Radiotherapy remains a major treatment option for
numerous patients, serving both as a radical therapy and as
palliative care (1,2). Since the discovery of X-rays by
Wilhelm Conrad Röntgen in 1895, the field of radiotherapy has
undergone marked evolution (3).
This advancement has been driven by the pioneering contributions of
renowned scientists such as Nikola Tesla, Mihajlo Idvorski Pupin
and Maria Sklodowska-Curie (4).
Their innovative efforts have established a solid foundation for
modern clinical applications of radiotherapy, which can be employed
individually or in combination with other therapies for both
curative and palliative purposes at all stages of cancer (5,6). More
than half of all patients with cancer undergo radiotherapy;
however, its effectiveness is often diminished by the emergence of
radioresistance, which can profoundly impact the quality of life of
patients (7,8). Radiation therapy exerts its effects by
destroying cancer cells either directly or indirectly through the
induction of DNA damage. Ionizing radiation (IR) can also activate
several prosurvival signaling pathways, including the p53, ataxia
telangiectasia mutated and NF-κB pathways, which enhance DNA damage
checkpoint activation, promote DNA repair and stimulate autophagy
(9–11). Together, these signaling pathways
provide protection to cancer cells against radiation-induced
damage, thereby contributing to their resistance to treatment
(12).
Autophagy is a vital protein degradation pathway in
cells, and is essential for maintaining cellular homeostasis and
overall health (13). Autophagy,
which was first identified in human liver cells, is categorized
into three forms in mammalian cells: Macroautophagy, microautophagy
and chaperone-mediated autophagy (14). The autophagy process typically
includes four main stages: Initiation, formation and maturation of
the autophagosome, precise fusion of the autophagosome with the
lysosome, and finally content degradation (15) (Fig.
1). During the autophagy process activated by radiotherapy, a
cellular mechanism directs old, damaged or malfunctioning
biomolecules and organelles to lysosomes for degradation (16,17).
This process is preserved through evolution and is triggered by
different internal and external stressors, including nutrient
shortage, absence of growth factors, IR or low oxygen levels
(18). Under such circumstances,
autophagy functions primarily as a survival tactic by clearing out
dysfunctional organelles or toxic aggregates that could otherwise
lead to apoptosis (19).
Furthermore, the lysosomal decomposition of excess cellular parts
supplies crucial raw materials and nutrients that can be reused to
create important biomolecules (20). Therefore, regulating tumor autophagy
levels to reduce radiotherapy resistance represents a novel
approach.
Long non-coding RNAs (lncRNAs) are defined as
transcripts longer than 200 nucleotides that do not encode proteins
(21). Despite their low
conservation across species, lncRNAs function as molecular switches
that influence cell survival, inflammation and lipid metabolism in
the vasculature by regulating autophagy (22). Research has established a
relationship between lncRNAs and resistance to tumor radiotherapy
(23,24). Additionally, lncRNAs serve various
roles, including acting as molecular signals, decoys, guides and
scaffolds (25). Therefore,
reviewing the role of autophagy-modulating lncRNAs in tumor
radioresistance can enhance the understanding of these regulatory
mechanisms and may lead to the identification of novel therapeutic
strategies aimed at increasing tumor radiosensitivity through the
modulation of autophagy.
The present review aims to present the current
understanding of the role of autophagy in cancer and its impact on
tumor radioresistance through interactions with lncRNAs. By
elucidating the function of autophagy-modulating lncRNAs in tumor
radioresistance, the present review aims to provide valuable
insights into the context-dependent applications of therapeutic
strategies.
The role of autophagy in cancer is complex and can
be viewed as a double-edged sword; it has the potential to inhibit
tumor development, while also being implicated in tumor initiation
(26). Autophagy operates at a
basal level in all cell types and actively contributes to tumor
prevention (27). As a critical
intracellular mechanism, autophagy effectively responds to
genotoxic stress through pathways involving reactive oxygen species
(ROS), helping to prevent the accumulation of mutations and
maintain genetic stability (28).
Furthermore, autophagy is responsible for the removal of damaged
organelles, ensuring that cellular damage does not accumulate,
thereby preserving homeostasis and normal cellular function
(29). This underscores its
precise, standardized and essential role in maintaining cellular
health and stability (30).
