Prostate cancer (PCa) is a leading cause of
cancer-related deaths in men worldwide (1). As medical technology evolves,
approaches for treating PCa are being regularly refined (2). Metastatic castration-resistant PCa
(mCRPC) poses significant therapeutic challenge (3). Current treatment modalities, including
hormone therapy, chemotherapy, and radiotherapy, show limited
effectiveness against mCRPC and frequently cause considerable
adverse effects (4). The
progression of metastatic PCa is influenced by multiple factors
such as tumor load, molecular traits, and resistance to therapies
(5).
Proteins located on the cell surface serve as
specific markers for tumors and are increasingly recognized as key
targets for targeted therapies in PCa (6). Research indicates that proteins such
as prostate-specific membrane antigen (PSMA) are significantly
overexpressed in PCa cells, making them promising options for
targeted treatment (7). These
proteins play a role in tumor proliferation and spread, as well as
in mechanisms that allow tumors to evade the immune system
(8). Focusing on these surface
proteins can enhance treatment efficacy and minimize adverse
effects (9).
The shortcomings of conventional treatment
strategies have led to the development of targeted therapies.
Although chemotherapy and radiation therapy continue to play
crucial roles in PCa management, their effectiveness is frequently
hindered by variations within tumors and resistance to medications
(10). Recently, therapies that
focus on cell surface proteins have gained attention as innovative
treatment options (11). This
strategy not only targets particular cancer cells but also enhances
the precision of drug delivery and increases the availability of
medications in the body (12).
Consequently, the management of mCRPC must differ from that of
hormone-sensitive diseases (13,14),
necessitating personalized strategies that target specific cell
surface markers [such as PSMA and six-transmembrane epithelial
antigen 1 (STEAP1)] and often employ combination therapies to
overcome resistance (15-17).
This review aims to comprehensively outline the
advancements in targeted treatments associated with PCa cell
surface proteins, focusing on the underlying molecular processes,
therapeutic approaches, and their clinical relevance. By examining
various strategies for targeted therapy and their implementation in
clinical settings, it seeks to offer improved treatment
alternatives for patients with PCa and inform future research
pathways.
mCRPC represents a distinct and advanced stage of
PCa characterized by disease progression despite androgen
deprivation therapy (18). The
management of mCRPC necessitates a differentiated approach compared
to hormone-sensitive PCa due to its unique biological behavior,
resistance mechanisms, and therapeutic vulnerabilities (19). Key challenges in mCRPC include
persistent androgen receptor (AR) signaling, intratumoral
heterogeneity, adaptive immune evasion, and the emergence of
treatment-resistant clones (20).
Current standard therapies for mCRPC, including
novel hormonal agents (such as enzalutamide and abiraterone),
chemotherapies (for example docetaxel), and radiopharmaceuticals
(such as 177Lu-PSMA-617), have demonstrated survival
benefits (21). However, their
efficacy is often limited by primary or acquired resistance, which
is driven by AR alterations, neuroendocrine differentiation, and an
immunosuppressive tumor microenvironment (TME) (22).
Therapeutic differentiation in mCRPC involves
several key approaches: i) Molecular stratification based on
genomic alterations (for example BRCA1/2 and PTEN), AR variant
expression, and PSMA avidity (23);
ii) sequential and combination therapies that leverage synergistic
effects between AR-directed agents, radioligands, immunotherapies,
and targeted agents (24); and iii)
liquid biopsy and biomarker monitoring utilizing circulating tumor
cells (CTCs) and cell-free DNA to track clonal evolution and
treatment response (25). Emerging
evidence supports the integration of multi-omics profiling and
artificial intelligence (AI) to guide personalized therapy in
mCRPC, emphasizing the necessity for dynamic treatment adaptation
in response to evolving tumor biology (26).
