Quercetin in oncology: evidence map and translational summary
This 2026 oncology research deep dive unpacks the science, the gaps, and the dose, safety and interaction questions that matter.
Intro
Quercetin is a dietary flavonol with a large, mechanistically diverse oncology literature. The evidence is strongly weighted toward cell cultures and rodent models: across breast, colorectal, gastric, prostate, lung, liver, pancreatic, ovarian, haematological, brain and other cancers.
Studies report growth inhibition, apoptosis, altered tumor metabolism, reduced stem-like phenotypes, and sensitization to selected anticancer drugs. These observations support biological activity, not clinical efficacy.
The main translational barriers are the gap between experimental concentrations and human exposure, rapid conjugation and elimination after oral intake, uncertain active species and tissue delivery, and context-dependent redox effects. One early phase-I study tested intravenous quercetin in patients with refractory cancer and identified renal toxicity at high doses; it did not establish anticancer efficacy or a safe oral supplement regimen.
Human oral pharmacokinetic work shows marked dependence on the glycoside and food matrix, and detected circulating glucuronides rather than free aglycone. Stem-cell, ferroptosis/NRF2, multi-drug-resistance, metabolism and immune-oncology findings are promising but remain predominantly preclinical.
There is no evidence-based oncology dose, timing schedule, or product-quality recommendation. This review maps the evidence by model and cancer type, then assesses mechanisms, pharmacology, safety, combinations and research priorities.
Quercetin deep dive jump menu
1. Overall evidence: impressive preclinical breadth, thin clinical bridge
5. Human pharmacokinetics, metabolism, dose, timing and safety
8. Evidence quality, open questions and practical conclusions
1. Overall evidence: impressive preclinical breadth, thin clinical bridge
What the laboratory research reports
Across reviews and experimental studies, recurring findings include:
Reduced cancer-cell growth and multiplication.
Cell-cycle arrest.
Apoptosis.
Autophagy.
Reduced migration and invasion.
Anti-angiogenesis.
Changes in signalling pathways, including PI3K–AKT–mTOR, MAPK, NF-κB, JAK/STAT, p53 and Wnt/β-catenin.
These findings provide a credible reason to investigate quercetin as a possible treatment candidate or addition to existing therapy. They do not show that a dietary supplement treats cancer.
A key difficulty is the gap between laboratory exposure and human exposure:
Cell experiments often use micromolar concentrations of quercetin.
After oral intake, quercetin is extensively metabolised and circulates mainly as conjugates.
The effects seen in cultured cells therefore cannot be assumed to occur after taking an oral supplement [1], [2], [3], [4].
Different cancer cells respond differently
A 2025 NCI-60-oriented abstract tested 77 cancer cell lines and reported substantial variation between them:
The reported IC50 ranged from 5.03 μM in one glioblastoma line to 5,780.61 μM in a renal carcinoma line.
Myeloid and prostate lines were relatively sensitive within that panel.
Ovarian/fallopian lines were less sensitive.
These results help generate research questions. They do not establish which patients—or which cancer types—would benefit from quercetin [5].
A separate review of cell-line results also highlighted tissue- and cell-dependent activity, rather than a universal response [6].
What the human studies show
The only clearly identified oncology patient study in this search was a 1996 phase-I trial that tested increasing doses of intravenous quercetin.
That study provided information about:
Quercetin’s pharmacology.
Kidney toxicity at high doses.
Isolated tumor-marker changes in individual patients.
Those tumor-marker changes do not establish anticancer efficacy.
Later human pharmacokinetic studies examined absorption of food-derived quercetin glycosides, rather than cancer outcomes [7], [8].
What this search did not establish
This search did not identify:
A randomised human trial establishing quercetin as an anticancer treatment.
A clinically validated regimen for using it alongside cancer therapy.
Evidence establishing ordinary dietary intake or supplements as a way to prevent or treat an individual’s cancer.
The overall picture is broad preclinical activity, but limited evidence connecting those findings to clinical benefit in people.
Quercetin is not a standard cancer treatment. The current case for it's anti-cancer use is mechanistic and preclinical.
