mitA Cancer Research Results

mitA, Mitotic arrest: Click to Expand ⟱
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Mitotic arrest is a cell-cycle state in which a cell is prevented from completing mitosis, usually because the spindle-assembly checkpoint detects improper chromosome alignment, defective kinetochore attachment, spindle damage, or incomplete chromosome segregation. Mitotic arrest commonly occurs during metaphase and is associated with sustained cyclin B1/CDK1 activity, checkpoint proteins such as MAD2, BUB1, BUBR1, and MPS1, and inhibition of the anaphase-promoting complex/cyclosome (APC/C).

In cancer cells, prolonged mitotic arrest may suppress tumour growth by preventing cell division and can lead to apoptosis, mitotic catastrophe, senescence, or abnormal exit from mitosis. Compounds that disrupt microtubules, centrosomes, kinetochores, or spindle-checkpoint signalling frequently induce mitotic arrest. However, some cells escape through mitotic slippage, which may produce polyploid or genetically unstable surviving cells.

Generally favourable anticancer direction: increased or prolonged mitotic arrest in tumour cells, particularly when followed by apoptosis or mitotic catastrophe. The effect should be interpreted cautiously if the study also reports mitotic slippage, polyploidy, or survival of genomically unstable cells.



Scientific Papers found: Click to Expand⟱
6690- DFC,    Diclofenac: A Nonsteroidal Anti-Inflammatory Drug Inducing Cancer Cell Death by Inhibiting Microtubule Polymerization and Autophagy Flux
- in-vitro, Cerv, HeLa
Inflam↓, Diclofenac, a nonsteroidal anti-inflammatory drug (NSAID) used to treat inflammatory diseases induces cellular toxicity by increasing the production of reactive oxygen species (ROS) and impairing autophagic flux.
ROS↑,
mitA↑, diclofenac induces mitotic arrest with a half-maximal effective concentration of 170 μM and cell death with a half-maximal lethal dose of 200 µM during 18-h incubation in HeLa cells.
ChemoSen↑, We found that diclofenac induces cell death further in combination with 5-fuorouracil, a DNA replication inhibitor than in single treatment in cancer cells.

6862- FBZ,    Research: The Urgent Need for Clinical Studies to Evaluate the Anti-Tumor Efficacy of Fenbendazole
- Review, Var, NA
mitA↑, FBZ destabilizes microtubules, critical for cell division, leading to mitotic arrest and apoptosis.
Apoptosis↑,
GLUT4↓, FBZ inhibits glucose uptake by downregulating GLUT transporters and hexokinase II, starving cancer cells reliant on aerobic glycolysis (Warburg effect).
HK2↓,
Warburg↓,
TumCCA↑, FBZ induces G2/M phase arrest and promotes apoptosis via p53 activation and caspase activation.
P53↑,
Casp↑,
TumCP↓, confirmed dose-dependent proliferation inhibition and apoptosis.
ROS↑, FBZ induces reactive oxygen species (ROS) accumulation, enhancing ferroptosis and apoptosis, particularly in 5-fluorouracil-resistant colorectal cancer cells.
Ferroptosis↑,
TumVol↓, A549 lung cancer xenografts in nude mice, reported significant tumor shrinkage with oral FBZ administration (1 mg/mouse every 2 days for 12 days).
Dose↝, The case of Joe Tippens, who reported complete remission from stage IV small-cell lung cancer after taking FBZ (222 mg daily) alongside vitamin E, CBD oil, and curcumin, has fueled public interest.
BioAv↓, FBZ’s poor water solubility and low systemic bioavailability limit its ability to reach therapeutic levels in tumors when administered orally.
RadioS↝, Given preclinical evidence of synergy with radiation or docetaxel, trials should explore FBZ’s role as an adjunct to conventional treatments, potentially enhancing efficacy in resistant cancers.
ChemoSen↑,

