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⟱
3176- Ash,    Apoptosis is induced in leishmanial cells by a novel protein kinase inhibitor withaferin A and is facilitated by apoptotic topoisomerase I-DNA complex
- in-vitro, NA, NA
PKCδ↓, TOP1∅, ROS↑, GSH↓, DNAdam↑, MMP↓, Cyt‑c↑,
3675- Ash,    Ashwagandha (Withania somnifera) Reverses β-Amyloid1-42 Induced Toxicity in Human Neuronal Cells: Implications in HIV-Associated Neurocognitive Disorders (HAND)
*memory↑, *neuroP↑, *Aβ↓, *LDH↓, *PPARγ↑, *cognitive↑,
3674- Ash,    Ashwagandha in brain disorders: A review of recent developments
- Review, NA, NA
*neuroP↑,
3673- Ash,    An overview on ashwagandha: a Rasayana (rejuvenator) of Ayurveda
- Review, NA, NA
*cognitive↑, *Inflam↓, *Strength↑, *VitC↑, *memory↑,
3672- Ash,    Critical review of the Withania somnifera (L.) Dunal: ethnobotany, pharmacological efficacy, and commercialization significance in Africa
- Review, NA, NA
*cardioP↑, *antiOx↑, *ROS↓, *neuroP↑, *Inflam↓, *Apoptosis↓,
3671- Ash,    Withania somnifera showed neuroprotective effect and increase longevity in Drosophila Alzheimer’s disease model
- in-vivo, AD, NA
*OS↑, *BACE↓,
3670- Ash,    Neurodegenerative diseases and Withania somnifera (L.): An update
- Review, AD, NA - Review, Park, NA
*Apoptosis↓, *Inflam↓, *ROS↓, *neuroP↑,
3669- Ash,    Withanamides in Withania somnifera fruit protect PC-12 cells from beta-amyloid responsible for Alzheimer's diseas
- in-vitro, AD, PC12
*lipid-P↓, *antiOx↑,
3668- Ash,    Withania somnifera reverses Alzheimer's disease pathology by enhancing low-density lipoprotein receptor-related protein in liver
- NA, AD, NA
*Aβ↓, *cognitive↑,
3179- Ash,    Withaferin A inhibits JAK/STAT3 signaling and induces apoptosis of human renal carcinoma Caki cells
- in-vitro, RCC, Caki-1
JAK↓, STAT3↓, Apoptosis↑,
3178- Ash,    Withaferin A Inhibits Neutrophil Adhesion, Migration, and Respiratory Burst and Promotes Timely Neutrophil Apoptosis
- Review, Nor, NA
ITGB1↓,
3177- Ash,    Emerging Role of Hypoxia-Inducible Factors (HIFs) in Modulating Autophagy: Perspectives on Cancer Therapy
- Review, Var, NA
Hif1a↓, ROS↑, ER Stress↑,
3676- Ash,    Effect of Withania somnifera (Ashwagandha) root extract on amelioration of oxidative stress and autoantibodies production in collagen-induced arthritic rats
- in-vivo, Arthritis, NA
*CRP↓, *ROS↓, *lipid-P↓, *GSTs↓, *GSH↑, *antiOx↑, *Inflam↓,
3175- Ash,  SFN,    Withaferin A and sulforaphane regulate breast cancer cell cycle progression through epigenetic mechanisms
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
DNMTs↓, HDAC↓, eff↑,
3174- Ash,    Withaferin A Acts as a Novel Regulator of Liver X Receptor-α in HCC
- in-vitro, HCC, HepG2 - in-vitro, HCC, Hep3B - in-vitro, HCC, HUH7
NF-kB↓, angioG↓, Inflam↓, TumCP↓, TumCMig↓, TumCI↓, Sp1/3/4↓, VEGF↓, angioG↓, uPA↓, PDGF↓, MCP1↓, ICAM-1↓, *NRF2↑, *hepatoP↑,
3173- Ash,    Nano-targeted induction of dual ferroptotic mechanisms eradicates high-risk neuroblastoma
- in-vitro, neuroblastoma, NA
GPx4↓, HO-1↑, lipid-P↑, Keap1↓, NRF2↑, Ferroptosis↑,
3172- Ash,    Implications of Withaferin A for the metastatic potential and drug resistance in hepatocellular carcinoma cells via Nrf2-mediated EMT and ferroptosis
- in-vitro, HCC, HepG2 - in-vitro, Nor, HL7702
Keap1↑, NRF2↓, EMT↓, TumCP↓, TumCI↓, selectivity↑, *toxicity↓, ROS↑, MDA↑, GSH↓, Ferroptosis↑,
3171- Ash,    Unlocking the epigenetic code: new insights into triple-negative breast cancer
- Review, BC, NA
DNMTs↓,
