LC is a type of malignant cancer originating from trachea, bronchial mucosa or glands (8). Previous research has revealed the multi-level mechanism of erianin against LC (9); its core role is derived from its unique biphenyl methyl structure, which enables it to specifically target and regulate the PI3K/Akt/mTOR signaling pathway (10). Notably, erianin induces ferroptosis by activating the Ca²⁺/calmodulin signaling pathway (11). Therefore, erianin induces both apoptosis and ferroptosis (11).

At the level of metabolic regulation, erianin has shown precise intervention in cancer energy metabolism (12,13). Previous studies have confirmed that erianin has inhibits aerobic glycolysis in non-small cell LC (NSCLC) (2,14), which accounts for 85% of LC (14). Moreover, lung adenocarcinoma (LUAD) is estimated to account for 40% of all lung cancer cases (15). Erianin effectively inhibits the proliferation of cisplatin-resistant cells by regulating the Wnt3/β-catenin signaling pathway (16,17), which provides a novel possibility for overcoming common clinical chemotherapy resistance. In addition, erianin inhibits the proliferation, migration, invasion and angiogenesis of LUAD cells and induces apoptosis by regulating the multiple epidermal growth factor-like domains 9 (MEGF9)/MAPK/ERK signaling pathway (18).

Nasopharyngeal carcinoma is a malignant cancer that originates from the nasopharyngeal mucosal epithelium. Erianin induces caspase cascade-dependent apoptosis, and blocks cell cycle progression by dually activating mitochondrial and death receptor pathways (19). At the same time, erianin inhibits ERK1/2 phosphorylation in a dose-dependent manner and promotes apoptosis by downregulating MMP-9 expression. In conclusion, erianin inhibits nasopharyngeal carcinoma cell proliferation through the ERK1/2-MMP-9 signaling pathway (19). These findings reveal the multi-target anti-nasopharyngeal carcinoma mechanism of erianin and provide options for targeted therapy.

Hepatocellular carcinoma, the main histological subtype of primary liver cancer, originates from the malignant transformation of liver parenchymal cells or mesenchymal tissue (20). Erianin affects the expression of cancer-associated genes by regulating pyruvate carboxylase (PC)-mediated Wnt/β-catenin signaling pathway, while promoting mitochondrial oxidative stress and inhibiting glycolysis and the proliferation of liver cancer cells (20).

At the molecular level, erianin induces ferroptosis by blocking the JAK2/STAT3/SLC7A11 signaling pathway (21) while regulating the PI3K/Akt and MAPK signaling pathways (22). Erianin can also activate the DNA damage repair pathway by inducing DNA damage, triggering G₂/M phase arrest and mitotic cell death, which is complementary to its metabolic regulation (23).

Erianin can simultaneously activate the mitochondrial apoptosis pathway (24) and oxidative stress response (25). Previous experiments in mice have demonstrated tumor growth inhibition without notable toxicity (21). Erianin can also regulate the immune microenvironment, which provides a theoretical basis for its combined application with other treatments, such as chemotherapy, biological immunotherapy, and traditional Chinese medicine (26).

EC is a highly malignant cancer type originating from the esophageal mucosal epithelium. Erianin can promote MMPs, block cell cycle progression and inhibit MAPK protein activation by dually regulating the JAK/STAT3 and MAPK signaling pathways, thus effectively blocking the proliferation and metastasis of EC cells (27).

In esophageal squamous cell carcinoma (ESCC), erianin exerts an anti-metastasis effect by promoting the ubiquitination and degradation of the outb deubiquitinase 1 (OTUB1) protein (28). Erianin also activates the cyclic guanosine monophosphate/cgmp-dependent protein kinase (cGMP/PKG) signaling pathway, induces apoptosis and inhibits ESCC cell migration (29).

Pancreatic cancer is a common and highly malignant digestive system cancer derived from pancreatic cells. For example, The American Cancer Society reports that PC is the 10th most common cancer in male and the 8th in female patients in terms of newly diagnosed cases (30). Previous research has shown that erianin significantly inhibits the proliferation and migration and induces the apoptosis of pancreatic cancer cells by dually regulating AKT/FOXO1 and apoptosis signal-regulating kinase 1 (ASK1)/JNK/p38 MAPK signaling pathways (31). Erianin directly interacts with MEK1/2 and blocks the activation of MAPK signaling, thus effectively inhibiting the proliferation of pancreatic cancer cells and the characteristics of cancer stem cells, including suppression of sphere-forming capacity and the downregulation of key stemness markers, such as CD133, CD 44, sex determining region y-box 2 (SOX 2), and octamer-binding transcription factor 4 (OCT 4) (32).

