Ashwagandha(Withaferin A) Cancer Research Results

Ash, Ashwagandha(Withaferin A): Click to Expand ⟱
Features:

Ashwagandha (Withaferin A) — Withaferin A (WA; WFA) is a bioactive steroidal lactone (a “withanolide”) found in Withania somnifera (ashwagandha/Indian ginseng), with most translational oncology discussion centered on WA as a small-molecule electrophile rather than the whole-herb supplement. It is best classified as a natural-product small molecule (steroidal lactone/withanolide) with pleiotropic proteostasis, cytoskeletal, redox-stress, and inflammatory signaling effects; in supplements, WA exposure depends strongly on extract standardization (root vs leaf, % withanolides) and formulation.

Primary mechanisms (ranked):

  1. Hsp90-axis disruption (incl. client protein destabilization) leading to proteostasis stress and multi-client oncoprotein depletion
  2. Covalent targeting of intermediate filaments (notably vimentin) with downstream effects on adhesion/migration, EMT programs, and angiogenic endothelium
  3. Pro-oxidative stress signaling in cancer cells with mitochondrial dysfunction, ER stress/UPR engagement, and apoptosis execution
  4. Inflammation and survival signaling suppression (notably NF-κB-centric programs; context-dependent immune modulation)
  5. Contextual transcriptional/epigenetic modulation (e.g., HDAC/DNMT-related signals) contributing to anti-proliferative phenotypes
  6. Metabolic stress signaling (glycolysis/HIF-1α/ATP depletion) as a secondary vulnerability in susceptible models

Bioavailability / PK relevance: WA shows measurable systemic exposure in animals (reported oral bioavailability in rats), but PK is variable across species, doses, and extract matrices; human exposure data exist from a phase I osteosarcoma study and from healthy-volunteer PK work on standardized Withania extracts measuring circulating withanolides (including WA). WA is lipophilic and subject to first-pass metabolism; typical pharmacodynamic in-vitro micromolar concentrations may exceed achievable unbound plasma levels depending on formulation and dosing.

In-vitro vs systemic exposure relevance: Many mechanistic cancer studies use ~1–10 µM WA; translation requires caution because free (unbound) systemic concentrations and tumor penetration are not well-constrained in humans, and whole-extract products can have low/variable WA content (model- and formulation-dependent).

Clinical evidence status: Limited human oncology evidence: a phase I study in advanced high-grade osteosarcoma reported feasibility/safety and proposed a daily dose level; an active clinical trial evaluates an ashwagandha/withaferin-A strategy with liposomal doxorubicin in recurrent ovarian cancer. Most anticancer support remains preclinical, while non-oncology human data for ashwagandha primarily address stress/sleep and are not evidence of anticancer efficacy.

The main active constituents of Ashwagandha leaves are alkaloids and steroidal lactones (commonly known as Withanolides).
-The main constituents of ashwagandha are withanolides such as withaferin A, alkaloids, steroidal lactones, tropine, and cuscohygrine.
Ashwagandha is an herb that may reduce stress, anxiety, and insomnia.
*-Ashwagandha is often characterized as an antioxidant.
-Some studies suggest that while ashwagandha may protect normal cells from oxidative damage, it can simultaneously stress cancer cells by tipping their redox balance toward cytotoxicity.
Pathways:
-Induction of Apoptosis and ROS Generation
-Hsp90 Inhibition and Proteasomal Degradation

Cell culture studies vary widely, typically ranging from low micromolar (e.g., 1–10 µM).
In animal models (commonly mice), Withaferin A has been administered in doses ranging from approximately 2 to 10 mg/kg body weight.
- General wellness, Ashwagandha supplements are sometimes taken in doses ranging from 300 mg to 600 mg of an extract (often standardized to contain a certain percentage of withanolides) once or twice daily.
- 400mg of WS extract was given 3X/day to schizophrenia patients. report#2001.
- Ashwagandha Pure 400mg/capsule is available from mcsformulas.com.