Among the numerous regulators of autophagy that have
been identified, beclin 1 (BECN1) is recognized as one of the most
crucial (31). As a vital
regulatory protein, BECN1 is essential for initiating autophagy and
serves a role in maintaining the delicate balance between cell
survival and death (32). Research
has indicated that heterozygous loss of the BECN1 gene enhances
tumor development in mice, highlighting its importance in
understanding the mechanisms underlying tumorigenesis (33). Notably, the deletion of the BECN1
gene is frequently observed in various malignant tumors, including
breast, ovarian and prostate cancer, underscoring its critical role
in cancer pathology (34–36). Furthermore, a study has demonstrated
that overexpression of BECN1 in breast cancer cells effectively
inhibited cell proliferation and colony formation, and reduced
tumor growth in nude mice (37). In
addition to BECN1, research has shown that the knockout of the
autophagy-related gene (ATG)5 and ATG7 genes in mice disrupts the
autophagy process, leading to exacerbated oxidative stress
responses and an increased risk of developing liver cancer
(38). These findings emphasize the
crucial role of autophagy in tumor prevention.
Although radiotherapy is a main approach for the
treatment of cancer, resistance frequently arises, resulting in
unsuccessful treatments (44). This
radioresistance arises from the capacity of tumors to disrupt
stress responses, such as DNA damage and repair processes, which
either promote or inhibit autophagy and aid in nutrient recycling
(45) (Fig. 2). For example, by modulating Unc-51
like autophagy activating kinase 1 (ULK1)-mediated autophagy,
butyrophilin subfamily 3 member A1 contributes to tumor progression
and radiation resistance in esophageal squamous cell carcinoma
(46). Xu et al (47) reported that blocking autophagic flux
and DNA repair in tumor cells could enhance the effectiveness of
radiotherapy for orthotopic glioblastoma. In addition to damaged
proteins, various intermediate molecules, their complexes, and
organelles such as mitochondria and micronuclei can serve as cargo
for the autophagy process (48).
Previous studies have revealed both pro-survival and anti-survival
characteristics of autophagic pathways (49,50).
Cancer cells frequently take advantage of the dual role of
autophagy to survive in metabolically difficult conditions, escape
immune system attacks, prevent cell death and induce metastasis
(51,52). Research has revealed that using both
radiation and berberine together suppresses autophagy and
alternative end-joining DNA repair, which are linked to
radioresistance, thereby enhancing sensitivity to radiation
(53).
The sensitivity of tumor cells to radiation is
frequently affected by autophagic processes (54). BECN1 moves to the nucleus after IR
exposure, resulting in G2/M cell cycle arrest (55). Furthermore, autophagy driven by ATG5
has been demonstrated to increase the radiosensitivity of prostate
cancer cells, especially when nutrients are scarce or glutamine is
depleted, and also when MYC is silenced (56). Chen et al (57) proposed that inhibiting the nuclear
factor erythroid 2-related factor 2 (NRF2) antioxidative pathway
could make U-2 osteosarcoma cells more sensitive to radiation, with
the NRF2 antioxidative response being controlled by
autophagy-driven activation of ERK 1/2 kinases. Consequently,
reducing the expression levels of BECN1, ATG5 or NRF2 has been
shown to decrease the IR sensitivity of cancer cells. Furthermore,
the inhibition of ATG7 by lncRNA HOTAIR, which is notably
upregulated in prostate cancer cell lines exposed to radiation, has
been associated with radioresistance in these cells (58). These results emphasize the essential
function of autophagy in influencing radiosensitivity and suggest
the possibility of targeting autophagic pathways to enhance
radiotherapy effectiveness (58).