Oral cancer is a malignant cancer that occurs in the oral cavity. Erianin induces the ferroptosis of oral cancer KB cells and inhibits their proliferation and metastasis by regulating the Nrf2/heme oxygenase-1 (HO-1)/glutathione peroxidase 4 (GPX4) signaling pathway (33). In oral squamous cell carcinoma, erianin exerts anticancer effects through a dual mechanism: Erianin blocks the cell cycle in the G₂/M phase, activates the apoptosis program and regulates autophagy (34) and induces autophagy-dependent apoptosis by inhibiting the palmitoyl-protein thioesterase 1/mTOR signaling pathway (35) and regulating the MAPK pathway (36).

GC is a highly malignant cancer originating from the gastric mucosal epithelium. Erianin significantly inhibits the proliferation, invasion and migration of GC cells by dually regulating the PI3K/AKT and liver kinase b1/salt-inducible kinase 2 or 3/par-3 family cell polarity regulator (LKB1/SIK2/3/PARD3) signaling pathways (37). At the molecular level, erianin not only blocks the activation of the PI3K/AKT pathway, but also effectively reverses the epithelial-mesenchymal transition (EMT) of GC cells by inhibiting LKB1/SIK2/3/PARD3 signal transduction (38).

In addition, a previous study based on network pharmacology confirmed that erianin serves a key role in the treatment of gastric precancerous lesions by regulating the harvey rat sarcoma viral oncogene homolog (HRAS)/PI3K/AKT signaling pathway (39).

CRC is a malignant cancer derived from the epithelial cells of the colon and rectum. Erianin significantly induces the apoptosis of CRC cells by dually regulating JNK and MAPK signaling pathways (40) and has a specific anticancer effect on BRAF V600 E or RAS mutant cells (41). In KRAS glycine-to-aspartic acid substitution at codon 13 (G13D) mutant CRC, erianin effectively inhibits cancer cell migration, invasion and EMT by inducing autophagy-dependent ferroptosis (42,43). Erianin induces ferroptosis by promoting GPX4 ubiquitination degradation (44) and upregulating ferredoxin 1 expression (45).

BC is a malignant cancer derived from breast epithelial cells (46). In triple-negative (TN)BC, erianin exerts anticancer effects through a dual mechanism: Erianin activates the mitochondrial apoptosis pathway and inhibits PI3K/Akt signal transduction (46,47) and regulates the cholesterol metabolism pathway by targeting sarcoma gene, which significantly inhibits cancer proliferation and migration (47,48). In estrogen receptor-positive BC, erianin effectively inhibits the proliferation and metastasis of T47D cells by regulating cell cycle progression, inducing apoptosis and balancing MMP/tissue inhibitor of metalloproteinase (TIMP) expression (49).

Erianin shows value in the treatment of bone metastasis of BC. As a novel nuclear factor of activated T cells, cytoplasmic 1 (NFATc1)-specific inhibitor, erianin can effectively block BC-induced pathological osteoclast genesis and decrease bone destruction in MDA-MB-231 breast cancer cell-induced bone loss mice (50).

Cervical cancer has the highest incidence of gynecological malignancy, with an incidence rate of 604,127 new cases reported in 2020 (51). Erianin shows a multi-level anticancer mechanism in the treatment of cervical cancer. In terms of immune regulation, erianin serves an important role through dual pathways: Erianin promotes the lysosomal degradation of PD-L1 and blocks the synthesis of hypoxia-inducible factor (HIF)-1α by inhibiting the mTOR/p70 ribosomal protein s6 kinase (S6K)/eukaryotic translation initiation factor 4e-binding protein 1 (4EBP1) pathway (52). Erianin also effectively restores the tumor killing ability of cytotoxic T lymphocytes by inhibiting the MAPK/ERK pathway (52). These immunomodulatory effects have been verified in in vivo experiments, showing anti-proliferative effects.

In terms of apoptosis regulation, erianin shows dose- and time-dependent anticancer properties (53). Erianin regulates the ERK1/2 signaling pathway, which causes HeLa cell cycle arrest in the G₂/M phase and activates the mitochondrial apoptotic pathway (53).