Be sure to read the page unpacking why natural medicines often lack large clinical trials
2. Evidence by cancer type
Interpretation: “Preclinical” below means cell culture and/or animal models; it does not imply a human response.
Several newer reports are abstract-only, so their claims should be treated as early signals until methods and replication are assessed.
Cancer area | What the retrieved studies report | Evidence judgement |
|---|---|---|
Breast | Cell and mouse studies report apoptosis, PI3K/AKT/mTOR modulation and reduced CSC-associated stem-like phenotypes [10], [11], [12]. Separate cell studies report ferroptosis-associated effects through TFEB/ferritin handling or NEDD4L–SLC7A11 [13], [14]. | Multiple mechanistic models and some mouse work; no established clinical benefit. Effects vary by cell model and proposed pathway. |
Colorectal/colon | HT29 CD133+ cells were less sensitive than bulk cells, but quercetin increased low-dose doxorubicin activity; other work reports hypoxic invasion suppression and reversal of P-glycoprotein-mediated resistance through SLC1A5/glutamine metabolism [15], [16], [17]. A 2026 mouse metastasis study links BCAT1/BCAA metabolism to CD8+ T-cell activity [18]. | Cell and animal evidence, with translationally interesting immune-metabolic mechanisms; no human treatment outcome. |
Gastric | Studies report apoptosis in gastric CSC-enriched models, ferroptosis through SLC1A5–NRF2/xCT/GPX4 and lysosomal/autophagic pathways, and reversal of selected drug resistance; a recent co-culture/xenograft abstract reports increased CD8+ cytotoxic markers with altered PD-L1 protein [19], [20], [21], [22], [23]. | Rich preclinical literature, but mechanistic heterogeneity and no clinical validation. |
Prostate | Models report inhibition of survival signalling and stem-like populations; quercetin plus docetaxel reversed resistance-associated traits in resistant cells and xenografts [24], [25]. | Promising resistance-focused preclinical evidence; not an alternative to standard prostate-cancer care. |
Lung | Broad in-vitro and animal literature is summarised in a systematic review; a 2026 NSCLC study reports ferroptosis via DDB2-AS1/miR-4728-5p/p53 and cisplatin-resistance reversal in models [26], [27]. | Preclinical, including one recent resistance mechanism; no patient efficacy evidence retrieved. |
Liver/HCC and intrahepatic cholangiocarcinoma | HCC reports include doxorubicin sensitisation and resistance modulation via p53/Bcl-xL or FZD7/β-catenin/ABC transporters; cholangiocarcinoma studies report ferroptosis and reduced invasion via NF-κB [28], [29], [30], [31]. A preclinical meta-analysis included nine studies and found reduced mouse tumor burden, while explicitly identifying the lack of clinical validation [32]. | Better animal-model breadth than many sites, but still preclinical; animal meta-analysis does not upgrade evidence to human efficacy. |
Pancreatic | Studies report effects on CSC self-renewal and apoptosis resistance, combination activity with gemcitabine, and altered STAT3–CPT1B lipid metabolism; a recent PDAC study links ferritinophagy to ferroptosis [33], [34], [35], [36]. | Promising disease-specific hypotheses; oral exposure and tumor delivery remain major unresolved issues. |
Ovarian/endometrial | Ovarian cell/xenograft reports include ferroptosis through HSPB1/Notch1 and reduced migration; endometrial CSC-enriched models report ERα-dependent STAT3/JAK2 suppression [37], [38], [39]. | Early preclinical only; ovarian cell lines were relatively insensitive in one cross-cancer panel, illustrating model dependence [5]. |
Haematological cancers | Leukemia models report apoptosis, cell-cycle effects, redox/ERK signaling, and doxorubicin sensitisation; one 2025 ALL study reports inhibition of glycolysis and oxidative phosphorylation-related endpoints [40], [41], [42], [43]. | Several in-vitro and xenograft reports, but no clinical efficacy evidence identified. |
Glioblastoma/brain | U87MG/T98G models and mouse work report lower glycolytic activity, tumor burden and improved animal survival [44]. | Animal survival is not patient survival; brain exposure and human pharmacokinetics are not established by these data. |
Oral/head-and-neck, melanoma, cervical, thyroid, bladder | Oral squamous-carcinoma studies report ferroptosis [45], [46]; a head-and-neck model reports lower tumor-initiating-cell traits [47]; mouse melanoma work describes immune changes [48]; a cervical-cancer study is cell-based [49]; thyroid-cell work describes CSC/metabolic effects [50]; and a mouse bladder-cancer study reports microbiome/serine-metabolism effects [51]. | Emerging and varied preclinical signals; each rests on distinct models and should not be pooled into a general effect estimate. |
Across cancer sites, reported direction is often inhibitory, but potency and mechanism differ substantially by cell line, dose, oxygenation, drug-resistance status, and formulation. These studies support a platform of testable mechanisms—not a single validated pan-cancer mechanism or a clinical cancer-type ranking [5], [6], [32].
