy (29). In
addition, some viruses can hijack the exosome formation mechanism
of host cells for their propagation (30).
Exosomal miRNAs are a class of small non-coding RNAs
that are usually 18-22 nucleotides in length and are encapsulated
in exosomes. These miRNAs are involved in the post-transcriptional
regulation of gene expression by binding to complementary sequences
on target miRNAs, leading to miRNA degradation or translational
repression (31,32). Exosomal miRNAs are selectively
packaged into exosomes, which allows them to be protected from
degradation by RNases and transported over long distances through
body fluids, such as blood, urine and milk (19). This intercellular communication
mechanism is critical for various physiological and pathological
processes including cancer progression, immune regulation and
tissue homeostasis (33). This
property makes exosomal miRNAs potential biomarkers for disease
diagnosis and prognosis as well as possible targets for the
treatment of cancers, including breast carcinoma.
Exosomal miRNA biosynthesis is a multi-step process
that involves the transcription, processing and selective packaging
of miRNAs into exosomes. Studies have shown that precursor miRNAs
(pre-miRNAs) associated with processing complexes such as Dicer,
Argonaute 2 and TAR RNA-binding protein can be detected in exosomes
derived from breast carcinoma cells. These pre-miRNAs are further
processed into mature miRNAs within exosomes, thereby establishing
a new mechanism for the integration of miRNAs into exosomes
(34). Typically, miRNA
biosynthesis begins in the nucleus, where miRNA genes are
transcribed by RNA polymerase II to produce primary miRNAs
(pri-miRNAs). These pri-miRNAs are then processed by the
Drosha-DGCR-8 complex into pre-miRNAs, which is a critical step in
the miRNA maturation process (35). The pre-miRNAs are transported from
the nucleus to the cytoplasm via Exportin-5, a transport protein
that facilitates the movement of pre-miRNAs across the nuclear
envelope. In the cytoplasm, Dicer enzymes further process the
pre-miRNAs into mature miRNA duplexes (36). This step is essential for the
functionalization of miRNAs so that they can be integrated into
exosomes. Fig. 2 depicts miRNA
biosynthesis.
Several mechanisms have been proposed to explain how
specific miRNAs are categorized into exosomes. One of the key
mechanisms involves the recognition of exosomal miRNA sequences or
motifs by RNA-binding proteins such as hnRNPA2B1, Y-box-binding
protein 1 and synaptotagmin-binding cytoplasmic RNA-interacting
protein (SYNCRIP). SYNCRIP is involved in the exosomal partitioning
of miRNAs by recognizing specific sequences such as the hEXO motif,
which enhances miRNA loading into exosomes. This process is crucial
for cell-cell communication and is regulated by the NURR domain of
SYNCRIP, which binds to miRNA targets with high affinity (37,38). HnRNPA2B1 binds to specific
sequence motifs in miRNAs, thereby controlling their loading into
exosomes. Its binding activity is influenced by SUMOylation and
alterations in either the motif or hnRNPA2B1 expression levels can
modulate the efficiency of miRNA sorting. Notably, hnRNPA2B1 is
essential for the selective sorting of miRNAs, such as miR-486a-5p,
which has cardioprotective effects (39,40). YBX 1 also facilitates the sorting
of miRNAs (such as miR-223) into exosomes by binding to specific
sequence motifs. It shuttles between different cellular
compartments, suggesting its dynamic role in miRNA sorting and
exosome formation (41). In
addition, the ESCRT machinery and associated proteins such as ALIX
and TSG101 play key roles in exosome biosynthesis and miRNA
integration. The ESCRT machinery and related proteins, such as ALIX
and TSG101, promote the budding of ILVs into MVBs. miRNAs are
selectively sorted into ILVs during this process, which is followed
by the formation of MVBs. When MVBs fuse to the cell membrane, ILVs
are released as an exosome (42,43).