3170- Ash,    Withaferin A protects against hyperuricemia induced kidney injury and its possible mechanisms
- in-vitro, Nor, NRK52E - in-vivo, NA, NA
*RenoP↑, *hepatoP↑, *creat↓, *BUN↓, *uricA↓, *Apoptosis↓, *α-SMA↓,
3169- Ash,    Withaferin A blocks formation of IFN-γ-induced metastatic cancer stem cells through inhibition of the CXCR4/CXCL12 pathway in the UP-LN1 carcinoma cell model
- in-vitro, GC, NA
CXCR4↓, CXCL12↓,
3168- Ash,    Withaferin A targeting both cancer stem cells and metastatic cancer stem cells in the UP-LN1 carcinoma cell model
- in-vitro, Var, NA
CXCR4↓, STAT3↓, CSCs↓,
3167- Ash,    Withaferin A Inhibits the Proteasome Activity in Mesothelioma In Vitro and In Vivo
- in-vitro, MM, H226
TumCP↓, cMyc↓, cFos↓, cJun↓, TIMP2↑, Vim↓, ROS↑, BAX↑, IKKα↑, Casp3↑, cl‑PARP↑,
1142- Ash,    Ashwagandha-Induced Programmed Cell Death in the Treatment of Breast Cancer
- Review, BC, MCF-7 - NA, BC, MDA-MB-231 - NA, Nor, HMEC
Apoptosis↑, ROS↑, DNAdam↑, OXPHOS↓, *ROS∅, Bcl-2↓, XIAP↓, survivin↓, DR5↑, IKKα↓, NF-kB↓, selectivity↑, *ROS∅, eff↓, Paraptosis↑,
5169- Ash,    The Tumor Inhibitor and Antiangiogenic Agent Withaferin A Targets the Intermediate Filament Protein Vimentin
- in-vitro, BC, MCF-7
AntiTum↑, angioG↓, Vim↓,
5398- Ash,    Withaferin-A inhibits colorectal cancer growth and metastasis by targeting the HSP90/HIF-1α/EMT axis
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW48
TumCG↓, TumCMig↓, TumCI↓, HSP90↓, Hif1a↓, EMT↓,
5396- Ash,    Withania Somnifera (Ashwagandha) and Withaferin A: Potential in Integrative Oncology
- Review, Var, NA
selectivity↑, ROS↑, Apoptosis↑, ChemoSen↑, RadioS↑, NF-kB↓, ER-α36↓, P53↑, *ROS∅, γH2AX↑, DNAdam↑, MMP↓, XIAP↓, IAP1↓, survivin↓, SOD↓, Dose↝, IL6↓, TNF-α↓, COX2↓, p‑Akt↓, NOTCH1↓, FOXO↑, Casp↑, MMP2↓, CSCs↓, *ROS↓, *SOD2↑, chemoP↑, ChemoSen↑, RadioS↑,
5395- Ash,    Withaferin A Targets Heat Shock Protein 90 in Pancreatic Cancer Cells
- vitro+vivo, PC, PANC1 - in-vitro, PC, MIA PaCa-2
TumCP↓, HSP90↓, Akt↓, CDK4↓, TumCG↓, Apoptosis↑, AntiCan↑,
5394- Ash,    Safety and pharmacokinetics of Withaferin-A in advanced stage high grade osteosarcoma: A phase I trial
- Trial, OS, NA
toxicity↝, hepatoP↓, BioAv↓, Apoptosis↑, ROS↑, TumCCA↑,
5393- Ash,    Studies on oral bioavailability and first-pass metabolism of withaferin A in rats using LC-MS/MS and Q-TRAP
- in-vivo, Nor, NA
*BioAv↝, *other↝, *Half-Life↓,
5175- Ash,    Withaferin A Induces Proteasome Inhibition, Endoplasmic Reticulum Stress, the Heat Shock Response and Acquisition of Thermotolerance
- in-vitro, Cerv, CCL-102
Inflam↓, AntiTum↑, Proteasome↓, ER Stress↑, HSPs↑, GRP94↑, Akt↑, eff↑, HSP70/HSPA5↑,
5174- Ash,    Withaferin A is a potent inhibitor of angiogenesis
- in-vitro, Nor, HUVECs
Inflam↓, *TumCP↓, cycD1/CCND1↓, NF-kB↓, angioG↓,
5173- Ash,  2DG,    Withaferin A inhibits lysosomal activity to block autophagic flux and induces apoptosis via energetic impairment in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468 - in-vitro, BC, T47D
autoF↓, lysosome↓, TumAuto↑, p‑LDH↓, ATP↓, AMPK↑, eff↑, TumCG↓, CTSD↓, CTSB↓, CTSL↑, cl‑PARP1↑, LDHA↓, TCA↓,
5172- Ash,    Withaferin-A suppress AKT induced tumor growth in colorectal cancer cells
Akt↓, TumCP↓, TumCMig↓, TumCI↓, EMT↓, Snail↓, Slug↓, β-catenin/ZEB1↓, Vim↓, angioG↓,
5171- Ash,    The tumor proteasome is a primary target for the natural anticancer compound Withaferin A isolated from "Indian winter cherry"
- vitro+vivo, Pca, LNCaP - vitro+vivo, Pca, PC3
Proteasome↓, BAX↑, p27↑, AR↓, TumCG↓,
5170- Ash,    Withaferin A inhibits NF-kappaB activation by targeting cysteine 179 in IKKβ