3. Mechanisms: areas of signal and contradiction
Redox, NRF2 and ferroptosis
Quercetin is not simply an antioxidant. Its redox behaviour is context- and dose-dependent: it can scavenge oxidants or activate antioxidant defences, yet in some tumor models it increases ROS, lipid peroxidation and cell death. A prior oncology review describes a biphasic antioxidant/pro-oxidant pattern, while experimental studies show that the observed direction depends on the model and cellular redox state [2], [3], [52].
The clearest recent mechanistic thread is ferroptosis, an iron-dependent lipid-peroxidation death process. Experimental work links quercetin to lysosomal TFEB activation, ferritin breakdown and iron release in cancer models [13], [53]. Separate studies report ferroptosis-associated effects in gastric cells through SLC1A5 and NRF2/xCT/GPX4 signalling [20], oral squamous cells through LGR4/NF-κB/GPX4 [46], ovarian models through HSPB1/Notch1 [37], lung cancer resistance models through DDB2-AS1/miR-4728-5p/p53 [27], and pancreatic models through NCOA4-mediated ferritinophagy [36].
Mechanism is often tested with pathway perturbation or ferroptosis inhibitors, which is more informative than pathway prediction alone; nevertheless, this remains model-specific preclinical evidence. NRF2 deserves particular caution: it can protect normal tissue by inducing antioxidant defenses, while tumor-cell NRF2 signaling can also support stress tolerance and drug resistance.
A recent liver-cancer abstract reports NRF2-related ferroptosis effects, while gastric-cancer work describes reduced NRF2 nuclear translocation with quercetin. So the takeaway is 'do not label NRF2 modulation uniformly beneficial' [20], [54].
Cancer stem-like cells and multi-drug resistance
CSC populations studied
CSC claims are based chiefly on marker-selected or sphere-enriched cell populations, including:
CD44+/CD24− breast cells.
CD133+ colorectal cells.
Gastric CSC-enriched cultures.
Prostate CSC-enriched cells.
Endometrial spheres.
Reported effects and signalling
Reported effects include reductions in:
Sphere or colony formation.
Stemness markers.
Invasion.
Tumorigenicity.
Several studies implicate:
PI3K/AKT/mTOR.
STAT3.
ERα.
Midkine.
EMT-associated signalling.
References: [10], [15], [19], [25], [33], [39], [47].
These assay-defined populations do not establish eradication of clinically persistent CSCs in patients.
Candidate drug-resistance mechanisms
Drug-resistance studies describe distinct candidate mechanisms:
P-gp/ABCB1 and other ABC efflux transporters or YB-1 [29], [55].
FZD7/β-catenin in HCC [29].
NRF2/HO-1 in 5-FU-resistant colon cells [56].
SLC1A5/glutamine metabolism [17].
Hypoxia-associated HIF-1α signalling [16].
Androgen-receptor/PI3K signalling in prostate models [24].
Reported activity with chemotherapy
Selected models report enhanced activity with:
Interpreting the evidence
This breadth is not proof of a common clinically usable resistance-reversing effect.
Transporter inhibition may also change exposure to medicines in normal tissues.