Studies have also highlighted the role of
post-transcriptional modifications, such as uridylation and
adenylation, in the sorting of miRNAs into exosomes. For example,
the addition of uridine residues to the 3'terminus of miRNAs
enhances their incorporation into the exosomes (44). Furthermore, the lipid composition
of the exosomal membrane, particularly in the presence of ceramide,
has been implicated in the sorting process (45). Once packaged into exosomes, miRNAs
are protected from degradation by RNases and can be transported to
recipient cells via circulation or other body fluids. After uptake
by recipient cells, exosomal miRNAs regulate gene expression and
influence various cellular processes, including proliferation,
apoptosis and metastasis, thus playing an important role in breast
carcinoma progression and therapy resistance (46).
A variety of miRNAs have been identified as key
factors in the development and progression of breast carcinoma.
These oncogenic miRNAs exert their oncogenic effects through a
variety of mechanisms, including the repression of tumor suppressor
genes, activation of pro-tumor signaling pathways and promotion of
epithelial-mesenchymal transition (47). High expression of oncogenic miRNAs
is associated with poor prognosis and advanced disease stage,
highlighting their potential as therapeutic targets and diagnostic
biomarkers for breast carcinoma. Table I lists miRNAs that contribute to
breast carcinoma development and progression (9,10,48-60).
Calcification, particularly microcalcification, is a
common radiological feature observed in mammographic imaging of
breast carcinoma. Calcifications are generally categorized into two
types: Macrocalcifications and microcalcifications.
Macrocalcifications are larger, coarser calcium deposits that are
typically benign and often related to aging, inflammation, or past
injuries. Radiologically, microcalcifications appear as fine,
granular specks, while macrocalcifications present as larger, often
round or irregular, dense opacities. Microcalcifications are
predominantly composed of hydroxyapatite, consisting of small
calcium phosphate deposits within the breast tissue and are often
associated with malignant lesions (94). Their chemical composition,
particularly the carbonate content and protein-matrix ratio,
correlates with the grading of pathological breast carcinoma and
may serve as a diagnostic and prognostic indicator (95). These calcifications are thought to
originate from cellular debris, necrosis, or active mineralization
processes mediated by tumor cells and the TME.
Exosomal miRNAs have been increasingly recognized as
important regulators of tumor progression and the TME. Although
there have been few direct studies on the relationship between
exosomal miRNAs and breast carcinoma calcification in existing
literature, the following potential mechanisms can be hypothesized
based on their known biological functions and associated signaling
pathways.
Downregulation of miR-30b has been observed in
recurrent breast carcinoma, whereas overexpression of its target
gene, CCNE2, may influence calcium channel activity through
the PI3K/AKT signaling pathway (99). Disruption of calcium homeostasis
via this mechanism may contribute to the formation of
microcalcifications. Additionally, miR-16 (103) exhibits antiangiogenic properties
by inhibiting the expression of vascular endothelial growth factor.
Impaired angiogenesis may result in localized hypoxia, which
activates hypoxia-inducible factors that subsequently upregulate
the expression of calcium-binding proteins.
Recent dual strategy advances in miRNA-based
therapeutics have emphasized the use of synthetic miRNA mimics to
restore tumor suppressor miRNAs. For example, the use of miRNAs
from the let-7 family (104) and
anti-miRNA oligonucleotides to inhibit oncogenic miRNAs such as
miR-21 (105) and miR-155
(106). A phase I clinical trial
demonstrated that MRX34, a liposomal miRNA-34a mimic, exhibited
antitumor activity in metastatic breast carcinoma by targeting the
PD-L1 and MET pathways, although challenges in delivery efficiency
remain (107,108). Novel nanoparticle-based delivery
systems such as exosome-like vesicles can be effective in improving
the stability and tumor targeting of miRNA analogs in TNBC models
(109). By contrast, anti-miRNA
inhibitors such as anti-miR-21 and anti-miR-155 oligonucleotides
inhibit oncogenic miRNAs. Preclinical studies have shown that
anti-miR-155 acts synergistically with immune checkpoint inhibitors
to reprogram the TME, reduce immunosuppressive myeloid cell
infiltration and enhance T cell responses in metastatic models
(110).