PSMA is a glycoprotein that spans the cell membrane
and is predominantly found in PCa cells, especially in aggressive
forms, such as metastatic, poorly differentiated, and
castration-resistant variants, where its elevated presence often
correlates with increased tumor severity (27). Although normal tissues, including
parts of the urinary system and certain nerve tissues, exhibit
lower PSMA levels, PSMA is markedly overexpressed on cancer cell
surfaces (6). This overexpression
plays a crucial role in tumor cell growth and survival within the
TME, and possibly in promoting new blood vessel formation in
tumors. The distinct expression pattern of PSMA, characterized by
high levels in tumors and minimal expression in non-tumor tissues,
makes it a promising therapeutic target (6). Treatment with radiopharmaceuticals,
such as Lu-PSMA-617, can effectively destroy cancer cells while
sparing healthy tissue (28).
Additionally, PSMA is not exclusive to PCa cells; it is also
present in some newly formed blood vessels associated with tumors
(29). The use of radiolabeled
compounds, such as 68Ga-PSMA-11, enhances the diagnostic precision
for detecting metastatic cancer (30). However, PSMA expression shows
intra-and intertumoral heterogeneity, which may lead to varying
treatment responses (31). In
addition, its low expression in normal tissues, such as the
salivary glands and kidneys, may cause off-target toxicity,
requiring close monitoring during treatment (32).
STEAP1 is frequently overexpressed in PCa,
especially in advanced and metastatic forms, with >85% of
prostate tumors exhibiting this expression (33). By contrast, normal tissues show
minimal expression, highlighting their potential as significant
targets for therapy (34). This is
further supported by the link with biomarkers found in
STEAP1-positive extracellular vesicles, which can assist in both
diagnosis and prognosis (35). As a
cell surface antigen, STEAP1 plays a role in various aspects of
tumor development, including cell growth, migration, survival,
intercellular communication, and metal metabolism (36). It also enhances tumor cell functions
through pathways such as PI3K/Akt and is linked to aggressive
characteristics such as invasion and metastasis (37). Previous research on PCa models have
demonstrated that STEAP1 exerts antitumor effects when used in
chimeric antigen receptor T (CAR-T) cell therapy (38). When combined with localized IL-12
therapy, it was shown to improve treatment effectiveness by
modifying the TME and countering antigen escape (29). Moreover, clinical trials are being
conducted using STEAP1-targeted T-cell inducers and antibody-drug
conjugates (ADCs) (39). In
summary, STEAP1 is a promising target in PCa; however, its
expression dynamics in advanced cancer and association with metal
metabolism need to be further elucidated.
Additional important proteins on cell surfaces
include trophoblast cell-surface antigen 2 (TROP-2), a
transmembrane protein frequently found at elevated levels in
various cancers, including PCa, making it a promising candidate for
ADCs (40). Ongoing clinical trials
are assessing the effectiveness of sacituzumab-govitecan in
treating urothelial carcinoma and PCa, with supportive evidence of
its anticancer properties emerging from animal studies (41). Likewise, prostate stem cell antigen
(PSCA) is present in ~90% of PCa cases and is associated with tumor
aggressiveness, leading to the development of targeted
immunotherapies such as CAR-T cells and ADCs (42). Nonetheless, obstacles such as the
immunosuppressive nature of the TME, potential off-target effects,
and variability in expression levels may pose challenges (43). Furthermore, delta-like ligand 3
(DLL3) is overexpressed in neuroendocrine PCa (NEPC), linking it to
tumor severity and patient prognosis (44). Monoclonal antibodies and
radioimmunotherapy, including 177Lu-labeled antibodies, have
demonstrated preclinical promise. However, concerns regarding their
expression in non-neuroendocrine tumors and patient variability
must be resolved (45). In
addition, emerging targets, such as cadherin EGF LAG seven-pass
G-type receptor 3 (CELSR3) and glypican-3 (GPC3), have also
attracted attention. CELSR3 is highly expressed in NEPC and is
involved in the regulation of cell polarity and migration through
the Wnt/PCP signaling pathway; its overexpression is associated
with tumor invasiveness. Research has explored its potential as a
target for CAR-T cells and ADC (46). GPC3 is upregulated in
castration-resistant PCa and promotes tumor growth by regulating
the Hh signaling pathway. Preclinical studies have shown that
GPC3-targeting antibodies can inhibit tumor progression, and phase
I clinical trials are underway (47) (Table
I).