See our treatment resistance hub which includes a page dedicated to learning about 'How some cancer cells pump drugs out'
Metabolic and signalling effects of Quercetin
Metabolic work describes effects on:
Glycolysis.
Oxidative phosphorylation.
Fatty-acid oxidation.
Glutamine transport and metabolism.
Branched-chain amino-acid handling.
Serine synthesis.
Lipid oxidation.
Examples include:
Reduced glycolysis in glioblastoma and ALL models.
CPT1-linked fatty-acid oxidation in breast models.
STAT3–CPT1B in pancreatic CSCs.
BCAT1/BCAA-linked immune-metabolic effects in colorectal metastasis.
References: [18], [35], [43], [44], [60].
The variety makes metabolic reprogramming a promising research lens. However, there is no replicated evidence for:
One tumor-metabolic target across cancer types.
A dietary dose that achieves these effects in human tumors.
Signalling pathways
The proposed pathways span:
PI3K/AKT/mTOR in breast-cancer cells [61].
MAPK/ERK in cervical-cancer cells [49].
NF-κB in HCC resistance models [29].
JAK/STAT in endometrial CSC-like cells [39].
p53 in cisplatin-resistant lung-cancer models [27].
Wnt/β-catenin in HCC resistance models [29].
Interpreting the evidence
As a methodological interpretation, pathway association alone does not establish causality:
Some studies use docking or network prediction.
Others perturb candidate pathways or use rescue experiments.
Perturbation evidence better tests a proposed mechanism, but still does not establish a clinical target..
4. Immune-oncology and combinations
Immune findings
Immune findings are promising but early.
In breast-cancer studies:
A co-culture study found that quercetin promoted a γδ T-cell subset and altered JAK/STAT1 and PD-L1-associated signals.
A mouse study reported persistent tumor-specific T-cell responses when dietary quercetin was combined with intratumoral doxorubicin.
Other mouse or cell-based reports describe:
Treg depletion in TNBC.
Increased CD8+ activity or PD-L1 changes in gastric cancer.
Altered macrophage/CD8+ populations in melanoma.
Immune-metabolic effects in colorectal metastasis.
References: [18], [23], [48], [64].
These findings do not establish compatibility or synergy with checkpoint inhibitors in patients.
A mouse study of quercetin plus anti-PD-1 in HCC reported immune-microenvironment and microbiota changes, but provides no patient outcomes [65].
Combination findings
Combinations often look favourable in preclinical systems, but synergy is specific to the:
Dose ratio.
Schedule.
Assay.
Model.
Reported combination effects include:
Enhanced doxorubicin effects in colorectal CSC-enriched cells [15].
Enhanced doxorubicin or docetaxel effects in breast-cancer cell or mouse models [58], [63], [66].
Combination effects with gemcitabine in pancreatic models [33], [35].
The broader review literature also describes sensitisation and normal-tissue protection. However, many combination findings remain cell or animal experiments [4], [67], [68].
Antioxidant activity: a treatment-specific question
Depending on timing and regimen, antioxidant activity could:
Protect normal tissue.
Potentially interfere with therapies that depend on oxidative injury.
The net effect cannot be inferred from “antioxidant” labelling and needs drug-specific clinical testing [2], [3].
5. Human pharmacokinetics, metabolism, dose, timing and safety
What human pharmacology actually shows
First-in-human oncology trial
In the first-in-human oncology phase-I trial:
Quercetin was given by short intravenous infusion, starting at 60 mg/m² and escalating.
Dose-limiting nephrotoxicity occurred at 1,700 mg/m².
Renal toxicity also occurred at lower high-dose levels.
The recommended 1,400 mg/m² bolus schedule was a phase-II research recommendation, not an oral supplement dose.
The terminal half-life was short: a median of 43 minutes in a two-compartment model.
Lymphocyte tyrosine phosphorylation was inhibited in 9 of 11 patients.
Two individual patients had tumor-marker changes, which cannot establish response or efficacy [7].
Oral exposure in healthy volunteers
A four-way crossover study of 12 healthy volunteers found that:
100 mg quercetin equivalents from onion or isolated quercetin-4′-O-glucoside produced peak plasma concentrations near 2.1–2.3 μg/mL at about 0.7 hours.