The synergistic effects of miRNA therapeutics with
conventional therapies have gained increasing attention. Hyaluronic
acid-based nanocarriers can target CD44-overexpressing TNBC cells
and efficiently co-deliver doxorubicin (DOX) and miR-542-3p. This
system provides an effective strategy for reversing TNBC resistance
by enhancing intracellular drug accumulation, upregulating the
expression of the p53 tumor suppressor protein, directly
downregulating the apoptosis inhibitory protein survivin,
overcoming chemotherapy resistance through multiple pathways and
markedly inducing synergistic apoptosis in vitro (111). Functional exosome-mediated
co-delivery system of DOX and hm-miR159 provides a promising and
innovative combination therapy to address the challenge of TNBC
chemoresistance (112).
Furthermore, emerging strategies that combine miRNA inhibitors with
immune checkpoint inhibitors can reprogram the TME in metastatic
breast carcinoma, thus offering a potentially powerful avenue for
enhancing immunotherapeutic efficacy (113).
Recent progress in the targeted delivery of
therapeutic miRNAs has greatly advanced their therapeutic
potential. In terms of carrier design, lipid nanoparticles and
exosome-mimetic vesicles have emerged as prominent platforms for
enhancing the stability, bioavailability and tumor-targeting
capability of therapeutic miRNAs. For instance, Ohno et al
(114) engineered exosomes
derived from HEK293 cells by displaying the GE11 peptide via
a Lamp2b fusion protein on their surface, constructing engineered
exosomes that specifically recognize EGFR. These exosomes
efficiently delivered miRNAs to EGFR-positive breast tumors in
vivo and markedly suppressed tumor growth. Similarly,
RGD-modified exosomes, which target αvβ3 integrin, have been used
to co-deliver miR-34a to TNBC. This approach not only directly
induces tumor cell apoptosis but also remodels the
immunosuppressive microenvironment by downregulating PD-L1, thereby
enhancing CD8+ T cell infiltration (115,116). Although several miRNA
formulations have entered early phase clinical trials, challenges
remain regarding delivery efficiency, immune tolerance and
large-scale production. Continued optimization of targeted delivery
systems is therefore crucial for the successful clinical
translation of miRNA-based therapeutics.
Exosomes carry various biomarkers associated with
breast carcinoma, such as carcinoembryonic antigen and carbohydrate
antigen 125, which have potent therapeutic diagnostic properties
(117). A systematic review
conducted up to March 2023 analyzed 46 articles and found that
exosomal miRNAs were markedly associated with the
clinicopathological features of breast carcinoma (118). The present review emphasized
that exosomal miRNAs such as miR-16, miR-21 and miR-155, have been
analyzed in at least three studies and are suitable for selection
as potential biomarkers. These miRNAs could provide information
regarding early diagnosis, disease progression, recurrence,
treatment response and metastasis. Analyzing exosomal miRNAs in
blood samples is a simple and noninvasive method that is important
for the early detection of breast carcinoma (118). A study published in 2024
explored the advancement of serum exosomal miR-21 as a molecular
diagnostic marker for breast carcinoma and its efficacy was
assessed for the early detection and clinical diagnosis of breast
carcinoma (119). However, its
application in early diagnosis presents several challenges. The
primary bottleneck is that the identification technology itself is
complex, time-consuming and expensive. In addition, its diagnostic
specificity must be improved to accurately differentiate breast
cancer from other malignancies. Finally, whether serum or plasma
should be preferred for cancer detection using exosomal miRNAs
needs to be studied further.