-Note half-life 4-6 hrs?.
BioAv
Pathways:
- well-recognized for promoting ROS in cancer cells, while no effect(or reduction) on normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Confusing results about Lowering AntiOxidant defense in Cancer Cells: NRF2↓, TrxR↓**, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, uPA↓, VEGF↓, ROCK1↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓(combined with sulfor), DNMT1↓, DNMT3A↓, P53↑, HSP↓, Sp proteins↓, TET↑
- cause Cell cycle arrest : TumCCA↑, cyclin E↓, CDK2↓, CDK4↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓, EMT↓, TOP1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, β-catenin↓, sox2↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, α↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Mechanistic pathway map for Ashwagandha (Withaferin A) in cancer biology

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Hsp90 proteostasis axis Hsp90 functional inhibition → client proteins ↓ (Akt/EGFR/HER2/Raf/Cdk etc.) → growth/survival signaling ↓ Stress-response engagement possible; tolerability is dose/formulation dependent R Multi-node oncogenic network destabilization Often presented as ATP-independent Hsp90 inhibition with downstream proteasomal degradation of clients; mechanistically central because it collapses multiple driver pathways at once.
2 Vimentin and intermediate filament remodeling Vimentin function/organization ↓ → migration/invasion ↓, EMT programs ↓ (context-dependent) Endothelial and stromal cytoskeleton can be affected; may underlie anti-angiogenic activity P Anti-motility / anti-metastatic leverage WA behaves as a reactive small molecule with reported covalent interaction with vimentin; cytoskeletal perturbation can be rapid and not strictly transcription-driven.
3 Mitochondrial ROS increase ROS ↑ → ΔΨm ↓, cyt-c ↑, caspase cascade ↑ → apoptosis ↑ Often ROS ↔ or ↓ with antioxidant response ↑ (model-dependent) P/R Selective redox toxicity in susceptible tumors Frequently paired with ER stress/UPR activation; selectivity is commonly framed as “push cancer over its redox limit,” but this is highly dose- and context-dependent.
4 ER stress and UPR axis ER stress ↑, UPR ↑ → proteotoxic stress → apoptosis/autophagy shifts (model-dependent) Adaptive UPR may occur; excessive dosing can stress normal tissues R Proteotoxic stress amplification Mechanistically synergistic with Hsp90 disruption and ROS signaling; can manifest as GRP78/BiP and related markers ↑ in some systems.
5 NF-κB inflammatory survival signaling NF-κB ↓ → cytokine/pro-survival programs ↓, invasion-associated signaling ↓ Anti-inflammatory signaling ↓ may be beneficial in some contexts; immune effects can be mixed G Survival/inflammation program suppression Often aligned with COX-2 and inflammasome-related readouts in inflammatory models; oncology relevance is strongest where NF-κB is a core survival node.
6 EMT and metastasis signaling EMT ↓, MMPs ↓, uPA ↓, CXCR4/SDF1 axis ↓ (model-dependent) Wound-healing programs can be affected (context-dependent) G Anti-invasive phenotype Partly downstream of cytoskeletal (vimentin) effects and NF-κB/TGF-β-linked programs; directionality can vary by tumor lineage and assay.
7 Glycolysis and HIF-1α HIF-1α ↓, glycolysis flux ↓, ATP ↓ (susceptible models) Usually ↔ at low exposure; metabolic stress possible at higher exposure G Metabolic vulnerability unmasking Often secondary to upstream stress (ROS/proteostasis) rather than a primary enzymatic inhibitor; interpret as (context-dependent).
8 Cell cycle checkpoint control Cell-cycle arrest ↑ (often G2/M reported), CDK/cyclin signaling ↓ Proliferating normal cells may also be sensitive at higher exposure G Anti-proliferative enforcement Common phenotype readout across WA studies; mechanistic “why” may differ by model (proteostasis vs ROS vs mitotic machinery/cytoskeleton).
9 NRF2 and antioxidant defense NRF2 ↓ and antioxidant enzymes ↓ reported in some cancer models; sometimes mixed ↔ NRF2 ↑ and antioxidant enzymes ↑ reported in some normal-tissue protection contexts G Redox buffering divergence Highly model-dependent; WA can behave as a stressor that either suppresses or activates NRF2-linked programs depending on timing, dose, and baseline redox state.
10 Clinical Translation Constraint Micromolar in-vitro dosing common; human oncology exposure/target engagement remains sparsely defined Supplement heterogeneity (WA content), drug-interaction risk, and organ-specific toxicity signals (notably liver; thyroid) constrain use — Formulation + PK + safety gating Human data exist (phase I osteosarcoma; ongoing ovarian combo), but WA is not an approved anticancer drug and standardized products/target engagement biomarkers are not yet mature.

