FIS1 Cancer Research Results

FIS1, Mitochondrial fission 1 protein: Click to Expand ⟱
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FIS1 — Mitochondrial fission 1 protein
FIS1 is a mitochondrial outer-membrane fission adaptor/receptor linked to DRP1-mediated mitochondrial dynamics. In cancer, FIS1 is an emerging target because mitochondrial fission supports proliferation, survival adaptation, metastatic behavior, and tumor-initiating/stem-like phenotypes in some models. Recent TNBC evidence suggests FIS1 is required for expansion of tumor-initiating cells and that FIS1 loss suppresses TIC activity without broadly collapsing mitochondrial function, making it a potentially more selective mitochondrial dynamics target than global DRP1 inhibition.

-Often pro-tumor, Supports mitochondrial fragmentation/dynamics in stress-adapted cells

FIS1 is relevant to Alzheimer’s disease as part of the pathological mitochondrial fission program. AD models and human tissue studies show an imbalance toward mitochondrial fission, involving increased DRP1 and FIS1 and reduced fusion proteins such as MFN1, MFN2, and OPA1. Aβ and phosphorylated tau are linked to abnormal DRP1-mediated mitochondrial fragmentation, and increased DRP1/FIS1 interaction has been reported in Aβ-treated neurons and AD patient-derived fibroblasts.
-Direction: Usually increased or overactive in AD-like pathology

Natural Product Reported FIS1 / Fission Effect Evidence Strength for FIS1 Cancer Relevance Database Classification Suggested Note
Curcumin Reported to decrease FIS1 and DRP1-associated mitochondrial fission in several mitochondrial injury models. Moderate to strong Indirect; FIS1-specific cancer evidence is limited. FIS1/DRP1 mitochondrial fission down-modulator Best-supported natural product to link with FIS1, but still mostly non-cancer evidence.
EGCG Reported to decrease FIS1 or regulate the DRP1/FIS1 mitochondrial dynamics axis in neuroprotection and injury models. Moderate Indirect; stronger evidence for mitochondrial quality control than cancer-specific FIS1 targeting. Possible FIS1 down-modulator Useful to tag under mitochondrial fission, mitophagy, and oxidative-stress adaptation.
Urolithin A Reported to decrease FIS1 and DRP1 while improving mitophagy and mitochondrial quality control. Moderate Indirect; mostly neurodegeneration/mitophagy evidence. FIS1/DRP1-associated mitochondrial quality-control modulator Better classified under mitophagy and mitochondrial quality control
Melatonin Often reported to reduce pathological DRP1/FIS1-mediated mitochondrial fission, but effects can be context-dependent. Moderate Indirect; cancer relevance is complex and context-dependent. Context-dependent mitochondrial dynamics modulator “normalizes mitochondrial dynamics” rather than simple FIS1 inhibition.
Resveratrol Can reduce pathological DRP1/FIS1 fission in some injury models, but may increase Fis1/Drp1 expression in aging-repair contexts. Mixed Indirect; direction may vary by model and dose. Context-dependent FIS1/DRP1 modulator not a simple FIS1 inhibitor; more a mitochondrial dynamics normalizer.
Quercetin Associated with FIS1 targeting in omics/computational studies; direct experimental FIS1 modulation is weaker. Weak to moderate Indirect; not validated as a FIS1-targeted anticancer compound. Putative FIS1-associated modulator Suitable as a low-confidence or “possible” FIS1 link.
Sulforaphane Inhibits mitochondrial fission mainly through DRP1-related mechanisms; direct FIS1 modulation is unclear. Weak for FIS1 specifically Indirect; relevant to cancer metabolism and oxidative stress, but not FIS1-specific. Broader DRP1/fission pathway modulator mitochondrial fission rather than direct FIS1 modulation.
Berberine Reported to inhibit DRP1-mediated mitochondrial fission; FIS1 is mainly implicated as part of the pathway rather than directly modulated. Weak for FIS1 specifically Indirect; potentially relevant to cancer metabolism but not validated through FIS1. Broader DRP1/fission pathway modulator not a direct FIS1 modulator unless using a broader mitochondrial fission category.


Scientific Papers found: Click to Expand⟱
6409- CUR,    Curcumin prevents cisplatin-induced renal alterations in mitochondrial bioenergetics and dynamic
- in-vivo, Nor, NA
*FIS1↓, curcumin prevented the increase of mitochondrial fission 1 protein (FIS1), the decrease of optic atrophy 1 protein (OPA1) and the decrease of NAD+-dependent deacetylase sirtuin-3 (SIRT3)
*SIRT3↑,
*PTEN↓, as well as the increase in the mitophagy associated proteins parkin and phosphatase and tensin homologue (PTEN)-induced putative kinase protein 1 (PINK1).
*chemoP↑, In conclusion, the protective effect of curcumin in cisplatin-induced AKI