Endometrial carcinoma is a malignant cancer originating from the endometrial epithelium. Erianin inhibits the proliferation and invasion of endometrial cancer cells by regulating the microRNA (miRNA or miR)-661/bcl-2-related ovarian killer signaling pathway (54).

Erianin has unique molecular mechanisms and therapeutic potential in the treatment of prostate cancer (55,56). Erianin increases the levels of C16 ceramide in androgen-sensitive prostate cancer cells, which is associated with the function of ceramide synthase 5 (CerS5) and triggers endoplasmic reticulum stress-associated apoptosis (56).

GBM is the most aggressive primary cancer of the central nervous system, GBM accounts for 45.6% of all primary brain malignancies. the incidence rate of GBM is 3.19 among 100,000 individuals from different age groups with a median age of 64 years (57). Erianin exhibits a dual cell death induction mechanism in the treatment of GBM (58). Erianin triggers GBM cell apoptosis by inhibiting the Bcl-2 protein and activating the bh3-interacting domain death agonist (Bid) protein (58). Erianin enhances the ferroptosis sensitivity of glioma stem cells and their temozolomide-resistant subsets by promoting the ubiquitination and degradation of the iron transporter SLC40A1 (59). This dual mechanism not only overcomes the drug resistance of the traditional chemotherapeutic drug temozolomide, but also improves the therapeutic effect by simultaneously targeting cancer cells and cancer stem cells. In addition, erianin inhibits EMT by targeting prolyl 4-hydroxylase subunit alpha 1, thereby restoring abnormal tumor blood vessels in GBM, reshaping the immunosuppressive tumor microenvironment and enhancing the efficacy of chimeric antigen receptor (CAR)-T immunotherapy and chemotherapy (60).

Neuroblastoma is a malignant cancer originating from embryonic neural crest cells in the sympathetic nervous system (61). Erianin shows a multi-target anticancer mechanism in the treatment of neuroblastoma (3). Previous research has shown that erianin inhibits the malignant phenotype of SH-SY5Y cells through dual regulation: Erianin promotes the apoptosis of tumor cells by downregulating the expression levels of cancer-promoting Homo sapiens (hsa)-miR-155-5p and hsa-miR-223-3p (62).

RCC is a highly heterogeneous malignant cancer derived from the renal tubular epithelial system. Erianin could promote N6-methyladenosine modification of arachidonate 12-lipoxygenase, 12s-type/P53 mRNA, regulate ferroptosis-associated signaling pathways and induce ferroptosis in renal cancer cells (63).

Bladder cancer is the second most prevalent malignant tumor of the urological system (5.85 cases per 100 000) (64). Erianin shows a multi-target anticancer mechanism in the treatment of bladder cancer (65). Specifically, erianin serves a key role through dual pathways: Erianin effectively induces ferroptosis in bladder cancer cells by inhibiting the NRF2 signaling pathway (65) and, by activating the JNK signaling pathway, triggers cell cycle G₂/M phase arrest and promotes apoptosis (66).

Melanoma is a common and highly malignant cancer of the skin, it causes 75% of skin cancer-associated mortality due to its high metastatic potential (64). Erianin exerts a significant effect through a dual mechanism: Erianin effectively promotes cancer cell apoptosis and inhibits cell migration by inhibiting the VEGF-α/PI3K/AKT signaling pathway (67) and inhibits the proliferation and survival of BRAF V600E or RAS mutant melanoma cells by simultaneously targeting MEK1/2 and c-raf proto oncogene serine/threonine protein kinase (CRAF) (41).

Leukemia is a common malignant clonal hematological disease that originates from bone marrow hematopoietic stem cells. Compared with 2020, by 2023, there were 2.4 additional instances per 100,000 people, and the fatality rate had increased to between 1.4 and 1.8 per 100,000 people (68). Erianin serves a significant role through dual pathways: Erianin effectively induces the death of acute myeloid leukemia cells by activating the PPARα signaling pathway and inhibiting PI3K/AKT signal transduction (69) and inhibits the proliferation and promotes the apoptosis of HL-60 leukemia cells by downregulating the expression of the anti-apoptotic protein Bcl-2, upregulating the expression of the pro-apoptotic protein Bax and arresting the cells in the G₂/M phase cell cycle (70).