Research on breast cancer cells, which naturally
resist apoptosis, further underscores the link between IR and
autophagic pathways (59). After IR
exposure, these cells show increased autophagic characteristics,
resulting in more iron accumulation. This accumulation, in
conjunction with subsequent ROS generation, oxidative stress and
DNA damage, may trigger cell death through a mechanism known as
ferroptosis (60,61). These insights have sparked a rising
interest in pairing autophagic inducers with IR to improve the
radiosensitivity of cancer cells. For instance, in a similar
approach, the treatment of non-small cell lung carcinoma (NSCLC)
cells with rapamycin alongside a histone deacetylase inhibitor has
been found to promote radiosensitization (62). This combined treatment has two
effects: It boosts autophagy and at the same time hinders DNA
damage repair processes. Observations in cultured cells and tumor
xenograft mouse models have demonstrated the effectiveness of the
strategy, pointing to a potential improvement in radiotherapy
outcomes (63).
Autophagy affects cancer cell survival in complex
ways, acting both as a supporter and an opponent of
radiosensitization (62,64). Various cancer cell types have been
shown to exploit enhanced autophagy as a survival strategy. For
instance, the application of autophagy inhibitors renders otherwise
radio-resistant bladder cancer (BLCA) cells more sensitive to
chemotherapy (65). Similarly,
silencing of ATG5, a key component of the autophagy process, has
been found to increase IR-induced cell death in nasopharyngeal
carcinoma (66). Furthermore, the
use of autophagy inhibitors in combination with IR has emerged as a
factor influencing the bystander and abscopal effects associated
with chemotherapy and radiotherapy (67). These findings underscore the
importance of context in the role of autophagy in cancer treatment
and highlight the potential of targeting autophagy pathways to
enhance treatment efficacy.
Radiotherapy is a common cancer treatment that
induces different forms of cell death, including autophagy
(74). Besides directly causing DNA
strand breaks, IR can lead to the production of significant amounts
of ROS in cells, resulting in oxidative stress damage (75). According to Yang et al
(76), mitophagy triggered by IR
boosts ferroptosis by raising the levels of free fatty acids inside
cells. Lysosomes serve a crucial role in autophagy, a cellular
degradation process (77). A
conserved protein associated with autophagy, Atgs/P62/LC3II,
controls the process (78). In
cancer cells, autophagy is a double-edged sword. In the initial
phases, it might restrict the development of tumors. Nevertheless,
it might also offer a survival advantage for adaptation and
detoxification in challenging conditions such as starvation, low
oxygen levels, and chemotherapy or radiotherapy (79). Investigators have reported that
autophagy activity rises following IR. This acts as a mechanism for
cells to survive when faced with cytotoxic agents, including IR and
temozolomide, in the treatment of glioblastoma (80,81).
Furthermore, researchers have revealed that IR promotes autophagy
via the Wnt/β-Catenin pathway (82). In conclusion, IR has an important
effect on tumor autophagy.
Numerous cancer types have been found to exhibit
abnormal expression of lncRNAs, and the relationship between
lncRNAs and autophagy has garnered interest across various cancer
types (Table I), including lung,
gastric, breast and prostate cancer (83). The majority of research suggests
that lncRNAs regulate autophagy mainly through mechanisms such as
microRNA (miRNA/miR) sponging (functioning as competing endogenous
RNAs), interactions between RNAs, RNA-protein regulation and
various other pathways (84,85).
Studies have indicated that lncRNAs are involved in various phases
of the autophagy process from the beginning to the maturation stage
(86,87). They assist in starting autophagic
phagocytosis by controlling essential proteins such as ULK1, mTOR
and BECN1, and they also affect the extension of autophagic
vesicles by regulating ATG3, ATG5, ATG4, ATG12 and ATG7 (88). The present review highlights the
complex and diverse functions of lncRNAs in regulating autophagy,
and their possible impact on cancer biology and treatment.
Proliferation is one of the most critical malignant
phenotypes observed in cancer, while apoptosis is equally
significant in the context of neoplastic development (89). Although their functions are
fundamentally opposite (proliferation promotes cell growth and
survival, while apoptosis leads to programmed cell death), their
interactions work synergistically to regulate cancer development.
