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Fluorescence Guided Activatable Cancer Theranostics: Its Development and Prospect
DOI: http://ITexLi.115104
agents like anthracycline analogs and others. Attaining the intended therapeutic
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outcomes within the hypoxic region becomes unfeasible due to the combination of
reduced oxygen levels and increased distance from the nearest blood capillary. This
situation represents an unfavorable prognostic and predictive factor, as it contributes
to various aspects such as chemoresistance, radioresistance, angiogenesis, vasculogenesis, invasiveness, metastasis, resistance to cell death, altered metabolism, and
genomic instability. In all challenging circumstances, different reductase enzymes
are upregulated during hypoxia, effectively reducing aromatic azo (NN), nitro
(NO2), and quinone moieties. Based on this inherent conversion, several theranostics have been created, wherein the cleavage of the azo bond (NN) or reduction
of the nitro group (NO2) to amine (NH2) facilitates the self-immolative discharge
of active therapeutic components into the low-oxygen area of the solid tumor. Recent
advancements in hypoxia-responsive theranostics have been consolidated in Table
While diverse strategic theranostics have been documented, none have yet pro
gressed to the clinical trial stage. Further efforts are required to develop hypoxia-sensitive theranostics that may enhance clinical benefits and address existing healthcare
challenges.
Light-activated theranostics
.
.
To date, we have discussed numerous endogenous stimuli-responsive theranostics
that actively deliver chemotherapeutic agents to various cell types/cancers based
on the presence of specific stimulants. It is important to note that these stimulants
are also present in normal cells but in relatively lower quantities, thus ensuring that
the therapeutic agents are selectively released solely in the tumor region cannot be
guaranteed. External stimulants, such as light, have been utilized to trigger the release
of therapeutics, a process commonly referred to as “photo caging,” where drugs are
shielded or “caged.” UV or laser irradiation facilitates the controlled release of therapeutics in a spatially and temporally precise manner. Some critical examples of the
photo trigger theranostic in a consulate form are provided in Table
The utilization of photo-triggered activation of anticancer drugs represents a
.
unique and innovative strategy. By employing this approach, it becomes possible to
activate the therapeutic agent with a higher degree of precision specifically at the
intended target tumor site.
Theranostics Active ingredients In vitro cells In vivo/ex-vivo Re f.
OPV-Luminol Luminol & ROS HeLa HeLa cell tumor
10/11 SN-38/CA-4 MCF-7 — [67]
CMP-NCL-CA4
(1–5)
CMP-L-Rh Combretastatin A-4 Colon 26 cells SC colon 26 tumors
1(Biotin-taggedONB-CC)
,, CA-074 Inhibitors MDA-MB-231/MCF-10A — [71]
combretastatin A-4,
Pc-(L-CA4)
chlorambucil MDA-MB-231 cells — [70]
Colon 26 cells SC colon 26 tumors [68]
mice model
mice model
[66]
[69]
Table 3.
Information onphoto-triggered theranostics.
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. Recent cutting-edge strategies in cancer theranostics
The forefront of medical advancement includes the innovative idea of selfimmolative theranostics, in which the therapeutic substance undergoes a controlled
chemical reaction, causing its self-degradation under certain circumstances. This
characteristic is frequently harnessed to prompt the release of the therapeutic payload precisely at the disease site, thereby improving its effectiveness and reducing
unintended effects elsewhere. In the previously mentioned approaches, the primary
focus is on delivering chemotherapeutic agents to cancer cells or tumors. However,
these strategies have not yet been assessed for their effectiveness against multidrugresistant cancers/metastasis cancer. It’s crucial to note that multidrug-resistant
cancer remains one of the most lethal forms of cancer, with the highest mortality
rates. With a focus on addressing multidrug-resistant cancer, Kim et al. strategically
engineered prodrug (depicted in Figure ), which combines a protein phosphatase 2A (PP2A) inhibitor with a DNA damage chemotherapeutic agent linked
via a GSH-responsive labile linker [72]. In this context, the protein phosphatase 2A
(PP2A) inhibitor, demethyl cantharidin (DMC), inhibits PP2A activity. This inhibition leads to elevated MDM2 expression, subsequently triggering the reduction
of p53-p21 mediated G1/S checkpoint arrest, thereby diminishing the DNA repair
pathway. Conversely, 5-fluorouracil inhibits the growth of DNA in newly born cells. It
disrupts DNA synthesis and, to a lesser extent, hinders RNA formation by integrating
itself into RNA molecules, resulting in the generation of faulty RNA. Additionally,
fluorouracil hampers uracil riboside phosphorylase activity, impeding preexisting uracil’s utilization in RNA synthesis. The strategic prodrug is preferentially
Figure 11.
Example of recently reported cutting-edge cancer theranosic.
Fluorescence Guided Activatable Cancer Theranostics: Its Development and Prospect
DOI: http://ITexLi.115104
localized in the mitochondria, where triphenyl phosphonium cation drives to localize
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in the mitochondria. After cellular glutathione cleaves the vulnerable –S–S– bond,
DMC and 5-fluorouracil are activated, ultimately disrupting the usual mitochondrial functions in cancer cells. Prodrug exhibited greater anticancer efficacy in
PP2A over-expressed breast cancer cell line (4T1) and colon cancer cells HCT116
compared to PP2A unexpressed cancer cell line. This heightened anticancer effect
was accompanied by increased production of reactive oxygen species (ROS), resulting in DNA damage. Subsequently, mitochondrial swelling occurred, leading to the
rupture of the mitochondrial outer membrane and the release of the pro-apoptotic
protein cytochrome C. In the in vivo mouse model with HCT 116-inoculated mice, the
combination of drugs in prodrug significantly reduced tumor volume and size by
three times more compared to using DMC or 5-fluorouracil alone. This exemplifies
the effectiveness of combination therapy in combatting cancer.