6981- Form,    Formononetin: a review of its source, pharmacology, drug combination, toxicity, derivatives, and drug delivery systems
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
BioAv↝, FMN has only one phenolic hydroxyl group, so it is poorly soluble in water and easily soluble in organic solvents such as methanol, ethyl acetate, and ether.
*memory↑, It had been found that FMN, isolated from Sophora secundiflora, could improve memory problems by restoring the level of oxidative stress in brain tissues and modulating acetylcholinesterase activity. I
*ROS↓, findings suggest that FMN can inhibit oxidative stress in the liver and restore mitochondrial function
*AChE↓,
*NF-kB↓, FMN, the expression levels of the above three decreased and NF-κB activation was inhibited, which may be related to the release of FMN blocking kelch-like ECH-associated protein-1 (Keap1) and activating the nuclear factor erythroid 2-related factor 2
*Keap1↝,
*NRF2↑,
*Inflam↓, FMN exerted anti-neuroinflammatory effects by targeting peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) and bidirectionally regulating NF-κB signaling pathway and Nrf2/Heme oxygenase-1 (HO-1) signaling pathway,
*PGC-1α↝,
*HO-1↓,
*p‑tau↓, thereby inhibiting tau protein hyperphosphorylation.
*cognitive↑, Significantly FMN improve cognitive dysfunction in mice caused by high-fat feeding
*BDNF↑, increased BDNF and 5-hydroxytryptamine (5-HT) levels, and mitigated the progression of depression in mice.
*5HT↑,
*Stroke↓, It could significantly reduce the level of inflammatory factors, increase the number of dendritic spines in neurons, and increase the expression of βIII-tubulin, growth-associated protein 43 (GAP-43), nerve growth factor (NGF) and BDNF.
*PARP1↓, FMN significantly reduced PARP1, PARG, apoptosis-inducing factor (AIF), cysteinyl aspartate-specific protease 3 (caspase-3) and p53 protein in rats with cerebral ischemia-reperfusion injury
*AIF↓,
*Casp3↓,
NP/CIPN↓, FMN had a favorable ameliorative effect on oxaliplatin-induced peripheral neuropathy and did not affect the chemotherapeutic function of oxaliplatin.
*neuroP↑, The neuroprotective mechanism of FMN is shown in Figure 2.
*NGF↑,
*TNF-α↓,
*IL1β↓,
*IL18↓,
*IL6↓,
*VCAM-1↓,
*pol-M2 MC↑,
*hepatoP↑, could reduce hepatotoxicity and improve liver function through inflammatory molecular pathways.
*AST↓, reduce serum AST, ALT, TNF-α and IL-1β levels. I
*ALAT↓,
*LC3II↑, the levels of LC3II, Beclin1, p62, cyclooxygenase-2 (COX2), COX4, MMP and adenosine triphosphate (ATP) were increased
*Beclin-1↑,
*p62↑,
*COX2↑,
*MMP↑,
*ATP↑,
*GSH↑, activity of antioxidant proteins glutathione (GSH), catalase (CAT), GSH-PX in the FMN treatment group recovered, and the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) decreased.
*Catalase↑,
*GPx↑,
*MDA↓,
*antiPs↑, it was found that the interferon (IFN) signaling pathway was inhibited, which could effectively reduce the expression of related inflammatory chemokines, and significantly improve the erythema, scales and thickness of skin lesions in the psoriasis m
*AntiDiabetic↑, FMN effectively mitigated alloxan-induced pancreatic β-cell and DNA damage, lowered blood glucose levels, and increased insulin content.
*glucose↓,
*Insulin↑,
*GutMicro↑, FMN could act as a prebiotic to regulate intestinal microbial flora, thereby improving host metabolism and preventing obesity
*Obesity↓,
COX2↓, FMN effectively inhibited the proliferation of KYSE170 and KYSE150 cells by significantly reducing the mRNA and protein expression levels of COX-2 and cyclin D1, while inducing G1 phase arrest.
cycD1/CCND1↓,
TumCCA↑,
EGFR↓, FMN binds to both WT and mutant EGFR, reducing EGFR kinase activity and inhibiting downstream signaling.
GSK‐3β↑, This, in turn, activated GSK-3β and decreased the expression of myeloid leukemia sequence 1 (Mcl-1), without causing significant toxicity to the vital organs of mice.
Mcl-1↓,
*toxicity↓,
TumCP↓, FMN inhibited the proliferation and growth of cervical cancer cells by inhibiting the expression of HIF-1-α and VEGF.
Hif1a↓,
VEGF↓,
ERK↓, can achieve antiproliferative and invasive effects through effective inhibition of the oncogenic ERK1/2 pathway and the Lamin A/C signaling pathway,
LAMs↓,
Cyt‑c↑, FMN, as a candidate anticancer drug, could release cytochrome C (cyto C) directly through the mitochondrial pathway and activate the cascade reaction of caspase-9, caspase-3 and PARP, which ultimately lead to FaDu cell death
Casp9↑,
Casp3↑,
PARP↑,
TumCD↑,
mitA↑, FMN inhibited mitosis by inactivating the BACH1/p53 signaling pathway, promoted the release of cyto C
BACH1↓,
P53↓,
ROS↑, FMN delivered ROS to mitochondria to release cyto C and activated caspase-3 and caspase-9 cascade reactions to induce apoptosis in MCF7 cells
PD-1↓, FMN has the potential to serve as a PD-1/PD-L1 inhibitor for clinical use
NF-kB↓, FMN mainly interfered with PD-L1 activation by inhibiting the STING-NF-κB signaling pathway
*Bacteria↓, possess other pharmacological activities, such as antibacterial, antiviral, and antiallergic
*AntiViral↑,
*mt-ROS?, FMN effectively reduced the accumulation of ROS and mitochondrial damage in hair cells by activating the PI3K/AKT-Nrf2 signaling pathway, restored the balance of GSH/GSSG.
*PI3K↓,
*chemoP↑, FMN was a potential therapeutic agent for cisplatin-induced ototoxicity.
ChemoSen↑, Therefore, combination therapy had better control effects on multiple targets and a lower risk of drug resistance, which had great application prospects for treating cancer.
eff↑, combination of FMN (30 μM) and sulforaphane (20 μM) exhibited a significant synergistic effect
*toxicity↓, Therefore, it was proved that FMN was safe and non-toxic and could be used for pharmacological and therapeutic purposes.
*BioAv↑, water solubility problem of FMN, succinylated FMN using Bacillus amyloliquefaciens FJ18 to form the compound FMN-7-O-β-D (6″-O-succinyl)-D-glucoside (FMP), which compared to FMN, the water solubility was increased more than 106-fold.
*BioAv↑, To solve those problems, structural modification and nano-delivery systems can be used as a promising solution
*eff↑, FMN can be combined with other treatments, such as immunotherapy, to enhance the therapeutic effect and improve the prognosis of patients;