This delicate balance between cell proliferation and apoptosis
serves a crucial role in tumor progression and resistance to
therapy (90). In digestive system
cancers, various lncRNAs have been identified to serve roles in
tumor progression and autophagy regulation (91). For instance, lncRNA SNHG11 is
upregulated in gastric cancer and is associated with poor patient
prognosis. lncRNA SNHG11 post-transcriptionally enhances ATG12
expression through miR-1276, thereby promoting autophagy, cell
proliferation and activation of the Wnt/β-catenin signaling pathway
(92). Similarly, in HCC, lncRNA
MALAT1 exhibits elevated expression levels compared with those in
normal tissues. Silencing MALAT1 has been shown to increase HCC
autophagy by promoting the conversion of LC3-I to LC3-II and
simultaneously suppressing HCC cell proliferation (93). Conversely, lncRNA NBR2 acts as a
tumor suppressor in HCC by inhibiting BECN1 and autophagy through
the ERK/JNK pathways, thereby restraining HCC cell proliferation
(94). In colorectal cancer (CRC),
lncRNA SLCO4A1-AS1 acts as an oncogenic element, exhibiting a
positive association with par-3 family cell polarity regulator
(PARD3) and sponging miR-508-3p. This lncRNA enhances the
proliferation of CRC cells and initiates autophagy through the
miR-508-3p/PARD3 pathway. Nonetheless, the regulatory effect is
interrupted by the application of the autophagy inhibitor
3-methyladenine (95). Another
lncRNA in CRC, FIRRE, directly interacts with polypyrimidine tract
binding protein 1 to enhance BECN1 mRNA stability, thus reducing
autophagy and promoting CRC cell proliferation (96). In the context of oral squamous cell
carcinoma (OSCC) and cholangiocarcinoma (CCA), several upregulated
lncRNAs have been shown to suppress autophagy. For instance,
LINC01207 is highly expressed in OSCC, where its upregulation
promotes cell proliferation but inhibits both apoptosis and
autophagy via the miR-1301-3p/lactate dehydrogenase A axis
(97). By contrast, overexpression
of LINC00958 reduces apoptosis while promoting autophagy by
upregulating autophagy-related proteins such as BECN1 and ATG5, and
increasing the LC3-II/LC3-I ratio, driven by p53 mediated by
sirtuin 1 (SIRT1) (98). In CCA,
lncRNA HOTAIR inhibits both apoptotic and autophagic processes,
thereby promoting the proliferation of CCA cells by targeting the
miR-204-5p/high mobility group box 1 axis (99). Pancreatic cancer (PANC), known for
its poor prognosis, remains a complex malignancy with unclear
progression mechanisms (100). A
study by Wu et al (101)
revealed that LZTS1-AS1, a highly expressed lncRNA in PANC cells
and tissues, promoted PANC cell proliferation while inhibiting
apoptosis and autophagy via the miR-532/twist family bHLH
transcription factor 1 axis. Overall, these findings highlight the
diverse and critical roles of lncRNAs in modulating autophagy and
influencing the malignant phenotypes of various cancer types.
The downregulation of lncRNA CASC2 enhances
apoptosis in NSCLC and diminishes ATG5-mediated autophagy by
regulating the miR-214/tripartite motif containing 16 axis in A549
and H1299 NSCLC cell lines (105).
Conversely, a reversed autophagic state has been noted in papillary
thyroid carcinoma (PTC), where overexpression of lncRNA SLC26A4-AS1
inhibited the proliferation of PTC cells and stimulated autophagy
by recruiting the transcription factor ETS1 and elevating inositol
1,4,5-trisphosphate receptor type 1 expression (106). Additionally, Qin et al
(107) revealed that lncRNA SNHG5
was stabilized by RNA binding motif protein 47 (RBM47) and directed
to FOXO3, resulting in decreased proliferation and the activation
of autophagy in PTC cells through the RBM47/small nucleolar RNA
host gene 5/FOXO3 pathway.
CASC19, a newly identified lncRNA located on
chromosome 8q24.21, consists of 324 nucleotides (110). A study has demonstrated that
CASC19 expression is upregulated in a variety of human cancer
types, including NSCLC, gastric cancer, CRC, PANC, ccRCC, glioma,
cervical cancer and nasopharyngeal carcinoma (111). Notably, some research has
indicated that CASC19 can enhance radioresistance in nasopharyngeal
carcinoma by modulating autophagy signaling pathways (112,113). Furthermore, the dysregulation of
CASC19 has been closely linked to numerous clinicopathological
characteristics (prognosis and pathological staging) and cancer
progression, particularly in HCC and gastric cancer (114,115). In summary, CASC19 influences
various cellular phenotypes, including cell proliferation,
apoptosis, cell cycle regulation, migration, invasion, EMT,
autophagy and therapeutic resistance (116).