TSF legend: P: 0–30 min    R: 30 min–3 hr    G: >3 hr
Scientific Papers found: Click to Expand⟱
1364- Ash,    Withaferin a Triggers Apoptosis and DNA Damage in Bladder Cancer J82 Cells through Oxidative Stress
- in-vitro, Bladder, J82
cl‑Casp3↑, cl‑Casp8↑, cl‑Casp9↑, cl‑PARP↑, ROS↑, MMP↓, DNAdam↑, eff↓,
1363- Ash,  doxoR,    Withaferin A Synergizes the Therapeutic Effect of Doxorubicin through ROS-Mediated Autophagy in Ovarian Cancer
- in-vitro, Ovarian, A2780S - in-vitro, Ovarian, CaOV3 - in-vivo, NA, NA
ChemoSen↑, ROS↑, DNAdam↑, TumCCA↑, LC3B↑, TumCG↓, cl‑Casp3↑,
1362- Ash,  GEM,    Synergistic Inhibition of Pancreatic Cancer Cell Growth and Migration by Gemcitabine and Withaferin A
- in-vitro, PC, PANC1 - in-vitro, PC, Hs766t
ChemoSen↑, ROS↑, Apoptosis↑, TumCMig↓, F-actin↓, YMcells↓, NF-kB↓,
1361- Ash,  SRF,    Withaferin A, a natural thioredoxin reductase 1 (TrxR1) inhibitor, synergistically enhances the antitumor efficacy of sorafenib through ROS-mediated ER stress and DNA damage in hepatocellular carcinoma cells
- in-vitro, Liver, HUH7 - in-vivo, Liver, HUH7
TrxR↓, ROS↑, DNA-PK↑, ER Stress↑, Apoptosis↑, eff↓,
1360- Ash,  immuno,    Withaferin A Increases the Effectiveness of Immune Checkpoint Blocker for the Treatment of Non-Small Cell Lung Cancer
- in-vitro, Lung, H1650 - in-vitro, Lung, A549 - in-vitro, CRC, HCT116 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
PD-L1↑, eff↓, ROS↑, ER Stress↑, Apoptosis↑, BAX↑, Bak↑, BAD↑, Bcl-2↓, XIAP↓, survivin↓, cl‑PARP↑, CHOP↑, p‑eIF2α↑, ICD↑, eff↑,
1359- Ash,    Withaferin A Induces ROS-Mediated Paraptosis in Human Breast Cancer Cell-Lines MCF-7 and MDA-MB-231
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
MMP↓, Alix/AIP‑1↓, ROS↑, Paraptosis↑, ER Stress↝,
1358- Ash,    Withaferin A: A Dietary Supplement with Promising Potential as an Anti-Tumor Therapeutic for Cancer Treatment - Pharmacology and Mechanisms
- Review, Var, NA
TumCCA↑, Apoptosis↑, TumAuto↑, Ferroptosis↑, TumCP↓, CSCs↓, TumMeta↓, EMT↓, angioG↓, Vim↓, HSP90↓, annexin II↓, m-FAM72A↓, BCR-ABL↓, Mortalin↓, NRF2↓, cMYB↓, ROS↑, ChemoSen↑, eff↑, ChemoSen↑, ChemoSen↑, eff↑, *BioAv↓, ROCK1↓, TumCI↓, Sp1/3/4↓, VEGF↓, Hif1a↓, EGFR↓,
1357- Ash,    Cytotoxicity of withaferin A in glioblastomas involves induction of an oxidative stress-mediated heat shock response while altering Akt/mTOR and MAPK signaling pathways
- in-vitro, GBM, U87MG - in-vitro, GBM, U251 - in-vitro, GBM, GL26
TumCP↓, TumCCA↑, Akt↓, mTOR↓, p70S6↓, p85S6K↓, AMPKα↑, TSC2↑, HSP70/HSPA5↑, HO-1↑, HSF1↓, Apoptosis↑, ROS↑, eff↓,
1367- Ash,    An anti-cancerous protein fraction from Withania somnifera induces ROS-dependent mitochondria-mediated apoptosis in human MDA-MB-231 breast cancer cells