200 mg equivalents from rutin or buckwheat tea produced lower peaks, about 0.3–0.6 μg/mL, later—at roughly 4–7 hours.
Plasma contained glucuronides, not free quercetin.
Terminal half-life was about 11 hours.
Thus, dose alone did not predict exposure: glycoside form and food matrix mattered [8].
Absorption and metabolism limitations
Reviews identify several obstacles:
Poor solubility.
Limited oral availability.
Rapid conjugative metabolism.
Inflammatory β-glucuronidase activity may locally regenerate aglycone, but the clinical significance is unproven [3], [69].
Dosing and timing
There is no validated anticancer:
Oral dose.
Timing rule.
Cycling schedule.
Formulation.
In-vitro exposure durations and animal mg/kg doses cannot be converted directly into a patient regimen.
The phase-I intravenous oncology data are historical pharmacology, not evidence that high-dose IV quercetin should be used outside research [7], [8].
Drug interactions
Drug-interaction concern is biologically plausible rather than settled clinically:
Tumor-model sensitisation often involves inhibition of P-gp/ABCB1 or related efflux transporters.
Co-administration can alter intracellular drug accumulation.
That mechanism could change exposure to concomitant drugs.
This search did not establish:
The size or direction of such interactions in patients.
A universal safe interval between quercetin and treatment.
For a person receiving cancer therapy, supplement use should be discussed with the oncology pharmacist/prescriber rather than timed or dosed from cell-model results.
Safety and metabolic safety
“Natural” and “well tolerated” are not equivalent to harmless at pharmacologic exposure.
The phase-I IV study’s dose-limiting renal toxicity is a concrete caution. Dietary exposure and high-dose IV administration are not interchangeable [7].
Recent reviews characterize oncology trial data as sparse and note unresolved questions about:
Pharmacokinetics.
Dose.
Interactions.
The retrieved oncology evidence does not define long-term safety in patients with:
Cancer.
Renal or hepatic impairment.
Poly-pharmacy.
Treatment-related organ vulnerability.
Metabolic effects on glucose, lipid and amino-acid pathways are primarily tumor-model findings. They do not establish a clinically useful or safe metabolic intervention [18], [35], [44], [60].
6. Formulation, sourcing and product quality
For sourcing, the peer-reviewed academic search did not identify a robust head-to-head survey validating commercial quercetin product identity, purity, contaminant levels, dissolution, stability or label accuracy. Therefore, no brand, supplier or “best” formulation can be recommended from peer reviewed evidence. Product standardisation and independent batch testing are important factors.
See the community's Trusted Supplies page for a high purity third party tested Quercetin (contains >97% Quercetin)
Bromelain supports Quercetin absorption after oral administration
7. Antimicrobial/anti-fungal relevance
What laboratory studies have found
Quercetin has shown anti-fungal activity in laboratory studies, particularly against Candida. Reported findings include:
Reduced biofilm formation—the attached communities of fungal cells that can make infections harder to treat.
Reduced development of hyphae, the thread-like growth associated with Candida invasion.
Increased susceptibility to fluconazole in some fluconazole-resistant Candida albicans strains.
For example, a 2015 study found that quercetin reduced biofilm formation and several virulence-related activities in a resistant C. albicans strain. It also increased fungal cell death when combined with fluconazole. These were laboratory experiments, not treatment results in patients.
A separate study tested 17 C. albicans isolates, including 15 collected from patients with vulvovaginal candidiasis. It reported activity against biofilms and enhanced effects with fluconazole under the tested conditions. Although some fungal samples came from patients, the experiments on those samples were performed in the laboratory—not as a clinical trial.
What animal studies add
The latter study also tested treatment in a mouse model of vaginal candidiasis. It reported reduced fungal burden and improvement in symptoms following quercetin and/or fluconazole treatment. This adds animal evidence, but does not establish effectiveness in humans or in cancer-related infections.
The studies identified above support preclinical anti-fungal activity but do not identify human clinical evidence.