The drug 177Lu-PSMA-617 is a radioligand used for
mCRPC that targets PSMA to deliver the radioactive isotope 177Lu
directly to cancer cells, leading to their destruction (48). Findings from the VISION trial
indicated that it notably enhanced both overall survival and
quality of life in patients, and its favorable tolerability has
established it as a standard treatment for mCRPC (49). Currently, there is growing interest
in exploring novel radioactive isotopes, such as 161Tb-PSMA, which
may offer promising avenues for combination therapies (50). Clinical studies have demonstrated
the safety and effectiveness of 161Tb-PSMA, suggesting that its use
along with 177Lu-PSMA-617 could potentially amplify therapeutic
outcomes (51). Overall,
radioligand therapy (RLT), such as 177Lu-PSMA-617, has been
demonstrated to significantly improve survival in patients with
mCRPC; however, drug resistance and heterogeneous expression remain
major challenges.
ADCs are designed to transport cytotoxic medications
directly to cancer cells using antibodies that specifically attach
to tumor antigens (52). This
targeted approach enhances the therapeutic effectiveness while
minimizing harm to healthy tissues (53). PSMA is recognized as a
well-established therapeutic target that facilitates efficient
delivery of ADCs. Clinical studies have indicated favorable results
and manageable side effects in patients with mCRPC, including a 50%
or more reduction in prostate-specific antigen levels during
second-line treatments, along with some instances of complete
responses (54). Additionally,
TROP-2, which is prominently expressed in metastatic PCa and linked
to poor prognosis, represents another significant target for ADCs,
showing encouraging clinical results (40). In contrast to conventional
chemotherapy, the targeted nature of ADCs mitigates widespread
toxicity and drug resistance (55).
ADCs achieve precise delivery; however, the internalization
efficiency of the target, linker stability, and off-target toxicity
limit their widespread applications.
BiTEs are designed to bind both tumor-specific
antigens and CD3 receptors on T cells, thereby effectively linking
T cells to cancer cells (56). This
connection not only activates T cells to kill tumor cells but also
facilitates the direct destruction of the tumor. For instance, AMG
160, which targets PSMA, elicits cytotoxic effects in PCa, whereas
BiTEs that target STEAP1 further improve therapeutic outcomes
(57). In addition to their direct
effects on tumors, BiTEs enhance the immune response against cancer
by promoting the release of cytokines from activated T cells,
which, in turn, activate nearby immune cells (58). Although the combination of BiTEs
with immune checkpoint inhibitors has the potential to address the
immunosuppressive environments found in ‘cold tumors’, such as PCa,
their application in clinical settings is hindered by issues such
as cytokine release syndrome (CRS) and other immune-related adverse
effects (irAEs) (59). BiTEs
activate T cells with strong cytotoxic effects; however, CRS and
neurotoxicity limit their clinical application.
CAR-T cell therapy is a groundbreaking
immunotherapeutic approach. Preclinical research has demonstrated
that CAR-T cells targeting the STEAP1 antigen in PCa cells can
effectively identify and eliminate tumor cells (60). Additionally, CAR-T therapy targeting
PSMA has been proven effective in patients with metastatic disease.
Studies conducted in vitro and in animal models revealed
enhanced anti-tumor properties, particularly when combined with
chemotherapy agents (60,61). Nonetheless, obstacles, such as the
immunosuppressive nature of the TME and the mechanisms of antigen
escape, hinder their overall effectiveness, leading to the
exploration of dual CAR-T cells paired with IL-23 antibodies to
enhance their proliferation and functionality (62). NEPC is a particularly aggressive
variant that poses distinct treatment challenges owing to the
presence of specific antigens. CAR-T cells targeting
carcinoembryonic antigen-related cell adhesion molecule 5 have
shown significant cytotoxic potential in preclinical studies,
thereby addressing some of the shortcomings of traditional
therapies (63). Although CAR-T has
made breakthroughs in hematologic tumors, its efficacy is limited
in solid tumors such as PCa, mainly due to: i) Immunosuppressive
cells [such as myeloid-derived suppressor cells (MDSCs)] and
factors (such as TGF-β) in the TME inhibiting T-cell function
(64); ii) physical barriers such
as fibrotic stroma hindering T-cell infiltration (65); and iii) antigen heterogeneity
leading to antigen escape (66). By
contrast, hematological tumors often exhibit more uniform antigen
expression and a less immunosuppressive microenvironment, which
facilitates the efficacy of CAR-T therapy (67). CAR-T cells exhibit potential in PCa,
however the obstacles presented by the solid TME and antigen escape
limit their efficacy, requiring combined strategies to overcome
this bottleneck.