- in-vitro, BC, MDA-MB-231
Apoptosis↑, ROS↑, Bax:Bcl2↑, MMP↓, Casp3↑, TumCCA↑,
1355- Ash,    Withaferin A-Induced Apoptosis in Human Breast Cancer Cells Is Mediated by Reactive Oxygen Species
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, HMEC
eff↑, mt-ROS↑, mitResp↓, OXPHOS↓, compIII↑, BAX↑, Bak↑, other↓, ATP∅, *ROS∅,
1181- Ash,    Withaferin A inhibits Epithelial to Mesenchymal Transition in Non-Small Cell Lung Cancer Cells
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
TumCMig↓, TumCI↓, EMT↓, p‑SMAD2↓, p‑SMAD3↓, p‑NF-kB↓,
1180- Ash,    Withaferin A Inhibits Liver Cancer Tumorigenesis by Suppressing Aerobic Glycolysis through the p53/IDH1/HIF-1α Signaling Axis
- in-vitro, Liver, HepG2
IDH1↑, Glycolysis↓, P53↑, Hif1a↓,
1179- Ash,    Withaferin-A Inhibits Colon Cancer Cell Growth by Blocking STAT3 Transcriptional Activity
- in-vitro, CRC, HCT116 - in-vivo, NA, NA
TumCP↓, TumCMig↓, STAT3↓, TumVol↓, TumW↓,
1178- Ash,    Withaferin A suppresses the expression of vascular endothelial growth factor in Ehrlich ascites tumor cells via Sp1 transcription factor
- in-vitro, Nor, HUVECs - in-vivo, NA, NA
*VEGF↓, *angioG↓, *ascitic↓, *Sp1/3/4↓,
1177- Ash,    Withaferin A downregulates COX-2/NF-κB signaling and modulates MMP-2/9 in experimental endometriosis
- in-vivo, EC, NA
TumVol↓, MMP2↓, MMP9↓, NF-kB↓, COX2↓, NO↓, IL1β↓, IL6↓,
1176- Ash,    Metabolic Alterations in Mammary Cancer Prevention by Withaferin A in a Clinically Relevant Mouse Model
- in-vivo, NA, NA
TumVol↓, Apoptosis↑, Glycolysis↓, PKM2↓, PGK1↓, ALDOAiso2↓,
1174- Ash,    Withaferin A Suppresses Estrogen Receptor-α Expression in Human Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vivo, BC, MDA-MB-231 - in-vitro, BC, T47D
p‑P53↑, Apoptosis↑, ERα/ESR1↓,
1173- Ash,    Withaferin A inhibits proliferation of human endometrial cancer cells via transforming growth factor-β (TGF-β) signalling
- in-vitro, EC, K1 - in-vitro, Nor, THESCs
TumCP↓, *toxicity↓, Apoptosis↑, TumCCA↑, TumCMig↓, TumCI↓, p‑SMAD2↓, TGF-β↓, *toxicity↓,
1172- Ash,    Withaferin A Inhibits Fatty Acid Synthesis in Rat Mammary Tumors
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
FASN↓, ACLY↓, ACC1↓, CPT1A↓, SREBP1↓,
3154- Ash,    Pharmacokinetics and bioequivalence of Withania somnifera (Ashwagandha) extracts – A double blind, crossover study in healthy adults
BioAv↑, BioAv↓,
3164- Ash,    Withaferin A alleviates fulminant hepatitis by targeting macrophage and NLRP3
*hepatoP↑, *IKKα↓, *NLRP3↓, *NRF2↑, *AMPK↑, *Inflam↓, *Apoptosis↓, *cl‑Casp3↓, *cl‑PARP1↓, *NLRP3↓, *ROS↓, *ALAT↓, *AST↓, *GSH↑,