- Review, Var, NA
NF-kB↓, Inflam↓, IKKα↓,
3166- Ash,    Exploring the Multifaceted Therapeutic Potential of Withaferin A and Its Derivatives
- Review, Var, NA
*p‑PPARγ↓, *cardioP↑, *AMPK↑, *BioAv↝, *Half-Life↝, *Half-Life↝, *Dose↑, *chemoPv↑, IL6↓, STAT3↓, ROS↓, OXPHOS↓, PCNA↓, LDH↓, AMPK↑, TumCCA↑, NOTCH3↓, Akt↓, Bcl-2↓, Casp3↑, Apoptosis↑, eff↑, NF-kB↓, CSCs↓, HSP90↓, PI3K↓, FOXO3↑, β-catenin/ZEB1↓, N-cadherin↓, EMT↓, FASN↓, ACLY↓, ROS↑, NRF2↑, HO-1↑, NQO1↑, JNK↑, mTOR↓, neuroP↑, *TNF-α↓, *IL1β↓, *IL6↓, *IL8↓, *IL18↓, RadioS↑, eff↑,
4679- Ash,    Induced cancer stem-like cells as a model for biological screening and discovery of agents targeting phenotypic traits of cancer stem cell
- in-vitro, NA, NA
CSCs↓,
4678- Ash,    Identification of Withaferin A as a Potential Candidate for Anti-Cancer Therapy in Non-Small Cell Lung Cancer
- vitro+vivo, NSCLC, H1975
ROS↑, AntiTum↑, CSCs↓, mTOR↓, STAT3↓, ChemoSen↑, Keap1↑, NRF2↓,
4677- Ash,    Withaferin A (WFA) inhibits tumor growth and metastasis by targeting ovarian cancer stem cells
- vitro+vivo, Ovarian, NA
CSCs↓, Securin↓, ALDH1A1↓,
4660- Ash,    Withaferin A Alone and in Combination with Cisplatin Suppresses Growth and Metastasis of Ovarian Cancer by Targeting Putative Cancer Stem Cells
- in-vitro, Ovarian, NA
CSCs↓, TumCG↓, TumMeta↓, CD44↓, CD34↓, OCT4↓, NOTCH1↓, HEY1↓,
4303- Ash,    Ashwagandha (Withania somnifera)—Current Research on the Health-Promoting Activities: A Narrative Review
- Review, AD, NA
*neuroP↑, *Sleep↑, *Inflam↓, *cardioP↑, *cognitive↑, *Aβ↓, *TNF-α↓, *IL1β↓, *IL6↓, *MCP1↓, *lipid-P↓, *tau↓, *ROS↓, *BBB↑, *AChE↓, *GSH↑, *GSTs↑, *GSR↑, *GPx↑, *SOD↑, *Catalase↑, ChemoSen↑, *Strength↑,
3689- Ash,    Ashwagandha attenuates TNF-α- and LPS-induced NF-κB activation and CCL2 and CCL5 gene expression in NRK-52E cells
- in-vitro, NA, NRK52E
*RenoP↑, *NF-kB↓, *MCP1↓, *RANTES↓,
3688- Ash,    Withaferin A Suppresses Beta Amyloid in APP Expressing Cells: Studies for Tat and Cocaine Associated Neurological Dysfunctions
- NA, AD, SH-SY5Y
*Aβ↓, *neuroP↑,
3687- Ash,    Role of Withaferin A and Its Derivatives in the Management of Alzheimer’s Disease: Recent Trends and Future Perspectives
- Review, AD, NA
*Aβ↓, *tau↓, *HSPs↝, *antiOx↑, *ROS↓, *Inflam↓, *neuroP↑, *cognitive↑, *NF-kB↓, *HO-1↑, *memory↑, *AChE↓, *BChE↓, *ChAT↑, *Ach↑,
3686- Ash,    Adaptogenic and Anxiolytic Effects of Ashwagandha Root Extract in Healthy Adults: A Double-blind, Randomized, Placebo-controlled Clinical Study
- Study, NA, NA
*Sleep↑,
3685- Ash,    Withania somnifera as a Potential Anxiolytic and Anti-inflammatory Candidate Against Systemic Lipopolysaccharide-Induced Neuroinflammation
- in-vivo, NA, NA
*TNF-α↓, *IL1β↓, *IL6↓, *iNOS↓, *COX2↓, *NOX↓, *cognitive↑, *Inflam↓, *NF-kB↓,
1356- Ash,    Withaferin A induces apoptosis by ROS-dependent mitochondrial dysfunction in human colorectal cancer cells
- in-vitro, CRC, HCT116
ROS↑, TumCCA↑, MMP↓, TumCG↓, Apoptosis↑, JNK↝,
3165- Ash,    Inhibitory effect of withaferin A on Helicobacter pylori‑induced IL‑8 production and NF‑κB activation in gastric epithelial cells
- in-vitro, Nor, NA
*IL8↓, *Inflam↓,
1366- Ash,    Selective Killing of Cancer Cells by Ashwagandha Leaf Extract and Its Component Withanone Involves ROS Signaling
- in-vitro, BC, MCF-7
ROS↑, P53↑,
1365- Ash,    Withaferin A Induces Oxidative Stress-Mediated Apoptosis and DNA Damage in Oral Cancer Cells
- in-vitro, Oral, Ca9-22 - in-vitro, Oral, CAL27
ROS↑, *toxicity↓, Apoptosis↑, TumCCA↑, MMP↓, p‑γH2AX↑, DNAdam↑, eff↓,