Exosomal miRNAs have been recognized as important
biomarkers for the prognostic assessment of breast carcinoma
because of their high stability and specificity. For example,
miRNA-373 is a specific biomarker for TNBC and its expression level
correlates with the degree of malignancy and prognosis of breast
carcinoma (120). Similarly, the
expression levels of miR-1246 and miR-155 are markedly elevated in
drug-resistant breast carcinoma cells compared to drug-sensitive
cells and this differential expression has been associated with
poor progression-free survival and overall survival in patients
(121). Additionally, dynamic
monitoring of exosomal miRNAs (such as miR-141, miR-182 and
miR-183) during neoadjuvant therapy can predict pathologic complete
response, thereby enabling more informed and personalized treatment
decisions (122).
Breast carcinoma remains an enormous global health
challenge that requires the continuous exploration of novel
diagnostic and therapeutic strategies. Exosomal miRNAs have emerged
as pivotal regulators of breast carcinoma pathogenesis, providing
valuable insights into tumor progression, metastasis and therapy
resistance. The present study reviewed the role of exosomal miRNAs
in breast carcinoma, highlighting their dual functions as oncogenic
drivers and tumor suppressors, as well as their utility as
diagnostic biomarkers and therapeutic potential. In the present
review, the dual oncogenic and inhibitory roles of exosomal miRNAs
were described, focusing on their multilevel regulatory mechanisms
in TME, drug tolerance and pathological calcification. Based on the
analysis of relevant literature, the present review proposed a
conceptual model of exosomal miRNA calcification axis, which
suggests that exosomal miRNAs may play a bridging role in breast
cancer calcification and progression by regulating cell metabolism,
immune inflammatory response and osteogenic signaling pathways.
However, there are several challenges and opportunities in
translating these findings into clinical practice. For example,
there is no perfect methodology for the extraction and purification
of exosomal RNAs. The differences in miRNA expression levels
between studies may be related to the heterogeneity of sample
sources, analytical methodologies and patient populations. Further
studies are needed to fully elucidate the role of exosomal miRNAs
in breast carcinoma calcification. The combination of advanced
imaging techniques, such as high-resolution mammography and
molecular imaging, as well as exosomal miRNA analysis, may provide
new insights into the mechanisms of calcification and its clinical
significance. Additionally, the development of exosomal miRNA-based
therapeutics may provide new avenues for the prevention and
treatment of breast carcinoma calcification. Overall, the present
review provided a systematic framework for the study of exosomal
miRNAs in breast cancer and demonstrates their potential value in
pathological calcification, precise diagnosis and treatment. In the
future, with technological progress and multidisciplinary research,
exosomal miRNAs are expected to become an important breakthrough in
understanding the complex biology of breast cancer and achieving
personalized treatment.
Not applicable.
ZMC was responsible for research conceptualization,
original draft preparation and reviewing the entire manuscript. PH
conducted supplementary analysis, responded to reviewers' comments
and updated and integrated relevant literature during the revision.
DYY performed calibration of the full text, organized the logical
flow and improved the language. SL contributed to the conception
and design of the study, participated in developing the manuscript
framework, critically revised the manuscript for important
intellectual content and provided final approval of the version to
be published. SQC guided and oversaw the entire research process,
supervised the completion of the present review and provided final
approval of the manuscript. Data authentication is not applicable.
All authors read and approved the final manuscript.
Not applicable.
Not applicable.
The authors declare that they have no competing
interests.
During the preparation of this work, DeepSeek was
used to provide suggestions for the logical organization and
language polishing of some paragraphs and ChatGPT was utilized to
assist in optimizing sentence expressions and enhancing text
fluency. Using these tools, the content was reviewed sentence by
sentence. The accuracy of the professional concepts was verified
and the expressions generated by the AI were adjusted to conform to
the research and the writing style of the authors. The originality
and scientific nature of the content were ensured and full
responsibility for the content of the publication was assumed by
the authors.
Not applicable.
No funding was received.
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