3163- Ash,  Rad,    Withaferin A, a steroidal lactone, selectively protects normal lymphocytes against ionizing radiation induced apoptosis and genotoxicity via activation of ERK/Nrf-2/HO-1 axis
*radioP↑, selectivity↑, *Casp3↓, *DNAdam↓, *ROS↓, *GSH↓, *NRF2↑, *HO-1↑, *Catalase↑, *SOD↑, *Prx↑, *ERK↑,
3162- Ash,    Molecular insights into cancer therapeutic effects of the dietary medicinal phytochemical withaferin A
- Review, Var, NA
lipid-P↓, SOD↑, GPx↑, P53↑, Bcl-2↑, E6↓, E7↓, pRB↑, CycB/CCNB1↑, CDC2↑, P21↑, PCNA↓, ALDH1A1↓, Vim↓, Glycolysis↓, cMyc↓, BAX↑, NF-kB↓, Casp3↑, CHOP↑, DR5↑, ERK↓, Wnt↓, β-catenin/ZEB1↓, Akt↓, HSP90↓,
3161- Ash,    Withaferin A inhibits ferroptosis and protects against intracerebral hemorrhage
- in-vivo, Stroke, NA
*neuroP↑, *MDA↓, *ROS↓, *SOD↑, *GPx↑, *NRF2↑, *HO-1↑,
3160- Ash,    Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal Plant Withania somnifera (L.) Dunal
- Review, Var, NA
TumCCA↑, H3↑, P21↑, cycA1/CCNA1↓, CycB/CCNB1↓, cycE/CCNE↓, CDC2↓, CHK1↓, Chk2↓, p38↑, MAPK↑, E6↓, E7↓, P53↑, Akt↓, FOXO3↑, ROS↑, γH2AX↑, MMP↓, mitResp↓, eff↑, TumCD↑, Mcl-1↓, ER Stress↑, ATF4↑, ATF3↑, CHOP↑, NOTCH↓, NF-kB↓, Bcl-2↓, STAT3↓, CDK1↓, β-catenin/ZEB1↓, N-cadherin↓, EMT↓, Cyt‑c↑, eff↑, CDK4↓, p‑RB1↓, PARP↑, cl‑Casp3↑, cl‑Casp9↑, NRF2↑, ER-α36↓, LDHA↓, lipid-P↑, AP-1↓, COX2↓, RenoP↑, PDGFR-BB↓, SIRT3↑, MMP2↓, MMP9↓, NADPH↑, NQO1↑, GSR↑, HO-1↑, *SOD2↑, *Prx↑, *Casp3?, eff↑, Snail↓, Slug↓, Vim↓, CSCs↓, HEY1↓, MMPs↓, VEGF↓, uPA↓, *toxicity↓, CDK2↓, CDK4↓, HSP90↓,
3159- Ash,    Neuroprotective effects of Withania somnifera in the SH-SY5Y Parkinson cell model
- in-vitro, Park, SH-SY5Y
*neuroP↑, *Inflam↓, *ROS↓, *cognitive↑, *memory↑, *GPx↑, *Prx↓, *ATP↑, *Vim↓, *mtDam↓,
3158- Ash,    Natural products triptolide, celastrol, and withaferin A inhibit the chaperone activity of peroxiredoxin I
- Study, NA, NA
Prx↓,
3157- Ash,    Withaferin A and Ovarian Cancer Antagonistically Regulate Skeletal Muscle Mass
- in-vivo, Ovarian, A2780S
*cachexia↑, *UPR↑, Strength↑,
3156- Ash,    Withaferin A: From ayurvedic folk medicine to preclinical anti-cancer drug
- Review, Var, NA
MAPK↑, p38↑, BAX↑, BIM↑, CHOP↑, ROS↑, DR5↑, Apoptosis↑, Ferroptosis↑, GPx4↓, BioAv↝, HSP90↓, RET↓, E6↓, E7↓, Akt↓, cMET↓, Glycolysis↓, TCA↓, NOTCH1↓, STAT3↓, AP-1↓, PI3K↓, eIF2α↓, HO-1↑, TumCCA↑, CDK1↓, *hepatoP↑, *GSH↑, *NRF2↑, Wnt↓, EMT↓, uPA↓, CSCs↓, Nanog↓, SOX2↓, CD44↓, lactateProd↓, Iron↑, NF-kB↓,
3155- Ash,    Overview of the anticancer activity of withaferin A, an active constituent of the Indian ginseng Withania somnifera
- Review, Var, NA
Half-Life↝, Inflam↓, antiOx↓, angioG↓, ROS↑, BAX↑, Bak↑, E6↓, E7↓, P53↑, Casp3↑, cl‑PARP↑, STAT3↓, eff↑, HSP90↓, TGF-β↓, TNF-α↓, EMT↑, mTOR↓, NOTCH1↓, p‑Akt↓, NF-kB↓, Dose↝,