NEAT1 is predominantly located in the nucleus,
although a smaller fraction is present in the cytoplasm (117). NEAT1 functions as a structural
component of nuclear paraspeckles and is involved in regulating
gene expression at both transcriptional and post-transcriptional
levels (118). Research has
demonstrated that NEAT1 contributes to radioresistance in HCC cells
by inducing autophagy through GABA type A receptor-associated
protein (119). The role of NEAT1
in carcinogenesis is multifaceted, encompassing interactions with
miRNAs, modulation of gene expression, regulation of epigenetic
factors and participation in various signaling pathways, such as
the PI3K-AKT and TGF-β1 pathways (120). Additionally, the involvement of
NEAT1 in cancer is complicated by its impact on CSCs and the tumor
microenvironment (121). The
interaction of NEAT1 with autophagy further adds to the complexity
of its functions in cancer biology (122). Understanding the interactions
between NEAT1, autophagy and radioresistance is crucial for
researchers as it may lead to the identification of novel
therapeutic targets and strategies aimed at disrupting oncogenic
processes, reducing treatment resistance and improving patient
survival (123). Consequently,
this understanding could facilitate the development of specialized
treatment approaches and regimens.
lncRNA TP53TG1 (National Center for Biotechnology
Information reference sequence, NR_015381.1), located on chromosome
12, is transcribed as an ~0.7-kilobase lncRNA molecule (124). Its expression can be induced under
conditions of cellular stress in a wild-type TP53-dependent manner
(125). As a relatively recent
discovery in the field of lncRNAs, TP53TG1 has been implicated to
serve oncogenic and anti-oncogenic roles across various cancer
types, such as gastric and breast cancer (126). For example, overexpression of
TP53TG1 promotes proliferation of colon cancer cells (127). In addition, Cheng et al
(128) found that lncRNA TP53TG1
exerted anticancer effects in cervical cancer by comprehensively
regulating the transcriptome profile of HeLa cells. Research has
indicated a close association between TP53TG1 and autophagy
(129). Furthermore, it has been
demonstrated that lncRNA TP53TG1 contributes to the radioresistance
of glioma cells through the miR-524-5p/RAB5A axis (130). Given these findings, TP53TG1
represents a promising target to enhance the sensitivity of tumors
to radiotherapy.
HULC, found on chromosome 6p24.3, has been
identified to be upregulated in HCC and is linked to cancer
advancement (131). The expression
of this transcript is regulated by miRNAs and transcriptionally
modulated by Sp1 family factors (132). HULC has been identified as a novel
biomarker in different types of cancer, such as prostate cancer and
CRC, serving a role as an oncogenic factor (133). Research conducted previously
indicated that inhibiting HULC could reduce angiogenesis in human
gliomas (134). Another study
demonstrated that HULC facilitated the advancement of CRC (135). A study has shown that lncRNA HULC
serves a role in radioresistance by reducing autophagy in prostate
cancer cells (136). Thus, lncRNA
HULC could serve as a therapeutic target to combat tumor resistance
to radiotherapy.
PVT1, a lncRNA, was initially identified as a driver
of variant translocations in mouse plasmacytomas (142). The human lncPVT1 gene is situated
on chromosome 8q24.21, sharing the same location as the MYC
oncogene (143). lncPVT1 has been
identified as a factor that accelerates the development of several
cancer types, such as nasopharyngeal cancer and lung cancer
(144,145). Radioresistance poses a major
challenge to tumor treatment success, and is connected to the
abnormal regulation of physiological functions in cancer cells,
including apoptosis, autophagy, stemness (for CSCs), hypoxia, EMT
and DNA damage repair (146,147). Recently, lncPVT1 has been linked
to the modulation of radioresistance in certain cancer types,
including nasopharyngeal cancer and lung cancer (148).