Osteosarcoma is a common highly malignant bone cancer derived from osteoblasts, accounting for ~35% of all primary bone malignancies. The male-to-female ratio is ~1.5:1.0 (71). Previous in vitro and in vivo experiments have shown that erianin induces cell cycle G₂/M phase arrest, apoptosis and autophagy in human osteosarcoma cells by activating the reactive oxygen species (ROS)/JNK signaling pathway and serves an anticancer role (72). Notably, erianin significantly inhibited tumor growth in a xenograft mouse model without notable toxicity (72).

In conclusion, erianin has shown broad-spectrum anticancer activity in a variety of systems and cancer (Fig. 2; Table I). The underlying mechanisms include ferroptosis and anticancer effects by regulating core signaling pathways such as the PI3K/Akt/mTOR, JAK/STAT, MAPK and Wnt/β-catenin pathways (Fig. 3). The anticancer mechanism of erianin has been verified by a multi-disease model, which laid a foundation for clinical transformation. Compared with single highly selective targeted drugs, erianin has wider indications, overcomes cancer heterogeneity, has stronger clinical practicability, inhibits cancer in multiple systems, decreases drug resistance, is suitable for patients with advanced or multiple refractory cancer and has potential as a combination therapy (73).

The broad-spectrum anticancer biological activity of erianin is based on the precise regulation of key signaling networks (Fig. 3). Erianin induces specific cell death modalities such as ferroptosis via the JAK/STAT pathway and reverses chemotherapy resistance (21) and reprograms metabolism through the Wnt/β-catenin pathway (16). These converging mechanisms constitute the molecular basis for the universality and therapeutic potential of erianin against heterogeneous types of malignancy.

However, erianin may possess drug toxicity, and needs to balance efficacy and safety. A previous study found that erianin is stable, has low toxicity and shows consistent sensitivity and reliability in rat plasma under specific storage conditions (including long-term storage at low temperatures, short-term stability at room temperature and freeze-thaw cycle stability) (74), which provides a practical basis for clinical application.

Erianin has shown extensive therapeutic potential in chronic inflammation-related diseases, such as ulcerative colitis, rheumatoid arthritis, osteoarthritis, chronic atrophic gastritis and psoriasis (87-94,95,96). Previous studies have shown that erianin exhibits anti-inflammatory activity by directly inhibiting the assembly and activation of NLRP3 inflammasomes (87,95). In ulcerative colitis, erianin serves a role through a dual mechanism: On the one hand, erianin reduces the expression of the pro-inflammation factors IL-6 and IL-8 by inhibiting the TLR4/TRAF6/NF-κB signaling pathway. On the other hand, erianin restores immune homeostasis by regulating the IL-2 levels (88). Similarly, erianin also has potential in the treatment of rheumatoid arthritis, where it inhibits the abnormal activation and polarization of T helper 17 cells by targeting the JAK/STAT3 signaling pathway (89). In addition, erianin serves a protective role in osteoarthritis by activating the GPX4/STING signaling pathway and inhibiting IL-1β-induced chondrocyte ferroptosis, oxidative stress and extracellular matrix degradation (90).

In chronic atrophic gastritis, erianin exhibits a regulatory role in maintaining autophagy homeostasis by balancing the activity of the MAPK/mTOR signaling pathway (91). The key core mechanisms of the anti-inflammatory effects of erianin include direct targeting of inflammasomes, regulation of key inflammation signaling pathways and maintenance of immune cell balance.

Psoriasis is a chronic recurrent inflammation skin disease characterized by excessive proliferation and abnormal differentiation of keratinocytes, resulting in impaired epidermal barrier function. Previous mechanistic studies have shown that erianin activates the JNK/c-Jun pathway in a ROS-dependent manner and inhibits AKT/mTOR signaling, thereby regulating the proliferation and differentiation of keratinocytes (92,96). These findings not only reveal the mechanism of erianin in the treatment of psoriasis, but also provide an experimental basis for the development of psoriasis treatment strategies based on ROS signal regulation.

Alopecia areata (AA) is a sudden-onset non-scarring hair disease (93). Erianin regulates the IFN-γ signaling pathway and inhibits cell populations closely related to the pathogenesis of AA (94). It is necessary to explore the causes and pathophysiological mechanisms of AA for the development of more effective treatment methods.