8. Evidence quality, open questions and practical conclusions
Why laboratory findings do not yet establish patient benefit
The biggest gap is whether the concentrations and exposure times used in experiments can be achieved safely in human tumors.
Much of the research uses:
Cancer cells grown in the laboratory.
Cell lines selected for drug resistance.
Sphere assays used to study CSC-like properties.
Human tumors grown in mice.
Small mouse studies.
These models help researchers explore possible effects. However, cancer cells are not patients, and a response in an animal does not establish clinical benefit.
Comparisons between studies are also difficult because researchers do not always use the same CSC markers or proposed signalling pathways.
Another important difference is the form of quercetin being studied. High-concentration experiments often use the aglycone form, whereas oral use produces circulating glucuronide and sulfate conjugates. The experimental exposure may therefore differ from what reaches tissues in people [5], [6], [8].
What stronger studies need to establish
The next decisive studies would need to answer five questions:
How much reaches the tumor or TME?
Establish how each formulation is absorbed, processed and distributed in people, including the exposure achieved in tumor tissue.Which forms are present?
Measure both quercetin itself and its metabolites.How does it interact with cancer medicines?
Test interactions through clinical pharmacology studies, rather than relying on transporter assays alone.Which tumours might respond?
Use biomarkers chosen in advance to group tumours by features such as NRF2/GPX4 activity, drug transporters, CSC-related characteristics or metabolic state.Does it help patients safely?
Test a standardised product in controlled oncology trials that measure safety, drug exposure and outcomes that matter to patients.
What the evidence means in practice
The current evidence does not yet support:
An over-the-counter quercetin regimen for treating cancer.
Routine use alongside cancer treatment.
Replacing proven therapy with quercetin.
Quercetin remains an interesting research candidate, particularly in studies of:
Ferroptosis.
Drug resistance.
CSC-like properties.
Tumor metabolism.
Immune signalling.
Human evidence shows that exposure depends on the formulation and that high-dose intravenous administration can injure the kidneys. It does not establish that oral quercetin treats cancer.
The responsible interpretation is: “research lead, not proven oncology treatment.”
Be sure to read our page where we explain Why natural medicines often lack large clinical trials
References
Further reading
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[2] N. Jana, G. Břetislav, S. Pavel, and U. Pavla, “Potential of the flavonoid quercetin to prevent and treat cancer - current status of research,” Klinicka onkologie : casopis Ceske a Slovenske onkologicke spolecnosti, 2018, doi: 10.14735/amko2018184.
[3] M. Sopjani, B. Krasniqi, E. Jashari, N. Xuan, F. G. D’Agostino, and C. Faggio, “Quercetin in cancer therapy: Molecular mechanisms, delivery strategies, clinical prospects, and safety.” Current Medicinal Chemistry, 2026, doi: 10.2174/0109298673448995251127063419.
[4] A. F. Brito et al., “Quercetin in cancer treatment, alone or in combination with conventional therapeutics?” Current medicinal chemistry, 2015, doi: 10.2174/0929867322666150812145435.
[5] A. Goraieb, A. Aggarwal, and K. W. Yip, “Abstract 6760: Anticancer mechanisms of quercetin revealed via a systems biology approach,” Cancer Research, 2025, doi: 10.1158/1538-7445.am2025-6760.
[6] K. Sak, “Site-specific anticancer effects of dietary flavonoid quercetin,” Nutrition and cancer, 2013, doi: 10.1080/01635581.2014.864418.
[7] D. R. Ferry et al., “Phase i clinical trial of the flavonoid quercetin: Pharmacokinetics and evidence for in vivo tyrosine kinase inhibition.” Clinical cancer research : an official journal of the American Association for Cancer Research, vol. 2, no. 4, pp. 659–68, 1996, Available: https://pubmed.ncbi.nlm.nih.gov/9816216
[8] E. U. Graefe et al., “Pharmacokinetics and bioavailability of quercetin glycosides in humans.” Journal of clinical pharmacology, vol. 41, no. 5, pp. 492–499, 2001, doi: 10.1177/00912700122010366.