Research interest in lncRNA therapeutics has only
emerged in the past decade, and so far, no treatments targeting
lncRNAs have reached clinical development (149). SP100-AS1, a lncRNA that targets
the antisense sequence of the SP100 gene, is upregulated in the
tissues of patients with CRC who are resistant to radiation,
according to RNA-sequencing analysis (150). Notably, reducing SP100-AS1
expression lowered radioresistance and decreased cell proliferation
and tumor growth in both laboratory and live models. To identify
the proteins and miRNAs interacting with SP100-AS1, mass
spectrometry and bioinformatics analyses were utilized. SP100-AS1
was shown to interact with and stabilize the ATG3 protein via the
ubiquitination-dependent proteasome mechanism (150). This interaction highlights the
possible involvement of SP100-AS1 in regulating autophagy-related
mechanisms and enhancing radioresistance in CRC. SP100-AS1 holds
potential as a therapeutic target to enhance the response of CRC to
radiation therapy (150). As
aforementioned, autophagy affects tumor cell proliferation,
survival and the response to treatment in intricate ways across
different types of cancer, such as nasopharyngeal cancer and CRC.
Methods to target autophagy might involve aiming at specific
proteins or pathways associated with autophagy, as well as using
agents that promote or block autophagy.
Scientists seek to improve treatment effectiveness
by utilizing the interaction between autophagy and processes
regulated by lncRNAs. They aim to develop more effective treatments
by integrating autophagy modulation with lncRNA-targeted methods
(151). Furthermore, these
combination therapies provide a comprehensive strategy to boost
patient outcomes (152).
There are both obstacles and prospects in the future
research of radiation oncology and lncRNAomics (153). For precise tumor targeting,
technological advancements such as hybrid MRI and positron emission
tomography scans are vital, although they entail significant costs
and demand specialized expertise (154). One major obstacle in lncRNA
research is the restricted knowledge gained from examining just a
small portion of lncRNAs, which limits the understanding of their
mechanisms, roles and structures (155). Despite significant progress in the
field, delivering oligonucleotides to solid tumors continues to be
a major challenge. Advancements in artificial intelligence and
sophisticated statistical modeling have enabled molecular-guided
treatment plans customized for each patient, representing a
significant achievement in precision medicine. Autophagy-modulating
lncRNAs represent a vast yet largely unexplored reservoir of
oncogenes, tumor suppressors and radioresponse modifiers.
Integrating this knowledge into treatment strategies, from
diagnosis and response prediction to the design of targeted
therapies, could greatly enhance management and outcomes for
patients with cancer (156). In
conclusion, the present review summarizes the effects of
autophagy-modulating lncRNAs on tumor radioresistance, providing
novel ideas for tumor radiosensitization.
lncRNAs that modulate autophagy are crucial elements
in the radioresistance of tumors. These lncRNAs are crucial in
different stages of cancer development and advancement, such as
tumor expansion, spread and resistance to treatment. Studies are
concentrating on using autophagy-based treatment methods to tackle
radioresistance in patients with cancer (157,158). Modifying autophagy can influence
the survival of tumor cells, their response to therapy and the
overall success of treatment. Creating targeted cancer treatments
requires a deep comprehension of the interaction between lncRNAs
and autophagy. Targeting specific lncRNAs could potentially adjust
autophagy and increase tumor radiosensitivity. Current clinical
trials and preclinical research are investigating the potential of
targeting autophagy and lncRNAs to enhance treatment outcomes for
patients with cancers resistant to radiation (159,160).
Not applicable.
The present study was supported by The Wings Scientific and
Technological Foundation of The First People's Hospital of Changde
City (grant no. Z2025ZC04) and Interdisciplinary Research Program
in Medicine and Engineering, The First Affiliated Hospital of
University of South China (grant no. IRP-M&E-2025-05)
Not applicable.
HL wrote and reviewed the drafts of the paper, while
ZH created the figures and tables, and revised the paper. Data
authentication is not applicable. All authors have read and
approved the final version of the manuscript.
Not applicable.
Not applicable.
The authors declare that they have no competing
interests.
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