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↑, 1,   ROS↑, 3,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

HK2↓, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   Casp↑, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 1,   Mcl-1↓, 1,   TumCD↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,   P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   mitA↑, 3,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1,   GSK‐3β↑, 1,  

Migration(tgid=13) ⓘ

BACH1↓, 1,   LAMs↓, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT4↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   PD-1↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↝, 1,   ChemoSen↑, 3,   Dose↝, 1,   eff↑, 1,   RadioS↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,  

Functional Outcomes(tgid=23) ⓘ

NP/CIPN↓, 1,   TumVol↓, 1,  
Total Targets: 40

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   HO-1↓, 1,   Keap1↝, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   mt-ROS?, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 1,   ATP↑, 1,   Insulin↑, 1,   MMP↑, 1,   PGC-1α↝, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   glucose↓, 1,  

Cell Death(tgid=5) ⓘ

Casp3↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

PARP1↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

PI3K↓, 1,  

Migration(tgid=13) ⓘ

VCAM-1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↑, 1,   IL18↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   pol-M2 MC↑, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   AChE↓, 1,   BDNF↑, 1,   NGF↑, 1,   p‑tau↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1,   antiPs↑, 1,   chemoP↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 1,   Obesity↓, 1,   toxicity↓, 2,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 1,  
Total Targets: 54

Scientific Paper Hit Count for: mitA, Mitotic arrest
1 Diclofenac
1 Fenbendazole
1 Formononetin
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

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