1368- Ash,  Cisplatin,    Withania somnifera Root Extract Enhances Chemotherapy through ‘Priming’
- in-vitro, Colon, HT-29 - in-vitro, BC, MDA-MB-231
tumCV↓, *toxicity↓, ROS↑, mitResp↓, ChemoSen↑,
2388- Ash,    Withaferin A decreases glycolytic reprogramming in breast cancer
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468 - in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-453
GlucoseCon↓, lactateProd↓, ATP↓, Glycolysis↓, GLUT1↓, HK2↓, PKM2↓, cMyc↓, Warburg↓, cMyc↓,
2003- Ash,    Withaferin A Induces Cell Death Selectively in Androgen-Independent Prostate Cancer Cells but Not in Normal Fibroblast Cells
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145 - in-vitro, Nor, TIG-1 - in-vitro, PC, LNCaP
TumCD↑, selectivity↑, cFos↑, ROS↑, *ROS∅, HSP70/HSPA5↑, Apoptosis↑, ER Stress↑, TumCCA↑,
2002- Ash,    Ancient medicine, modern use: Withania somnifera and its potential role in integrative oncology
- Review, Var, NA
antiOx↑, Inflam↓, TumCP↓, OS↑, RadioS↑, radioP↑, chemoP↑,
2001- Ash,    Withania somnifera: from prevention to treatment of cancer
- Review, Var, NA
toxicity↓, TumW↓, Dose?, eff↝, Ki-67↓, survivin↓, XIAP↓, PERK↑, p‑RSK↑, CHOP↑, DR5↑, Dose↝, BG↓, DNMTs↓,
1433- Ash,  SFN,    A Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
eff↑, Bcl-2↓, BAX↑, tumCV↓, DNMT1↓, DNMT3A↓, HDAC↓,
1373- Ash,    Endoplasmic reticulum stress mediates withaferin A-induced apoptosis in human renal carcinoma cells
- in-vitro, Kidney, Caki-1
ER Stress↑, p‑eIF2α↑, XBP-1↑, GRP78/BiP↑, CHOP↑, eff↓,
1372- Ash,    Withaferin-A Induces Apoptosis in Osteosarcoma U2OS Cell Line via Generation of ROS and Disruption of Mitochondrial Membrane Potential
- in-vitro, OS, U2OS
Apoptosis↑, ROS↑, MMP↓, Casp3↑,
1371- Ash,    Reactive oxygen species generation and mitochondrial dysfunction in the apoptotic cell death of human myeloid leukemia HL-60 cells by a dietary compound withaferin A with concomitant protection by N-acetyl cysteine
- in-vitro, AML, HL-60
ROS↑, MMP↓, cl‑Casp3↑, cl‑Casp9↑, cl‑PARP↑, eff↓,
1370- Ash,    Withaferin A induces mitochondrial-dependent apoptosis in non-small cell lung cancer cells via generation of reactive oxygen species
- in-vitro, Lung, A549
ROS↑, eff↓,
1369- Ash,    Withaferin A inhibits cell proliferation of U266B1 and IM-9 human myeloma cells by inducing intrinsic apoptosis
- in-vitro, Melanoma, U266
tumCV↓, Apoptosis↑, BAX↑, Cyt‑c↑, Bcl-2↓, cl‑PARP↑, cl‑Casp3↑, cl‑Casp9↑, ROS↑, eff↓,
5397- CUR,  SFN,  RES,  EGCG,  Ash  Targeting Cancer Stem Cells with Phytochemicals: Molecular Mechanisms and Therapeutic Potential
- Review, Var, NA
CSCs↓,
4665- QC,  Ash,  Api,    Targeting cancer stem cells by nutraceuticals for cancer therapy
- Review, Var, NA
CSCs↓,