Showing Research Papers: 1 to 50 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 ⓘ

Ferroptosis↑, 2,   GPx4↓, 1,   GSH↓, 2,   HO-1↑, 2,   Keap1↓, 1,   Keap1↑, 2,   lipid-P↑, 1,   MDA↑, 1,   NQO1↑, 1,   NRF2↓, 2,   NRF2↑, 2,   OXPHOS↓, 2,   ROS↓, 1,   ROS↑, 12,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 4,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

ACLY↓, 1,   AMPK↑, 2,   cMyc↓, 1,   FASN↓, 1,   LDH↓, 1,   p‑LDH↓, 1,   LDHA↓, 1,   TCA↓, 1,  

Cell Death ⓘ

Akt↓, 3,   Akt↑, 1,   p‑Akt↓, 1,   Apoptosis↑, 8,   BAX↑, 2,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 2,   Cyt‑c↑, 1,   DR5↑, 1,   Ferroptosis↑, 2,   HEY1↓, 1,   IAP1↓, 1,   JNK↑, 1,   JNK↝, 1,   p27↑, 1,   Paraptosis↑, 1,   Proteasome↓, 2,   survivin↓, 2,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 2,   GRP94↑, 1,   HSP70/HSPA5↑, 1,   HSP90↓, 3,   HSPs↑, 1,  