BiTEs and CAR-T cells are both T cell-directed
therapies; however, each has advantages and disadvantages. BiTEs
are easy to prepare, act quickly, and can be easily combined with
immune checkpoint inhibitors (57);
however, they have a short half-life and require continuous
infusion, and the risk of CRS is high (59). Although CAR-T is durable and can
expand in vivo, it is complex to prepare, costly, and easily
inhibited by the TME in solid tumors (62,65).
In summary, BiTEs offer a cost-effective, rapid response option for
short-term intervention, whereas CAR-T therapy provides durable,
personalized control, but faces manufacturing and TME challenges in
PCa. The choice should be guided by treatment goals and
patient-specific factors.
The use of nanoparticle-based drug delivery systems,
which include functionalized nanoparticles, such as gold and
polymeric carriers, allows for the precise targeting of cancer
cells that express PSMA (68). This
approach significantly improves drug bioavailability and can
decrease systemic toxicity by 50-70% (68). These systems enhance the solubility
and circulation duration of drugs, encourage tumor-specific
accumulation to enhance effectiveness, and minimize side effects,
while enabling treatment response monitoring through imaging
methods (69). Furthermore,
ultrasound-responsive nanocarriers are effective in delivering
small interfering RNA to suppress gene expression in PCa cells
(70). Nonetheless, the transition
to clinical applications encounters obstacles, such as
biocompatibility, immune reactions, and mechanisms of drug
resistance. Nanocarriers enhance drug targeting and
bioavailability; however, biocompatibility, immunogenicity, and
large-scale production are challenges for translation.
Different treatment strategies have distinct
advantages and disadvantages. RLT (such as 177Lu-PSMA-617) has a
high response rate in PSMA-high-expressing mCRPC but may cause
myelosuppression (71); ADCs have
strong targeting but carry the risk of off-target toxicity
(72); BiTEs activate T cells
rapidly but can easily lead to cytokine release syndrome (73); and CAR-T therapy has been successful
in hematologic neoplasms but is limited in solid tumors such as PCa
owing to TME suppression, resulting in limited efficacy (74). Longitudinal comparisons showed that
both BiTEs and CAR-T cells are T cell-directed therapies, but BiTEs
are cost-effective, quick to deploy, and suitable for short-term
interventions, while CAR-T modifications are durable but complex to
manufacture, making them more suitable for individualized long-term
treatment (75) (Fig. 1).
The reduction in antigen expression and the
phenomenon of antigen escape are significant factors in how tumor
cells avoid detection by the immune system (76). This downregulation is often
associated with various strategies employed by tumor cells to
elicit immune responses. In PCa cells, the levels of PSMA and
similar antigens frequently decrease due to factors such as genetic
alterations, epigenetic modifications, and the effects of the TME
(77). Lower PSMA expression can
lead to a diminished response to immunotherapy, allowing tumor
cells to evade immune monitoring (78). Furthermore, decreased antigen
expression can hinder T-cell activation, thus impairing the overall
immune response (79). Research
indicates that antigen escape is intricately linked to the
heterogeneity of tumor cells, where variations in antigen
expression among different tumor cells contribute to the complexity
and variability of immune responses against tumors (80). To cope with antigen downregulation,
multitarget CAR-T cells (such as PSMA and STEAP1) or combined
epigenetic regulators (such as HDAC inhibitors) can be used to
stabilize antigen expression (81,82).