Showing Research Papers: 51 to 93 of 93
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 93

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 1,   ATF3↑, 1,   Ferroptosis↑, 2,   GPx↑, 1,   GPx4↓, 1,   GSR↑, 1,   HO-1↑, 3,   ICD↑, 1,   Iron↑, 1,   lipid-P↓, 1,   lipid-P↑, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 1,   OXPHOS↓, 1,   Prx↓, 1,   ROS↑, 18,   mt-ROS↑, 1,   SIRT3↑, 1,   SOD↑, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ATP∅, 1,   BCR-ABL↓, 1,   CDC2↓, 1,   CDC2↑, 1,   compIII↑, 1,   mitResp↓, 3,   MMP↓, 6,   Mortalin↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

ACC1↓, 1,   ACLY↓, 1,   ALDOAiso2↓, 1,   cMyc↓, 3,   CPT1A↓, 1,   FASN↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 5,   HK2↓, 1,   IDH1↑, 1,   lactateProd↓, 2,   LDHA↓, 1,   NADPH↑, 1,   PGK1↓, 1,   PKM2↓, 2,   SREBP1↓, 1,   TCA↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 1,   Apoptosis↑, 13,   BAD↑, 1,   Bak↑, 3,   BAX↑, 7,   Bax:Bcl2↑, 1,   Bcl-2↓, 4,   Bcl-2↑, 1,   BIM↑, 1,   Casp3↑, 4,   cl‑Casp3↑, 5,   cl‑Casp8↑, 1,   cl‑Casp9↑, 4,   Chk2↓, 1,   Cyt‑c↑, 2,   DR5↑, 3,   Ferroptosis↑, 2,   HEY1↓, 1,   MAPK↑, 2,   Mcl-1↓, 1,   p38↑, 2,   Paraptosis↑, 1,   p‑RSK↑, 1,   survivin↓, 2,   TumCD↑, 2,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,   p70S6↓, 1,   RET↓, 1,   Sp1/3/4↓, 1,   TSC2↑, 1,  