Autophagy & Lysosomes ⓘ

autoF↓, 1,   lysosome↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 4,   DNMTs↓, 2,   P53↑, 2,   cl‑PARP↑, 1,   cl‑PARP1↑, 1,   PCNA↓, 1,   γH2AX↑, 1,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   Securin↓, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

ALDH1A1↓, 1,   CD34↓, 1,   CD44↓, 1,   cFos↓, 1,   CSCs↓, 7,   CTSB↓, 1,   CTSD↓, 1,   CTSL↑, 1,   EMT↓, 4,   FOXO↑, 1,   FOXO3↑, 1,   HDAC↓, 1,   mTOR↓, 2,   NOTCH1↓, 2,   NOTCH3↓, 1,   OCT4↓, 1,   PI3K↓, 1,   STAT3↓, 4,   TOP1∅, 1,   TumCG↓, 6,  

Migration ⓘ

CXCL12↓, 1,   ER-α36↓, 1,   ITGB1↓, 1,   MMP2↓, 1,   N-cadherin↓, 1,   PDGF↓, 1,   PKCδ↓, 1,   Slug↓, 1,   Snail↓, 1,   TIMP2↑, 1,   TumCI↓, 4,   TumCMig↓, 3,   TumCP↓, 5,   TumMeta↓, 1,   uPA↓, 1,   Vim↓, 3,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 5,   Hif1a↓, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 2,   ICAM-1↓, 1,   IKKα↓, 2,   IKKα↑, 1,   IL6↓, 2,   Inflam↓, 4,   JAK↓, 1,   MCP1↓, 1,   NF-kB↓, 6,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 4,   Dose↝, 1,   eff↓, 2,   eff↑, 5,   RadioS↑, 3,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

AR↓, 1,   IL6↓, 2,   LDH↓, 1,   p‑LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 3,   chemoP↑, 1,   hepatoP↓, 1,   neuroP↑, 1,   toxicity↝, 1,  
Total Targets: 136

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 2,   GSR↑, 1,   GSTs↓, 1,   GSTs↑, 1,   HO-1↑, 1,   lipid-P↓, 3,   NRF2↑, 1,   ROS↓, 6,   ROS∅, 3,   SOD↑, 1,   SOD2↑, 1,   uricA↓, 1,   VitC↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   BUN↓, 1,   LDH↓, 1,   PPARγ↑, 1,   p‑PPARγ↓, 1,  

Cell Death ⓘ

Apoptosis↓, 3,   iNOS↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↝, 1,  

Protein Folding & ER Stress ⓘ

HSPs↝, 1,  

Migration ⓘ

TumCP↓, 1,   α-SMA↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CRP↓, 1,   IL18↓, 1,   IL1β↓, 3,   IL6↓, 3,   IL8↓, 2,   Inflam↓, 8,   MCP1↓, 2,   NF-kB↓, 3,   RANTES↓, 1,   TNF-α↓, 3,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   BChE↓, 1,   ChAT↑, 1,   tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 5,   BACE↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 2,   Dose↑, 1,   Half-Life↓, 1,   Half-Life↝, 2,  

Clinical Biomarkers ⓘ

creat↓, 1,   CRP↓, 1,   IL6↓, 3,   LDH↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 3,   chemoPv↑, 1,   cognitive↑, 6,   hepatoP↑, 2,   memory↑, 3,   neuroP↑, 7,   OS↑, 1,   RenoP↑, 2,   Sleep↑, 2,   Strength↑, 2,   toxicity↓, 2,  
Total Targets: 66

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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