Myocarditis is a type of myocardial inflammation disease that leads to severe arrhythmia. It is the primary cause of dilated cardiomyopathy and may lead to heart failure (97). Erianin has shown notable anti-inflammatory activity and organ protection in acute inflammatory diseases, such as myocarditis and acute lung injury (98-100). In myocardial inflammation, erianin exerts therapeutic effects through a dual mechanism: Inhibiting the NF-κB and NLRP3 signaling pathways, decreasing M1 macrophage polarization and improving myocardial fibrosis and dysfunction to alleviate autoimmune myocarditis (98). By activating the Keap1/Nrf2 antioxidant pathway, reducing anthracycline-induced cardiotoxicity such as doxorubicin (DOX) and improving cardiac systolic function, erianin provides dual protection against chemotherapy-associated heart damage (99).

The lung is susceptible to acute inflammation and subsequent injury due to its extensive microvascular network and direct exposure to external stimuli. P-selectin is a potential therapeutic target for acute inflammation (100). Erianin mitigates lipopolysaccharide-induced acute lung injury in mice, reducing total cells, neutrophils and protein content in bronchoalveolar lavage fluid (BALF), as well as suppressing pro-inflammatory cytokines in both lung tissue and BALF (100).

In vivo, erianin inhibits NF-κB pathway activation in lung tissue, but does not attenuate inflammation responses in human pulmonary microvascular endothelial cells (HPMECs) in vitro (99). Mechanistically, erianin blocks neutrophil adhesion and transient adhesion-mediated movement along the surface of HPMECs by decreasing the binding affinity between P-selectin and p-selectin glycoprotein ligand-1 without altering P-selectin expression or membrane translocation (101).

This multi-target action characteristic makes erianin a potential candidate for the treatment of inflammation-associated diseases, and provides a theoretical basis for the development of new anti-inflammatory strategies.

Human enterovirus 68 (EVD68) is an emerging viral pathogen that has received increasing attention due to its association with severe respiratory disease, such as asthma exacerbations, community-acquired pneumonia and typical acute respiratory illness (102-104). Erianin inhibits the production of EVD68 by inducing G₂/M blockade (105), thus suggesting the potential application of erianin in antiviral research.

Oxygen free radicals and lipid peroxides are associated with the etiology of aging and diseases such as cancer, multiple sclerosis, Parkinson's disease, senile dementia, autoimmune disease and asbestosis (106). Erianin can effectively inhibit the abnormal activation of the ERK1/c-Jun signaling pathway following traumatic brain injury (TBI), and reduce oxidative stress and inflammation response in brain tissue (107). This reveals the antioxidant mechanism of erianin in TBI treatment.

Erianin exhibits a dual mechanism of action in overcoming cancer multidrug resistance (MDR). In an oxaliplatin-resistant model of colon cancer, erianin downregulates the expression of drug efflux protein P-glycoprotein (P-gp) by specifically inhibiting the JAK2/STAT3 signaling pathway, thereby effectively reversing the MDR phenotype of cancer cells (108). Erianin can also directly target the colchicine binding site of β-tubulin and impair the integrity of the cytoskeleton by inhibiting microtubule polymerization (109). This mechanism not only overcomes paclitaxel resistance (109), but also explains broad-spectrum anticancer activity of erianin.

Key mechanisms of erianin in overcoming cancer drug resistance include the regulation of drug transport systems and targeting of key components of the cytoskeleton, as well as the regulation of signaling pathways and direct cytotoxicity (108,109). This makes erianin a potential candidate drug to overcome cancer drug resistance, which provides a molecular mechanism basis and theoretical support for the development of novel MDR reversal strategies (109). Selective regulation mechanism of erianin on the resistance of different types of chemotherapeutic drug remains to be further elucidated.

Staphylococcus aureus is a Gram-positive opportunistic pathogen. Sortase A (SrtA) is a key transpeptidase of Gram-positive bacteria. Erianin blocks the entry and binding of T-G peptide chain and lipid II of surface protein to the SrtA biological active center and effectively inhibits the anchoring function of transpeptidase (110). This finding reveals the mechanism of erianin against S. aureus infection and provides important theoretical basis and potential therapeutic targets for the development of novel anti-infection strategies based on SrtA inhibition.

Erianin has shown neuroprotective effects in neurological diseases such as traumatic brain injury, cerebral ischemia-reperfusion injury and Parkinson's disease (105,111-113), and its mechanism of action primarily involves the regulation of key signaling pathways. In acute BI, erianin exerts a protective effect through a dual mechanism: In cerebral ischemia-reperfusion injury, erianin inhibits microglia-mediated neuroinflammation by regulating the PI3K/AKT and NF-κB pathways (111). In TBI, erianin attenuates neuronal injury by inhibiting the ERK1/c-Jun signaling pathway (105).