The diversity of PCa tumors significantly
contributes to their ability to evade the immune system (83). Within PCa, various tumor cell
subtypes may exhibit resistance to immunotherapy, whereas others
respond positively to such treatments (84). This variability leads to differences
in antigen expression, enabling some tumor cells to avoid immune
detection by reducing or completely losing expression of crucial
antigens (85). Additionally,
elements within the TME that inhibit immune function, including
tumor-associated macrophages and MDSCs, further facilitate the
immune evasion of these tumor cells, intensifying the heterogeneity
of the tumors (86-88).
Consequently, investigating combination therapies aimed at
enhancing immune responses and improving treatment effectiveness
against tumors is critically important (89).
Management of the immunosuppressive tumor
environment is a crucial focus in PCa research. Factors associated
with tumor-induced immunosuppression, such as S100A4, play a
significant role in the initiation and progression of PCa (90). This protein is elevated in numerous
tumors and is associated with unfavorable outcomes in patients with
PCa (91). The use of anti-S100A4
antibodies could potentially counteract this immunosuppressive
effect in PCa, leading to improved treatment responses (92). Targeting S100A4 with anti-S100A4
antibodies may effectively reverse the immunosuppressive state of
PCa, thereby improving patient response rates to treatment
(90). The combination of
immunomodulatory approaches and targeted therapies has great
potential. For example, YY001, a novel EP4 antagonist, is vital for
shaping the immune landscape of PCa (93). Research indicates that YY001 can
reduce the differentiation and activity of MDSCs, while promoting
T-cell growth and antitumor functions (93). By modulating cytokine and chemokine
levels, YY001 can effectively restore a more favorable immune
environment within tumors, functioning synergistically with
anti-PD-1 antibodies to significantly enhance antitumor immune
activity (93). The effectiveness
of this combined approach highlights the potential of integrating
immunomodulatory and targeted therapies for PCa treatment.
The combination and evaluation of multi-omics
information, including genomics, transcriptomics, and proteomics,
have enabled the discovery of novel biomarkers and treatment
targets for PCa (101). Notably,
mutations in genes such as BRCA1/2 are significantly linked to
patient outcomes. Treatments targeting these mutations, such as
PARP, have demonstrated efficacy (102). Molecular subtyping allows for the
identification of high-risk patients and enhances the likelihood of
successful treatment outcomes. Advanced AI techniques, such as deep
and machine learning, aid in the accurate analysis of biomarkers
and refinement of personalized treatment strategies (103). In addition, tracking CTCs is
essential. The number of CTCs and the expression of surface
proteins (such as PSMA and STEAP1) can indicate tumor severity,
prognosis, and response to therapy (104), whereas liquid biopsy methods can
efficiently isolate CTCs for ongoing clinical assessment (105). The management of mCRPC should be
individualized based on several key factors, including i) tumor
burden and metastatic sites; ii) expression levels of cell surface
targets (such as PSMA PET/CT standardized uptake value); iii)
genome characteristics (such as DNA repair defects); and iv) prior
treatment history (106-108).
Studies have shown that PSMA-targeted therapy can achieve a
response rate of 60-70% in patients with mCRPC and high PSMA
expression, while the effect is limited in patients with low
expression, emphasizing the importance of target assessment before
treatment (109-111).
Investigation of innovative surface proteins,
including CELSR3, which is notably overexpressed in NEPC, is
crucial for controlling cell growth and movement (46). Additionally, GPC3, which is linked
to tumor aggressiveness, opens up new possibilities for the
targeted treatment of PCa. CAR-T cells targeting CELSR3 have
demonstrated significant tumor-suppressive activity in
patient-derived xenograft models (37), while GPC3-targeted ADCs showed
promising results in phase I trials for liver cancer, and its trial
for PCa has been initiated (112).