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[10] X. Li et al., “Quercetin suppresses breast cancer stem cells (CD44+/CD24−) by inhibiting the PI3K/akt/mTOR‐signaling pathway,” Life Science, 2018, doi: 10.1016/j.lfs.2018.01.014.
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[19] X. Shen, Y. Si, Z. Wang, J. Wang, Y. Guo, and X. Zhang, “Quercetin inhibits the growth of human gastric cancer stem cells by inducing mitochondrial-dependent apoptosis through the inhibition of PI3K/akt signaling,” International journal of molecular medicine, 2016, doi: 10.3892/ijmm.2016.2625.
[20] L. Ding et al., “Quercetin induces ferroptosis in gastric cancer cells by targeting SLC1A5 and regulating the p-Camk2/p-DRP1 and NRF2/GPX4 axes.” Free Radical Biology & Medicine, 2024, doi: 10.1016/j.freeradbiomed.2024.01.002.
[21] J. Huang, J. Chen, and J. Li, “Quercetin promotes ATG5-mediating autophagy-dependent ferroptosis in gastric cancer,” Journal of Molecular Histology, 2024, doi: 10.1007/s10735-024-10186-5.
[22] H. B. Hyun, J. Y. Moon, and S. K. Cho, “Quercetin suppresses CYR61-mediated multidrug resistance in human gastric adenocarcinoma AGS cells,” Molecules, 2018, doi: 10.3390/molecules23020209.
[23] Y. Liu et al., “Quercetin inhibits gastric cancer growth and enhances t cells immunity by modulating the PI3K-AKT signaling pathway,” Bioorganic chemistry, 2026, doi: 10.1016/j.bioorg.2026.110420.
[24] X. Lu et al., “Quercetin reverses docetaxel resistance in prostate cancer via androgen receptor and PI3K/akt signaling pathways,” International Journal of Biological Sciences, 2020, doi: 10.7150/ijbs.41686.
[25] S. Erdogan et al., “Midkine downregulation increases the efficacy of quercetin on prostate cancer stem cell survival and migration through PI3K/AKT and MAPK/ERK pathway.” Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2018, doi: 10.1016/j.biopha.2018.08.061.
[26] S. V. Jasemi, H. Khazaei, S. Fakhri, Z. Samimi, I. Aneva, and M. H. Farzaei, “Quercetin modulates the signalling pathways and therapeutic targets in the pathophysiology of lung cancer: A systematic review,” Letters in Drug Design & Discovery, 2023, doi: 10.2174/1570180820666230719121525.
[27] M. Li et al., “Quercetin overcomes cisplatin resistance by inducing ferroptosis via the DDB2‐AS1/miR‐4728‐5p/p53 axis,” Phytotherapy Research, 2026, doi: 10.1002/ptr.70216.
[28] G. Wang, J. Zhang, L. Liu, S. Sharma, and Q. Dong, “Quercetin potentiates doxorubicin mediated antitumor effects against liver cancer through p53/bcl-xl,” PloS one, 2012, doi: 10.1371/journal.pone.0051764.
[29] Z. Chen et al., “Reversal effect of quercetin on multidrug resistance via FZD7/β-catenin pathway in hepatocellular carcinoma cells.” Phytomedicine, 2018, doi: 10.1016/j.phymed.2018.03.040.
[30] Y. Song et al., “Quercetin inhibits intrahepatic cholangiocarcinoma by inducing ferroptosis and inhibiting invasion via the NF-[formula: See text]b pathway,” The American journal of Chinese medicine, 2023, doi: 10.1142/s0192415x23500337.
[31] Y. Song et al., “Quercetin inhibits intrahepatic cholangiocarcinoma by inducing ferroptosis and inhibiting epithelial-mesenchymal transformation via the NF-κB pathway,” 2021, doi: 10.21203/rs.3.rs-947377/v1.
[32] Z. Tan et al., “Integration of meta-analysis and network pharmacology to investigate the pharmacological mechanisms of quercetin on hepatocellular carcinoma.” Frontiers in Bioscience, 2025, doi: 10.31083/FBL46289.
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