Erianin significantly alleviates neuroinflammation in a Parkinson's disease model by inhibiting the NF-κB/NLRP3 inflammasome pathway (112). Erianin promotes neuronal differentiation by regulating ERK1/c-Jun signaling (113). The aforementioned studies have revealed that the key mechanisms of neuroprotection of erianin include regulating the inflammatory response (NF-κB/NLRP3 pathway), maintaining neuronal survival (PI3K/AKT pathway) and promoting nerve regeneration (ERK1/c-Jun pathway). This makes erianin a potential candidate drug for the treatment of neurological disease and provides an important theoretical basis for the development of neuroprotection strategies based on signaling pathway regulation.

Decreased vascular endothelial (VE)-cadherin expression in hepatic vascular endothelial cells is associated with hepatic steatosis in the early stage of non-alcoholic fatty liver disease (NAFLD); erianin could reduce hepatic steatosis by enhancing Nrf2-mediated VE-cadherin expression (114).

In conclusion, a number of studies have confirmed that erianin exhibits pharmacological activity beyond its antitumor activity (5,6). Erianin functions as a pleiotropic agent capable of restoring homeostasis across diverse pathological microenvironments (Fig. 4; Table II). Erianin is used in a treatments, ranging from reducing diabetic complications and inhibiting pathological angiogenesis, to alleviating acute and chronic inflammation, as well as for other biological activities, including neuroprotection, anti-hepatic steatosis, anti-microbial effects (antiviral and antibacterial), anti-oxidation and reversal of drug resistance. These bioactivities are driven by the ability of erianin to modulate key signaling pathways, primarily the inflammatory NF-κB/NLRP3 pathway, the oxidative stress-responsive Nrf2 pathway and cytoskeletal dynamics. By simultaneously targeting upstream receptors and downstream effectors, erianin serves as a multi-target candidate for complex disease management. However, the poor water solubility and low bioavailability of erianin limit its practical applications (6). In recent years, researchers have effectively improved the water solubility and bioavailability of erianin by chemical modification, new manufacturing technology and structural optimization (Fig. 5; Table III) (5).

The development of an erianin nano-delivery system has improved the clinical application bottleneck of this natural product. Solubility, targeting and therapeutic effect of erianin have been improved through preparation techniques (131). In cancer therapy, the DOX and erianin-loaded CaCO₃-based nanoparticles (DECaNPs) system shows multiple advantages, such as inducing calcium overload, neutralizing the acidic tumor microenvironment, activating oxidative stress damage, promoting immunogenic cell death, and enhancing immunotherapy (132). Similarly, the curcumin encapsulated nanoparticles (CEN) system combined with celastrol and erianin through self-assembly technology (133), shows benefits including enhancing cancer accumulation, improving drug solubility, and reduced systemic toxicity while maintaining potent anticancer activity. In the treatment of skin disease, the embedded dual-mesoporous silica nanoparticles (E/DMSNs) system enhances the inhibitory effect on keratinocytes through mitochondrial and endoplasmic reticulum stress pathways (134) and the light-responsive carrier achieves controlled release delivery of erianin (131).

Nano-delivery system solves the core problems of poor water solubility and low bioavailability of erianin (131). However, this technology faces three major challenges, including the balance between preparation stability and drug loading efficiency, optimization of large-scale production process and verification of long-term safety. Future research should aim to overcome these technical bottlenecks while maintaining targeted advantages to accelerate the clinical transformation of erianin nanoformulations.

The erianin liposome delivery system provides an effective strategy to solve the poor aqueous solubility and off-target effects in its clinical application. Previous studies have shown that the solubility and targeting of erianin are improved by folic acid-chitosan modified dual drug-loaded liposomes (135) and transferrin-coupled liposomes (Tf-LP-ERN) (136). These systems enhance the accumulation of drugs in cancer cells through specific ligand-receptor interactions (such as folate receptor and transferrin receptor-mediated endocytosis), while using the sustained release characteristics of liposomes to prolong drug efficacy (136-138).

Although the liposome delivery system has good biocompatibility and high safety, it faces challenges, including complex preparation processes leading to batch-to-batch differences, poor physical stability affecting the storage period and high production costs restricting industrial production (136-138). Overcoming these technical bottlenecks is required to achieve the clinical application of erianin liposome preparations. In summary, carrier modification technology has a range of applications in erianin through nano-delivery and liposome delivery systems (Fig. 6).