By reprogramming mitochondrial metabolism, the cancer esterase-activated prodrug overcomes multidrug resistance activity, leading to delayed prodrug activation and enabling evasion of drug efflux mechanisms [73]. After esterase hydrolysis,
releasing of dichloroacetate (DCA) and doxorubicin leads to p21Waf1 upregulation,
reduction of PDH phosphorylation, and cleavage of caspase-3, and PARP-1 allows to
show high anticancer activity in multidrug resistance MCF-7. It effectively suppressed
tumor growth in the MCF/Dox xenograft mice model, with no indication of hepatotoxicity in the treated animals.
An additional theranostic prodrug, labeled as [74], is triggered by various
cellular reactive oxygen species (ROS) and has demonstrated its effectiveness in
combating metastatic cancer. Typically, cancer cells exhibit heightened levels of
multiple ROS, but a single ROS may not be adequate to activate the anticancer drug
within the theranostic platform. Therefore, a carbamate-linked theranostic labeled
as was developed, incorporating biotin-PEGylation. Following 15days of injecting
metastatic cervical cancer cell-bearing mice with doses dependent on the treatment, a
remarkable inhibition of tumor growth (99%) was observed, coupled with the depletion of HIF-1α, leading to a survival period of over 45days for the treated mice.
Another formidable aspect is tumor recurrence, wherein 90% of anticancer
medications fall short of providing the anticipated therapeutic effectiveness, resulting in increased mortality rates [75]. Ironically, recurrence is frequently triggered
by chemotherapy as a result of the accumulation of nuclear genomic mutations
throughout the treatment regimen. Antineoplastic agents that induce nuclear-DNA
damage, such as alkylating agents, are prevalent chemical mutagens and have been
associated with tumor recurrence. To address this ongoing challenge in cancer treatment, ciprofloxacin-conjugated (MT-CFX) (
Figure ) was employed to improve
mitochondrial targeting [76]. The payload release within the mitochondria triggers
oxidative damage to proteins, mitochondrial DNA (mtDNA), and lipids. A significant
preference for damaging mtDNA over nuclear DNA (nDNA) was observed in cancer
cells. It showed anticancer activity in various cancer cells namely, MDA-MB-231(IC50:
31.31μM), SW620 (IC50: 31.82μM), DU145 (IC50: 55.51μM), A549 (IC50: 23.77μM),
PC3 (IC
: 86.45μM) compared to the normal cells, BJ (IC50: 631.82μM), MCF10A
50
(IC50: ≥1000μM). The fluorophore-linked variant of , known as Bo-Mt-CFX, administered via intravenous injection (0.5mmol/kg) in an MDA-MB-231 xenograft mouse
model, resulted in more than a threefold reduction in both the tumor volume and size.
Hypoxia poses another challenge in overcoming multidrug resistance in tumors.
Kim et al. introduced theranostic (Figure ) in conjunction with photodynamic
therapy and chemotherapy to address this challenge [77]. The theranostic construct
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underwent reduction within the hypoxic tumor microenvironment, resulting in the
liberation of a near-infrared-emissive fluorophore and an active chemotherapeutic
drug. Consequently, during photodynamic therapy (PDT), theranostic aided
in eliminating normoxic tumor cells located in the superficial layer of the tumor.
Additionally, the activatable chemotherapy facilitated the eradication of hypoxic
tumor cells situated in the core of the tumors, thereby enhancing treatment efficacy
for solid tumors in mice. This double-aided approach introduces a new dimension in
cancer therapy, especially multidrug resistance cancer.
In this discussion, there is a notable focus on addressing multidrug resistance in
cancer therapy through diverse and sophisticated strategic approaches. These methods include the activation of reactive oxygen species (ROS) and the incorporation of
multidrug components. This approach integrates both the therapeutic and diagnostic
components, aiming to overcome resistance mechanisms exhibited by cancer cells
against multiple drugs. Through a combination of various therapeutic modalities
and diagnostic techniques, this approach seeks to enhance treatment efficacy while
providing insights into the resistance mechanisms at play, thereby enabling personalized and more effective cancer therapy.
. Conclusions and prospective outlook
In conclusion, the development and exploration of stimuli-responsive theranostics
(GSH, H2O2, H2S, pH, β-galactosidase, hypoxia) have brought significant advancements to the field of cancer treatment and diagnostic capabilities. The numerous
strategies and methodologies discussed herein reflect the tremendous potential of
these emerging technologies. As researchers continue to delve into the intricacies of
various stimuli-responsive platforms, there remains a wealth of opportunities and
potential for further exploration and development in this domain. Currently, optically modulated theranostics remain primarily of academic interest. Advancing these
to clinical trial phases requires generating additional data through high-throughput
assays, comprehensively exploring mechanisms, and collecting pharmacokinetic and
pharmacodynamic information.
Looking ahead, the prospective outlook for stimuli-responsive theranostics is
exceedingly promising. Continued research and development in this area hold the
key to addressing the existing limitations and challenges associated with traditional
cancer treatment modalities. By leveraging the dynamic nature of these responsive
systems, it is conceivable that refined and highly targeted therapeutic interventions
can be achieved, thereby maximizing efficacy while minimizing off-target effects and
potential toxicity. With a comprehensive understanding of the underlying mechanisms and a focused effort toward the development of novel and optimized therapeutic strategies, stimuli-responsive theranostics are poised to play a pivotal role in the
future of personalized and precision medicine.
Acknowledgements
SB thanks DST-SERB, India, for the research grant (CRG/2023/005905).
Fluorescence Guided Activatable Cancer Theranostics: Its Development and Prospect
DOI: http://ITexLi.115104
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