6408- CUR,    Protective Effects of a Natural Product, Curcumin, against Amyloid β Induced Mitochondrial and Synaptic Toxicities in Alzheimer'S Disease
- in-vitro, AD, SH-SY5Y
*mtDam↓, Mitochondrial function and cell viability were elevated in curcumin treated cells.
*eff↓,
*eff↑, Further, the protective effects of curcumin were stronger in pretreated SHSY5Y cells than in post-treated cells, indicating that curcumin works better in prevention than treatment in AD-like neurons.
*FIS1↓, significantly increased in Drp1, by 2.0 fold (p=0.004), and in Fis1, by 2.1 fold (
*lipid-P↓, lipid peroxidation were found ( p=0.002) in Aβ treated relative to untreated cells (figure 4). However, sig- nificantly decreased levels were found in the curcumin treated cells ( p=0.02) relative to untreated cells.
*ATP↑, Significantly increased levels of ATP were found in cells treated with curcumin

6410- EGCG,    Evaluation of the neuroprotective effect of EGCG: a potential mechanism of mitochondrial dysfunction and mitochondrial dynamics after subarachnoid hemorrhage
- in-vitro, Nor, NA
*FIS1↓, EGCG ameliorated oxyhemoglobin (OxyHb)-induced impairment of mitochondrial dynamics by regulating the expression of Drp1, Fis1, OPA1, Mfn1, and Mfn2. EGCG dramatically lowered the expression of Drp1 and Fis1
*neuroP↑, EGCG increased the neurological score by decreasing cell death through the cyt c-mediated intrinsic apoptotic pathway.
*Ca+2↓, suggesting that EGCG blocked the Ca 2+ influx via L-type VGCC
*VGCC↝,
*ROS↓, Briefly, ROS increased from 2.15 ± 0.18 in the control group to 3.08 ± 0.31 in the OxyHb group ( p < 0.05 vs. control), and then reduced to 2.34 ± 0.22 in the EGCG group
*DNAdam↓, EGCG downregulated the mitochondrial DNA (mtDNA) copy number after SAH
*Apoptosis↓, EGCG inhibition of apoptosis after SAH

6411- EGCG,    Pharmacological and Genetic Approaches to Downregulate FIS1 Mitigate Neuropathic Pain
- in-vivo, Nor, NA
*FIS1↓, As expected, EGCG treatment significantly decreased the expression of FIS1 and DRP1 in the SC-DH of SNI mice, while it had no effect on the expression of MFF
*Pain↓, downregulation of FIS1 expression within the SC-DH restored mitochondrial morphology and function, thereby exerting analgesic effects in neuropathic pain.
*ROS↓, It is noticed that EGCG, the main bioactive component of catechins, can improve mitochondria and cell function by inhibiting ROS-induced ferroptosis

6412- Uro,  EGCG,    A Combination Therapy of Urolithin A+EGCG Has Stronger Protective Effects than Single Drug Urolithin A in a Humanized Amyloid Beta Knockin Mice for Late-Onset Alzheimer’s Disease
- in-vivo, AD, NA
*Aβ↓, The levels of amyloid beta (Aβ) 40 and Aβ42 are reduced in both treatments, however, the reduction is higher for combined treatment.
*eff↑, combined treatment of urolithin A+EGCG is effective and stronger, indicating that combined therapy is promising to treat late-onset AD patients.
*cognitive↑, Recent familial AD mouse models revealed that urolithin A ameliorated cognitive impairment, prevented neuronal apoptosis and enhanced neurogenesis in APP/PS1 mice.
*neuroG↑,
*BBB↑, reported that EGCG bypassed the blood–brain barrier (BBB)
*TNF-α↓, EGCG was able to suppress the expression of TNFα, IL-1β, IL-6
*IL1β↓,
*IL6↓,
*p‑tau↓, EGCG was able to enhance the clearance of AD-related phosphorylated tau species, indicating that EGCG could be used as an adjuvant agent for AD treatment
*FIS1↓, decreased mRNA levels of fission genes Drp1 (by 1.96-fold) and Fis1 (by 2.32-fold) were observed in urolithin A-treated hAbKI mice relative to untreated mice. (urolithin A+EGCG) showed similar activities, but fold changes were higher
*ATP↑, Indicating that urolithin A and urolithin A+EGCG boost mitochondrial ATP.
*lipid-P↓, combination treatment of urolithin A+EGCG, the lipid peroxide levels were significantly reduced


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

FIS1↓, 5,  

Redox & Oxidative Stress ⓘ

lipid-P↓, 2,   ROS↓, 2,   SIRT3↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 2,   mtDam↓, 1,  

Cell Death ⓘ

Apoptosis↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

neuroG↑, 1,   PTEN↓, 1,   VGCC↝, 1,  

Migration ⓘ

Ca+2↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   IL6↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   eff↑, 2,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   cognitive↑, 1,   neuroP↑, 1,   Pain↓, 1,  
Total Targets: 25

Scientific Paper Hit Count for: FIS1, Mitochondrial fission 1 protein
3 EGCG (Epigallocatechin Gallate)
2 Curcumin
1 Urolithin
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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