Concurrently, gene therapy-utilizing carriers, such as
poly(lactic-co-glycolic acid) (PLGA) nanoparticles, can effectively
transport nucleic acid medications aimed at PSMA (47). Treatment efficacy can be enhanced by
employing a multifaceted approach that influences tumor dynamics
and encourages immune cell infiltration (113). Advances in nanotechnology have
enabled the development of immunotherapies. Functionalized
nanoparticles can transport immunomodulatory agents and checkpoint
inhibitors directly to tumor locations, enhancing biodistribution
and facilitating synergistic combination therapies through the
simultaneous delivery of various therapeutic compounds (114). Multi-omics and AI technologies
drive individualized therapy; however, target validation, biomarker
standardization, and clinical trial design remain key to achieving
precision medicine.
In the context of targeted therapy for PCa, a major
challenge in choosing PSMA is the heterogeneity of the targets
(115). Differences in PSMA
expression across various tumor types and their microenvironments
result in notable variations in treatment effectiveness among
individuals (116). To address
this heterogeneity, multimodal imaging (such as PSMA-PET/MRI) can
be used to assess target expression and develop bispecific
antibodies that simultaneously target both PSMA and STEAP1. Beyond
this heterogeneity, there is the potential for unintended toxicity
that can harm non-target tissues (117). This issue can be mitigated by the
use of functionalized nanoparticles and targeted ligands, which
improve the precision of therapeutic agents (118). By utilizing tumor-targeting
peptides in conjunction with nanoparticles, selective absorption of
cancer drugs can be achieved, whereas biocompatible carriers help
minimize systemic toxicity and ensure accurate delivery to PCa
cells (119).
Immunotherapy can result in a range of irAEs when
treating PCa and other urological malignancies, including mild
symptoms such as rashes and fatigue as well as serious conditions
such as endocrine dysfunction and potentially fatal pneumonia
(120). Consequently, it is
crucial to promptly recognize these issues through consistent
monitoring of symptoms and patient feedback (121). Management approaches involve
providing symptomatic relief for less severe cases and
administering immunosuppressive medications, including steroids, to
patients with moderate-to-severe irAEs, alongside patient education
(122,123). Similarly, CAR-T cell therapy
demonstrates promising effectiveness but requires rigorous safety
oversight to monitor adverse reactions such as CRS and
neurotoxicity (124). This
requires ongoing evaluation of vital signs and neurological health,
offering symptomatic care and tocilizumab when appropriate and a
thorough pretreatment assessment to identify risk factors (125). In future, priority should be given
to exploring the dynamic expression patterns of targets, the
mechanisms of immunotoxicity, and the establishment of predictive
models to optimize the treatment window.
Advancements in targeted therapies for PCa cell
surface proteins, including PSMA, STEAP1, and TROP-2, have
significantly improved the management of mCRPC. Innovative
approaches such as RLT (including 177Lu-PSMA-617), ADCs, bispecific
antibodies, and CAR-T cell therapy have demonstrated promising
results. Nonetheless, challenges, such as antigen escape,
immunosuppressive environments, and drug resistance, persist.
Addressing these issues requires the development of combination
therapies, including targeted drug pairings and the integration of
RLT with immunotherapy, alongside personalized treatments informed
by biological markers, such as genomic characteristics and CTC
analysis. Future research should focus on the following directions:
i) Elucidating the molecular mechanisms of antigen escape,
particularly the roles of epigenetic regulation and TME-mediated
immune suppression. ii) Prioritizing the clinical evaluation of
combination strategies, such as RLT (for example 177Lu-PSMA-617)
and immune checkpoint inhibitors (including anti-PD-1). iii)
Accelerating the translational development of therapies against
emerging targets (such as CELSR3- and GPC3-directed ADCs or CAR-T
cells). iv) Developing integrated biomarker panels (for example
combining ctDNA, CTCs, and radiomics) and standardizing toxicity
management guidelines to improve patient quality of life. By
fostering interdisciplinary collaboration to expedite the clinical
application of novel therapies, targeted PCa treatment can advance
to a more precise and effective era.
Not applicable.
Funding: The present review was funded by the Medical Research
Project of Sichuan Medical Association (grant no. S2024047).
Not applicable.
HL conceived and designed the review, drafted the
manuscript, as well as read and approved the final mansucript. Data
authentication is not applicable.
Not applicable.
Not applicable.
The author declares that he has no competing
interests.
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