Transcription & Epigenetics ⓘ

H3↑, 1,   other↓, 1,   pRB↑, 1,   tumCV↓, 3,   YMcells↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 6,   eIF2α↓, 1,   p‑eIF2α↑, 2,   ER Stress↑, 5,   ER Stress↝, 1,   GRP78/BiP↑, 1,   HSF1↓, 1,   HSP70/HSPA5↑, 2,   HSP90↓, 5,   PERK↑, 1,   XBP-1↑, 1,  

Autophagy & Lysosomes ⓘ

LC3B↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNA-PK↑, 1,   DNAdam↑, 2,   DNMT1↓, 1,   DNMT3A↓, 1,   DNMTs↓, 1,   m-FAM72A↓, 1,   P53↑, 4,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 5,   PCNA↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   CDK2↓, 1,   CDK4↓, 2,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   CycB/CCNB1↑, 1,   cycE/CCNE↓, 1,   P21↑, 2,   p‑RB1↓, 1,   TumCCA↑, 8,  

Proliferation, Differentiation & Cell State ⓘ

ALDH1A1↓, 1,   CD44↓, 1,   cFos↑, 1,   cMET↓, 1,   cMYB↓, 1,   CSCs↓, 5,   EMT↓, 4,   EMT↑, 1,   ERK↓, 1,   FOXO3↑, 1,   HDAC↓, 1,   mTOR↓, 2,   Nanog↓, 1,   NOTCH↓, 1,   NOTCH1↓, 2,   p85S6K↓, 1,   PI3K↓, 1,   SOX2↓, 1,   STAT3↓, 4,   TumCG↓, 1,   Wnt↓, 2,  

Migration ⓘ

Alix/AIP‑1↓, 1,   annexin II↓, 1,   AP-1↓, 2,   ER-α36↓, 1,   F-actin↓, 1,   Ki-67↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,   N-cadherin↓, 1,   ROCK1↓, 1,   Slug↓, 1,   p‑SMAD2↓, 2,   p‑SMAD3↓, 1,   Snail↓, 1,   TGF-β↓, 2,   TumCI↓, 3,   TumCMig↓, 4,   TumCP↓, 5,   TumMeta↓, 1,   uPA↓, 2,   Vim↓, 3,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 1,   EGFR↓, 1,   Hif1a↓, 2,   NO↓, 1,   PDGFR-BB↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   NF-kB↓, 6,   p‑NF-kB↓, 1,   PD-L1↑, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

ERα/ESR1↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 6,   Dose?, 1,   Dose↝, 2,   eff↓, 8,   eff↑, 9,   eff↝, 1,   Half-Life↝, 1,   RadioS↑, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

BG↓, 1,   E6↓, 4,   E7↓, 4,   EGFR↓, 1,   ERα/ESR1↓, 1,   IL6↓, 1,   Ki-67↓, 1,   PD-L1↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   OS↑, 1,   radioP↑, 1,   RenoP↑, 1,   Strength↑, 1,   toxicity↓, 1,   TumVol↓, 3,   TumW↓, 2,  
Total Targets: 211

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GPx↑, 2,   GSH↓, 1,   GSH↑, 2,   HO-1↑, 2,   MDA↓, 1,   NRF2↑, 4,   Prx↓, 1,   Prx↑, 2,   ROS↓, 4,   ROS∅, 2,   SOD↑, 2,   SOD2↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Casp3?, 1,   Casp3↓, 1,   cl‑Casp3↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Protein Folding & ER Stress ⓘ

UPR↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,   cl‑PARP1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,  

Migration ⓘ

Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

IKKα↓, 1,   Inflam↓, 2,  

Protein Aggregation ⓘ

NLRP3↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ascitic↓, 1,   AST↓, 1,  

Functional Outcomes ⓘ

cachexia↑, 1,   cognitive↑, 1,   hepatoP↑, 2,   memory↑, 1,   neuroP↑, 2,   radioP↑, 1,   toxicity↓, 4,  
Total Targets: 43

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:36  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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